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BACKGROUND: Fluid shear stress plays an important role in osteoblast proliferation and apoptosis. However, whether Caveolin-1 is involved in the process of fluid shear stress-induced proliferation and apoptosis in osteoblasts is unknown. OBJECTIVE: To explore the role of Caveolin-1 in fluid shear stress-regulated osteoblast proliferation and apoptosis. METHODS: The MC3T3-E1 osteoblasts in good growth status were selected and loaded with fluid shear stress at an intensity of 1.2 Pa for different times (0, 30, 60, 90 minutes). The expression of Caveolin-1 protein was observed and conditions with a time of 60 minutes were screened for the experiment. MC3T3-E1 cells were divided into control group, fluid shear stress group, fluid shear stress+pcDNA 3.1 group (control), fluid shear stress+pcDNA Cav-1 group (plasmid overexpression), and intervened with fluid shear stress and overexpression of Cav-1, respectively. The expression of molecules related to proliferation and apoptosis in MC3T3-E1 cells was detected by qRT-PCR and western blot. In addition, the proliferative activity of MC3T3-E1 cells was detected by cell counting kit-8 and EdU assay; and cell apoptosis was detected by Hoechst 33258 and flow cytometry. RESULTS AND CONCLUSION: The expression of Caveolin-1 in MC3T3-E1 cells was significantly down-regulated after loading fluid shear stress, and the expression level was lowest after 60 minutes. Overexpression of Caveolin-1 attenuated the proliferation-promoting and apoptosis-suppressing effects of fluid shear stress in MC3T3-E1 cells. In conclusion, Caveolin-1 has a vital role in fluid shear stress-regulated osteoblast proliferation and apoptosis, which may offer a potential therapeutic strategy for osteoporosis. [ABSTRACT FROM AUTHOR]

Caveolin-1 (CAV1) is a structural protein of caveolae on the plasma membrane and is an important regulatory factor for liver function. CAV1 regulates hepatic lipid deposition, lipid and glucose metabolism, mitochondrial function, and hepatocyte proliferation through various molecular pathways. Therefore, CAV1 plays a crucial role in maintaining liver physiology during the metabolic regulatory processes such as hepatic steatosis and hepatocyte proliferation. Furthermore, CAV1 is also involved in the development and progression of different types of liver injury, hepatitis, and liver cirrhosis. This article reviews the role of CAV1 in liver-related diseases and its mechanism in the regulation of liver macrophages, so as to provide a theoretical basis for targeting CAV1 in the treatment of liver-related diseases. [ABSTRACT FROM AUTHOR]

Objective: To investigate the effects of hyperbaric oxygen therapy at different time windows on serum tight junction protein (ZO-1), caveolin-1 (Caveolin-1) and Toll-like receptor 4 (TLR4) /nuclear transcription factor-κB (NF-κB) signaling pathway in patients with acute cerebral infarction (ACI) . Methods: 158 ACI patients who were treated in The First Affiliated Hospital of Air Force Military Medical University from April 2020 to April 2023 were selected as the research objects, patients were divided into group A (accept routine treatment, hyperbaric oxygen therapy was given within 12 h～7 d after the onset of the disease) and group B (accept routine treatment, hyperbaric oxygen therapy was performed within 12 h onset) by random number table method, with 79 cases in each group.The changes of each scale score, cerebral blood perfusion, serum ZO-1, Caveolin-1 levels and TLR4/NF-κB signaling pathway related indicators were compared in two groups. Results: After treatment, the National Institutes of Health Stroke Scale (NIHSS) in group B was lower than that in group A, and the activity of daily living (ADL) score was higher than that in group A (P＜0.05) . After treatment, the cerebral vascular reserve capacity (CVR), bilateral cerebral artery peak flow velocity and bilateral cerebral artery peak average flow velocity in group B were higher than those in group A (P＜0.05) . After treatment, serum Caveolin-1 in group B was lower than that in group A, and serum ZO-1 was higher than that in group A (P＜0.05) . After treatment, TLR4 and NF-κB in group B were lower than those in group A (P＜0.05) . Conclusion: Hyperbaric oxygen therapy in ACI patients within 12 hours of onset can effectively promote the recovery of neurological function and regulate the levels of serum ZO-1 and Caveolin-1, which may be relate to the inhibition of TLR4/NF-κB signaling pathway activation. [ABSTRACT FROM AUTHOR]

Caveolin-1 ( Cavl) is a structural protein component of the Caveolae and a major regulator of a variety of signaling molecules involved in a variety of cellular processes including signal transduction, endocytosis, cholesterol distribution and cell migration, and is a candidate target for the prevention and treatment of many diseases. With further research, the role of Cavl in maintaining bone metabolic balance was also discovered. In this paper, the gene structure and protein structure of Cavl were reviewed, and the regulatory mechanism of Cavl on bone metabolism was respectively summarized from osteogenic and adipogenic differentiation of Mesenchymal Stem Cells ( MSCs) and osteoclastic differentiation of Hematopoietic Stem Cells ( HSCs). [ABSTRACT FROM AUTHOR]

Objective To explore the effects and mechanism of caveolin-1 on the senescence-associated secretory phenotype （SASP), such as matrix metalloproteinase （MMPs), tissue factor （TF), interleukin-6（IL-6), interleukin-8 （IL-8), and tumor necrosis factor-α（TNF-α) in senescent macrophages induced by oxidized low-density lipoprotein （ox⁃ LDL). Methods The macrophages infected with Ctrl shRNA or Cav1 shRNA were treated with oxLDL or equal volume of PBS for 24 h, and β-galactosidase staining was used to assess the cell senescence. Transwell assay was used to observe cell migration ability. The expression levels of matrix metalloproteinases （MMPs) and TF protein in macrophages were de⁃ tected by Western blotting. The secretion content of IL-6, IL-8, and TNF-α in supernatants was measured by ELISA. The macrophages were infected with Cav1 shRNA or cotreated with mitogen-activated protein kinase p38（p38MAPK) specific agonist P79350, and the expression of p-p38 phosphorylation protein in macrophages was assayed by Western blotting. Results OxLDL induced the senescence of macrophages and activated p38 MAPK signaling pathway, with the increase of cell migration. After down-regulating the expression of caveolin-1 virus infection, the p38 MAPK signaling pathway was inhibited, the cell senescence decreased, the expression of MMP-9, MMP-2, and TF protein in cells de⁃ creased and the content of IL-6, IL-8, and TNF- α in supernatants decreased, with statistically significant differences （all P<0. 05). Treatment with the p38 MAPK specific agonist P79350 reversed the effect of the decrease in SASP follow⁃ ing down-regulation of caveolin-1. Conclusions Caveolin-1 may attenuate migration of the senescent macrophages, inhibit the release of inflammatory cytokines, and decrease the formation of SASP via activating the p38 MAPK signaling pathway. [ABSTRACT FROM AUTHOR]

BACKGROUND: Caveolin-1 is widely distributed in various kinds of cells, such as endothelial cells, epithelial cells, and vascular smooth muscle cells, and plays an important role in promoting endothelial cell proliferation and angiogenesis. Therefore, it has been increasingly highlighted in ischemic diseases. OBJECTIVE: To explore the effects of caveolin-1 on cardiac microvascularization, ventricular remodeling and mitochondrial respiratory function in rats with myocardial infarction based on angiotensin 1-7 signaling pathway. METHODS: Sixty male Sprague-Dawley rats were randomly divided into normal group (group A), model (group B), empty transfection (group C), Caveolin-1 transfection (group D) and triazamidine (an angiotensin converting enzyme 2 agonist; group E), and combination group (Caveolin-1+triazamidine), with 10 rats in each group. Administration in each group was given via the caudal vein, once a day, beginning at 12 hours after modeling. The left coronary artery ligation method was adopted to establish myocardial infarction models in the latter five groups. After 28 days of injection, cardiac function of rats was detected by color Doppler ultrasound, microvascular density was detected by cardiac gel ink staining, and pathological morphology of myocardial tissue was detected by hematoxylin-eosin staining. Mitochondrial respiratory function was detected by oxygen electrode method. The expression of Caveolin-1, angiotensin 1-7 signaling pathway and cardiac microvascular related indicators were detected by western blot assay. RESULTS AND CONCLUSION: Compared with group A, the cardiac function of rats in group B was significantly reduced (P < 0.05). Compared with group B, the cardiac function of rats in groups D-F was improved to different extents (P < 0.05). The cardiac function of rats was better in group F than groups D and E (P < 0.05). Compared with group A, rats in group B had damaged myocardial structure, irregular arrangement of myocardial cells, markedly inflammatory cell infiltration, and significantly decreased cardiac microvessel density (P < 0.05). Compared with group B, rats in groups D-F showed significantly improved myocardial pathomorphology and increased cardiac microvessel density (P < 0.05). The cardiac microvessel density in group F was higher than that in groups D and E (P < 0.05). Compared with group A, state 3 respiration level and respiratory control rate were significantly decreased in group B (P < 0.05), while state 4 respiration level was significantly increased (P < 0.05). Compared with group B, state 3 respiration level and respiratory control rate in groups D-F were increased (P < 0.05), while state 4 respiration level was decreased (P < 0.05). Compared with groups D and E, state 3 respiration level and respiratory control rate were increased in group F (P < 0.05), while state 4 respiration level was decreased (P < 0.05). Compared with group A, group B had significantly downregulated expressions of Caveolin-1, angiotensin converting enzyme 2, angiotensin 1-7, MAS receptor and platelet endothelial cell adhesion molecule-1 protein (P < 0.05). Compared with group B, the expressions of above proteins in groups D-F were significantly increased (P < 0.05); and compared with groups D and E, the expressions of above proteins in group F were significantly increased (P < 0.05). To conclude, Caveolin-1 can effectively improve cardiac microvessel density, ventricular remodeling and mitochondrial respiratory function in rats with myocardial infarction. The mechanism may be related to the targeted regulation of angiotensin 1-7 signaling pathway. [ABSTRACT FROM AUTHOR]

Objective: To explore the predictive value of intracranial pressure parameters combined with serum caveolin-1 and aquaporin-4（AQP-4） on the poor prognosis of patients with hypertensive intracerebral hemorrhage （HICH） after operation. Methods: 106patients with HICH who were admitted to Hebei Provincial Chest Hospital from January 2020 to January 2022 were selected, and the patients were followed up for 3 months after operation. The patients were divided into good prognosis group（55 cases） and poor prognosis group（51 cases） according to Glasgow Outcome Scale （GOS） score. Intracranial pressure parameters [pressure response index （PRx）, mean wave amplitude （MWA） and intracranial pressure dose under the threshold of 20 mm Hg（Dicp20） ]were monitored after operation, and serum caveolin-1 and AQP-4 levels were detected. Multivariate logistic regression was used to analyze the factors of poor prognosis in patients with HICH after operation. The value of intracranial pressure parameters combined with serum caveolin-1 and AQP-4 in predicting postoperative poor prognosis of patients with HICH was analyzed by receiver operating characteristic curve （ROC）.Results: The PRx, MWA, Dicp20 and serum caveolin-1, AQP-4 levels in the poor prognosis group were higher than those in the good prognosis group （P ＜0.05）. Low preoperative Glasgow coma score （GCS） score, high PRx, high Dicp20, high caveolin-1 and high AQP-4 were risk factors for poor prognosis of HICH（P＜0.05）. The area under the curve of combining PRx, Dicp20, caveolin-1 and AQP-4 to predict poor prognosis of HICH patients at 3 months after operation was 0.823, which was larger than that predicted by PRx,Dicp20, caveolin-1 and AQP-4 alone. Conclusion: High PRx, Dicp20, caveolin-1 and AQP4 are risk factors for postoperative poor prognosis in patients with HICH, and the combination of intracranial pressure parameters PRx, Dicp20 and serum caveolin-1, AQP4 has a high value in predicting postoperative poor prognosis in patients with HICH. [ABSTRACT FROM AUTHOR]

Objective To investigate the effect of miR-192 on proliferation, migration and extracellular matrix of mesangial cells under high glucose condition. Methods Human mesangial cells were cultured in vitro for 24 h and divided into six groups: the normal glucose concentration (NG, 5.6 mmol/L glucose) group, the high glucose concentration (HG, 25 mmol/L glucose) group, the normal glucose concentration+miR-192 mimics (NG+mimics) group, the high glucose concentration+miR-192 mimics (HG+ mimics) group, the normal glucose concentration+miR-192 inhibitor (NG+inhibitor) group and the high glucose concentration+miR-192 inhibitor (HG+inhibitor) group. After 24 h of intervention, cell viability was detected by CCK-8 assay, the cell migration ability was detected by Scratch healing test, and expression levels of miR-192, caveolin 1 (CAV-1), epidermal growth factor (EGF), collagen type 1 (COLⅠ) and fibronectin (FN) mRNA and related proteins were detected by qPCR and Western blot assay. Results Compared with the NG group, the proliferation and migration rates were increased, the expression levels of EGF, FN and COLⅠmRNA and protein were increased, and the expression of CAV-1 mRNA and protein decreased in the HG group (all P＜0.05). When miR-192 inhibitor was added to the NG group and the HG group, the cell proliferation and migration were decreased, the expression of EGF, FN and COLⅠ mRNA and protein were decreased, while the expression levels of CAV-1 mRNA and protein were increased (all P＜0.05). Changes were more significant in the HG group after the addition of miR-192 inhibitor. After adding miR-192 mimics to the NG group and the HG group, the cell proliferation and migration increased, expression levels of EGF, FN and COLⅠ mRNA and protein increased, and the expression of CAV-1 decreased (all P＜0.05). Conclusion High glucose increases the proliferation and migration of glomerular mesangial cells through miR-192-CAV-1-EGF pathway, leading to the formation of extracellular matrix and participating in the occurrence and development of diabetic nephropathy. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Modern Laboratory Medicine is the property of Journal of Modern Laboratory Medicine Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

BACKGROUND: Previous studies have shown the up-regulated expression of calcium-sensitive receptors in the neonatal mouse model of persistent pulmonary hypertension. The up-regulation trend is more obvious in the calcium-sensitive receptor agonist group, while the expression is declined somewhat in the calcium-sensitive receptor inhibitor group. OBJECTIVE: To explore the mechanism of calcium-sensitive receptors in pulmonary remodeling in neonatal mice with hypoxia-induced persistent pulmonary hypertension. METHODS: Eighty newborn C57BL/6 mice were randomly divided into four groups. Mice in the hypoxic group, the hypoxic+agonist group (hereinafter referred to as agonist group), and the hypoxic+antagonist group (hereinafter referred to as antagonist group) were placed in a hypoxic chamber simultaneously (oxygen concentration 12%). In addition, the agonist and antagonist groups were given intraperitoneal injection of calcium-sensitive receptor agonist GdCl3 (16 mg/kg) and inhibitor NPS2390 (1 mg/kg) once a day respectively. Mice in the normoxia group were exposed to air and injected with the same amount of normal saline daily as that in the hypoxic group. After 14 days, heart and lung tissues were removed. The thickness of ventricular wall and pulmonary vascular wall was measured and alveolar morphology was observed. The level of B-type brain natriuretic peptide was determined by enzyme linked immunosorbent assay. Western blot and immunohistochemistry were used to detect the expression and localization of caveolin-1 protein in mouse lung tissue, and qRT-PCR was used to detect the expression of caveolin-1 mRNA. The study protocol was approved by the Experimental Animal Ethic Committee of the First Affiliated Hospital of Shihezi University School of Medicine (approval No. 2018-172-01). RESULTS AND CONCLUSION: After 14 days of hypoxia, the wall thickness of small pulmonary arterioles in mice increased, and the thickness ratio of right ventricle to left ventricle and B-type brain natriuretic peptide level increased in the hypoxic group compared with the normoxia group. The average alveolar lining interval was widened and the radial alveolar count decreased in the hypoxic group compared with the normoxia group. Western blot and qRT-PCR results showed that the expression levels of caveolin-1 protein and mRNA were up-regulated hypoxic group compared with the normoxia group (P < 0.05). These changes were more significant in the agonist group (P < 0.05), while the inhibitor group reversed the changes caused by hypoxia (P < 0.05). To conclude, calcium-sensitive receptor affects the vascular remodeling in the lung of neonatal mice with persistent pulmonary hypertension, and the mechanism may be related to the changes in the caveolin-1 expression. [ABSTRACT FROM AUTHOR]

Objective To investigate the relationships between serum Caveolin-1, Caspase-3 and early neurological deterioration (END) in patients with acute ischemic stroke (AIS) . Methods Totally 148 patients with AIS were selected as the AIS group, and then they were divided into the END group (n=57) and non-END group (n=91) according to whether they had END. Fifty-three healthy people were selected as the control group in the same period. The clinical data of each group were collected, and the serum Caveolin-1 and Caspase-3 were detected by enzyme-linked immunosorbent as⁃ say. Multivariate Logistic regression analysis was used to analyze the influencing factors of END in AIS patients, and the receiver operating characteristic curve was used to analyze the predictive value of serum Caveolin-1 and Caspase-3 levels for END in AIS patients. Results The levels of serum Caveolin-1 and Caspase-3 in the AIS group were higher than those in the control group (both P<0. 05). National Institutes of Health Stroke Scale (NIHSS) score, blood glucose, Caveolin-1 and Caspase-3 were the influencing factors for END in AIS patients (all P<0. 05). The area under the curve of Caveolin-1 combined with Caspase-3 in predicting END in AIS patients was greater than that of either one alone (P<0. 05). Conclusion The elevated levels of serum Caveolin-1 and Caspase-3 in patients with AIS are independent risk factors for the occurrence of END, and they can be used as predictors of the occurrence of END. [ABSTRACT FROM AUTHOR]

Objective: To investigate the correlation between the levels of caveolin-1 (Caveolin-1), vascular endothelial calcherin (VE-cadherin), CXC-chemokine ligand 5 (CXCl-5) in cerebrospinal fluid and inflammatory factors in children with bacterial meningitis (BM), and to analyze the diagnostic value of Caveolin-1, VE-cadherin and CXCl-5 in BM. Methods: 106 cases of BM children (BM group), 76 cases of viral meningitis (VM group) and 72 cases of children without nervous system injury (control group) who were admitted to our hospital from January 1, 2016 to May 1, 2020 were selected. The levels of Caveolin-1, VE-cadherin and CXCl-5 in the cerebrospinal fluid of children in BM group and VM group were detected, and the levels of tumor necrosis factor-α(TNF-α), procalcitonin (PCT), C-reactive protein (CRP) and interleukin-6 (IL-6) in serum of the three groups were detected. Pearson correlation analyzed the relation between Caveolin-1, VE-cadherin, CXCl-5 and TNF-, PCT, CRP, IL-6 correlation. Receiver operating characteristic curve (ROC) analyzed the value of Caveolin-1, VE-cadherin and CXCl-5 in the diagnosis of BM. Results: The levels of Caveolin-1, VE-cadherin and CXCl-5 in cerebrospinal fluid in BM group were higher than those in VM group (P<0.05), the levels of serum TNF-α, PCT, CRP and IL-6 were higher than those in VM group and control group (P<0.05), and the levels of serum TNF-α, PCT, CRP and IL-6 in VM group were higher than those in control group (P<0.05). The levels of Caveolin-1, VE-cadherin and CXCl-5 in cerebrospinal fluid in BM group were positively correlated with the levels of serum TNF-α, PCT, CRP and IL-6 (P<0.05). ROC curve analysis showed that the area under the curve (AUC) of combined Caveolin-1, VE-cadherin and CXCl-5 in diagnosis of BM was 0.888, which was higher than that of single diagnosis of above indicators of 0.690, 0.661, 0.639 respectively. Conclusion: The levels of Caveolin-1, VE-cadherin and CXCl5 in cerebrospinal fluid of children with BM are higher than those of VM, which may play a role in the pathogenesis of BM through mediating the inflammatory response of nervous system. Combined with these three indicators have high value in the differential diagnosis of BM. [ABSTRACT FROM AUTHOR]

Copyright of Progress in Modern Biomedicine is the property of Publishing House of Progress in Modern Biomedicine and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: To explore whether Huangqi-Honghua combination protect brain from cerebral ischemia reperfusion injury through promoting angiogenesis by inducing the Cav-1/VEGF(Caveolin-1/vascular endothelial growth factor) signal pathway. Methods:Sixty rats were randomly divided into five groups: control group, model group and Huangqi-Honghua 40:1, 20:1, 5:1 groups(12 rats per group). The rat cerebral ischemia reperfusion injury models were induced by nylon monofilament. After 21 days of administration, the neurological scores were evaluated, the infarct volumes were calculated. Immunohistochemical method was used to detect the microvessel density(MVD) in brain tissue. RT-PCR and Western-blotting was used to detect the m RNA and protein expression levels of Cav-1 and VEGF. Results: After 21 days of administration, the neurological scores of each group were decreased, especially the Huangqi-Honghua groups(P<0.01), and infarct volume(P<0.05~ P<0.01)in Huangqi-Honghua groups were significantly lower than the model group. Compared with model group, the level of MVD, Cav-1 and VEGF m RNA and protein expression levels were significantly higher in Huangqi-Honghua treatment group(P<0.05~ P<0.01). Conclusions: Huangqi-Honghua combination has protective against cerebral ischemia injury, the Cav-1/VEGF pathway may be involved and then promote the angiogenesis. Additionally, the best proportion of Huangqi-Honghua was 5:1. [ABSTRACT FROM AUTHOR]

Objective To investigate the effect of moxibustion on the expression of Caveolin-1, p38MAPK, and pp38MAPK in the articular cartilage of knee osteoarthritis (KOA) rabbits. Methods Forty rabbits were randomly divided into the control group, model group, moxibustion group, and blocker group. Except the control group, KOA models were established by injecting papain into articular cavities of rabbits in the other three groups. Moxibustion was carried out at Dubi point and Zusanli point in the moxibustion group, and p38 blocker S8203580 was injected into articular cavities of rabbits in the blocker group. Rabbits were sacrificed after 3 weeks of treatment to obtain the cartilage tissues, while the rabbits in the control group and model group were not treated. The expression levels of Caveolin-1, p38 MAPK, and p38 MAPK were detected by Western blotting. Results The relative expression levels of Caveolin-1 were 2. 09 ± 0. 07, 1. 45 ± 0. 05, and 1. 09 ± 0. 07, respectively, and the relative expression levels of p-p38 MAPK/p38 MAPK were 3. 25 ± 0. 08, 2. 52 ± 0. 17, and 2. 07 ± 0. 14, respectively, in the model group, moxibustion group and inhibitor group, which were higher than those of the control group (1. 00 ± 0. 05) (all P < 0. 05). Compared with the model group, the expression levels of Caveolin-1 protein and p38 MAPK protein activity in the cartilage of the moxibustion group and blocker group decreased (both P < 0. 05). Compared with the blocker group, the expression levels of Caveolin-1 protein and p38 MAPK protein activity in the cartilage of moxibustion group increased (both P < 0. 05). Conclusions The expression levels of Caveolin-1 and the activity of p38 MAPK protein decrease in the cartilage of KOA rabbits after moxibustion treatment. Inhibition of abnormal activation of Caveolin-1/p38 MAPK signal pathway may be one of the molecular mechanisms of moxibustion. [ABSTRACT FROM AUTHOR]

Objective To explore the effect of low-intensity pulsed ultrasound (LIPUS) on long bone fracture healing and to examine caveolin-1 gene expression in the radius defects of rabbits. Methods A total of 24 New Zealand rabbits with 3-mm bone defects at lower 1/3 in both radii were randomly assigned to 4 groups (n=6). Daily LIPUS treatment was performed to the right fracture sites at a intensity of 30 mW/cm2 for 20 minutes, while the left sites received sham treatment with power off. To assess the effects of LIPUS on bone defects, X-ray imaging and hematoxylin-eosin staining were applied 7,14,21,28 days after the surgery. Additionally,the immunohistochemical staining was used to determine the subcllular localization of caveolin-1 and semi-quantify the caveolin-1 level, qPCR was performed to detect the mRNA level of caveolin-1,gene Col2a1 and Col10a1, and osteocalcin. Results On day 14, the radiological score of the right radii and mineralized callus area were significantly higher than that of the left ones, both of them were elevated with time flied. Histological examination suggested that the differentiation and apoptosis of chondrocytes along with the formation and bridging of the bone trabeculas appeared earlier in the right radius defects. The immunohistochemical staining showed that on day 7 and 14, the level of caveolin-1 increased with the proliferation and differentiation of condrocytes, and was significantly higher in callus tissues on the right sites. On day 21 and 28, the mesenchymal stem cells migrated to the surface of cartilage matrix started to differentiate into osteoblasts, the level of caveolin-1 decreased, and was significantly lower on the right sites. The result of qPCR indicated that compared with the left sites the caveolin-1 gene expression on the right sites was significantly higher on day 7, while significantly lower on day 21. The mRNA expression levels of Col2a1, Col10a1 and osteocalcin on the right sites were significantly higher on day 7 and 14,but they were significantly lower on day 21 and 28, except for Col10a1 on day 28. Conclusions Advancing endochondral ossification is considered to be a crucial mechanism during long bone fracture healing promoted by LIPUS. The caveolin-1 gene expression first increased in the chondrocytes then decreased in the mesenchymal stem cells during the process. [ABSTRACT FROM AUTHOR]

As a kind of marker protein of caveolae, Caveolin-1 (Cav-1) mediates multiple physiological and pathological processes, including the formation of caveolae, vesicular transport, maintenance of the homeostasis of cellular cholesterol, signal transduction and tumor genesis. Cav-1 is extensively present in multiple lung cells, and it plays an extremely important role in acute lung injury (ALI). The morbidity and mortality of the severe stage of ALI, the acute respiratory distress syndrome (ARDS) are extremely high. In recent years, a lot of research has demonstrated that Cav-1 plays an essential role in the pathogenesis of ALI. This paper reviewed the relations between Cav-1 and ALI, as well as its role in the genesis and development of ALI. [ABSTRACT FROM AUTHOR]

Objective To investigate the effect of Cav1F92A modified rat bone marrow mesenchymal stem cells ( rBMSCs/ Cav1F92A ) on pulmonary vascular proliferation lesions in rats with pulmonary arterial hypertension ( PAH) and to explore its possible mechanism. Methods Forty Wister rats were randomly divided into the Cav1，Cav1F92A，PAH，and normal control groups with 10 in each. PAH was induced by intraperitoneal injection of 1% monocrotaline ( MCT) (60 mg/kg) in adult male Wistar rats in the Cav1，Cav1F92A，and PAH groups. Meanwhile，rats in the control group were injected with the same volume of normal saline. At week 2 after PAH models were established，1 mL rBMSCs/Cav1 and 1 mL rBMSCs/Cav1F92A(1 x 10#/mL) were transplantated into the rats of the Cav1 and Cav1F92A groups by tail vein injection， while rats in the PAH group were not treated. Rats in each group were sacrificed and the lung tissues were dissected after 3 weeks of transplantation. The changes of pulmonary vascular lumen and vessel wall thickness were observed under microscope by HE staining. The gene expression of Bbc3，B cell translocation of lung tissue 2 ( Btg2 ) ，Dab2，peroxisome proliferator activated receptor ( Ppard)，and Rock1 and leucine rich alpha-2 glycoprotein 1 ( Lrg1) in the lung tissues was detected by using real-time quantitative PCR. The protein expression of endothelin 1 ( ET-1 ) and smooth muscle myosin heavy chain ( Myocardin) was investigated by Western blotting. Results Compared with the normal control group，the pulmona-Z vascular lumen became narrow，nearly closed，and the vascular wall became hyperplastic and hypertrophic significantly in the PAH group. Compared with the PAH group，the thickening degree of pulmonary vascular wall was reduced in the Cav1 and Cav1F92A groups but more obviously decreased in the Cav1F92A group，but the pulmonary vascular wall was thicker than that in the normal control group. Compared with the normal control group，the relative mRNA expression of Bbc3 and Btg2 in the lung tissues of the PAH group decreased，but the mRNA expression of Dab2，Ppard， Rockl，and Lrgl relative ，and the protein expression of ET-1 and Myocardin increased ( all P<0.01 ). Compared with the PAH group， the Bbc3 and Btg2 mRNA expression increased but Dab2，Ppard，Rockl and Lrgl mRNA expression decreased in the Cav1 and Cav1F92A groups，especially in the Cav1F92A group ( P<0.05 or P<0.01) ； the Bbc3 and Btg2 mRNA expression in the lung tissues was higher than that in the PAH and Cav1 groups ( P<0.05 or P<0.01) . Compared with the PAH and Cav1 groups，the protein expression of ET-1 and Myocardin in the lung tissues decreased in the Cav1F92A group ( both P<0.01). Conclusion rBMSCs/Cav1F92A can effectively alleviate vascular proliferative lesions in PAH rats by up-regulating the expression of Bbc3 and Btg2，Ppard， Dab2，and Rock1，and down-regulating the expression of ET-1 and Myocardin，and thus inhibiting the vascular smooth muscle cell proliferation，fibrosis，and vascular contraction. [ABSTRACT FROM AUTHOR]

BACKGROUND: Caveolin-1, as the most important functional protein in caveolae, is involoved in a variety of cell biological processes, and is closely related to the occurrence and development of breast cancer. OBJECTIVE: To explore the effect of caveolin-1 on epidermal growth factor (EGF) in fibroblasts after co-cultured with breast cancer cells. METHODS: Caveolin-1 expression in fibroblast lines ESF-1 was interfered with siRNA, and the optimal effect was determined through QRT-PCR and western blot assay. (1) The optimal silencing model of ESF-1-Caveolin-1 SiRNA-N.2 was obtained, which was co-cultured with breast cancer cells BT474 as experimental group, single-cultured ESF-1 and ESF-1-Caveolin-1 SiRNA-N.2 as controls. The expression level of EGF in ESF-1 was detected by QRT-PCR at 24 and 48 hours of culture; the expression level of EGF in the culture medium was detected by ELISA at 48 and 72 hours of culture. (2) ESF-1-Caveolin-1 SiRNA-N.2 (experimental group) and ESF-1 (control group) were respectively co-cultured with BT474, and single-cultured BT474 as blank control group. The proliferation of BT474 was detected by cell counting-kit 8 assay after 24- and 48-hour culture. RESULTS AND CONCLUSION: The mRNA expression level of EGF in the experimental group was significantly higher than that in the other two groups (P < 0.05), and the EGF expression level in the ESF-1-Caveolin-1 SiRNA-N.2 group was significantly higher than that in the ESF-1 group (P < 0.05). The protein expression level of EGF was ranked as follows: experimental group > ESF-1-Caveolin-1 SiRNA-N.2 group > ESF-1 group (P < 0.05). The proliferation of BT474 cells was significantly increased after co-cultured with BT474 cells and ESF-1 siRNA Caveolin-1 cells, especially with BT474 cells (P < 0.05). Our findings suggest that Caveolin-1 siRNA can promote the expression of EGF in fibroblasts, especially co-cultured with breast cancer cells. Furthermore, caveolin-1 siRNA accelerates the proliferation of breast cancer cells after co-cultured with fibroblasts. [ABSTRACT FROM AUTHOR]

Objective To investigate the therapeutic effect and mechanism of Caveolin-1 (Cav1) mutant to F92ACav1 modified rat bone marrow mesenchymal stem cells (rBMSCs/F92A-Cav1) on rats with pulmonary hypertension (PAH). Methods PAH was induced by intraperitoneal injection of 1% monocrotaline (MCT, 60 mg/kg) in adult male Wistar rats. The PAH rats were randomly divided into four groups( 10 rats/group) after 2 weeks of MCT injection:PAH group (only MCT), Cav1 group( transduced with LV-Cav1 modified r BMSCs), F92A-Cav1 group (transduced with LV-F92A-Cav1 modified r BMSCs),and the control group. Gene modified r BMSCs (1 × 106/ml) were transplanted into PAH rats in each group by tail vein injection. After 3 weeks of transplantation,the percentage of media wall thickness (MT%) and right ventricular hypertrophy index( RVHI) were evaluated by Image-Pro Plus 6 software,serum NO concentration was checked by Griess method, and the expression of phosphoinositide 3-kinase (PI3K) and protein kinase B (AKT) was detected by Western blotting. Results MT%, RVHI, PI3K and AKT was all increased but NO was decreased in the PAH group as compared with that of the control group (P < 0. 05 or P < 0. 01). Compared with the PAH group, MT%, RVHI, PI3K and AKT was decreased but NO was increased in the Cav1 and F92A-Cav1 groups, especially in the F92A-Cav1 group (P < 0. 01). Conclusion F92A-Cav1 can abrogate the inhibitory effect of wild-type Cav1 on e NOS and promote the release of NO, then inhibit the activation of PI3K/Akt signaling pathway and thus exert its therapeutic effect on PAH rats. [ABSTRACT FROM AUTHOR]

Objectives: To observe the effect of electroacupuncture (EA) at "Jiaji"(EX-B2) on body mass, motor function, expression of caveolin-1 (Cav-1) in nucleus pulposus cells and annulus fibrosus tissue, telomerase activi-ty, relative telomere length and different cell cycle ratio of nucleus pulposus cells in rabbits with intervertebral disc degeneration(IVDD), so as to investigate its mechanism underlying delaying senescence of the degenerated lumbar intervertebral disc nucleus pulposus cells., Methods: Twenty-five male New Zealand rabbits with mature bones were divided into control, sham operation, model, EA, and acupuncture groups, with 5 rabbits in each group. The IVDD model was established by inserting kirschner wires to the vertebral bone surface between the lumbar (L)4 and L5 vertebrae, followed by applying continuous axial pressure for 28 d. EA (2 Hz/15 Hz, 1-2 mA) or acupuncture (only insertion of acupuncture needles into bilateral EX-B2, but without electrical stimulation) was applied to bilateral EX-B2 for 20 min, once daily, 6 times a week for 4 weeks. The hindlimb locomotor function (locomotor score) was assessed by using Faden's and colleagues' methods. The general conditions of rabbits in each group were observed, and their body weight changes were measured every week. Nucleus pulposus cells were isolated using enzyme digestion method. After the treatment, the Cav-1 positive cell counts in nucleus pulposus cells and annulus fibrosus tissues were detected by immunohistochemistry, and the telomerase activity of nucleus pulposus cells was detected by PCR-ELISA. The relative telomere length of nucleus pulposus cells was measured by real-time quantitative polymerase chain reaction (real-time qPCR), and the cell cycle of nucleus pulposus was detected by flow cytometry., Results: Compared with the sham operation group, the body mass from 4 to 11 week, locomotor score at 4, 7 and 11 week, telomerase activity, relative telomere length and the proportion of cells in G2/M phase of nucleus pulposus cells were significantly decreased ( P <0.01), while Cav-1 positive cell counts of nucleus pulposus and annulus fibrosus tissue, and the proportion of nucleus pulposus cells in the G0/G1 phase considerably increased ( P <0.01) in the model group. Relevant to the model group, the EA group rather than the acupuncture group had an increase in the body mass from 8 to 11 week, locomotor score at 11 week, telomerase activity, relative telomere length of nucleus pulposus cells, and the proportion of nucleus pulposus cells in G2/M phase ( P <0.01), and a decrease in the Cav-1 positive cell counts of nucleus pulposus and annulus fibrosus tissue and the proportion of cells in G0/G1 phase ( P <0.01). No significant differences were found between the model and acupuncture groups in all the indexes mentioned above., Conclusions: EA at EX-B2 has a bene-ficial effect in improving motor function in rabbits with IVDD, which may be related to its functions in reducing the expression of Cav-1 in nucleus pulposus cells and annulus fibrosus, improving cycle arrest, enhancing the telomerase activity and the relative telomere length of nucleus pulposus cells, delaying the senescence of nucleus pulposus cells of the degenerated lumbar intervertebral discs.

Objective: To investigate the expression of caveolin-1(Caveolin-1) in the lung tissue of rats with COPD and its correlation with airway remodeling. Methods: 20 cases of 10 week-old Wister rats were randomly divided into the control group and the experimental group, 10 rats in each group. The rats in control group were fed by normal feeding, while the rats in experimental group were fed by the method of smoking and lipopolysaccharide (LPS). All the rats were killed at feeding for 91 days and the lung function were measured. Then immunohistochemical method was used to detect the expression of caveolin-1 in lung tissue, and enzyme-linked immunosorbent adsorption test (ELISA) was used to detect the interleukin IL-8 (IL-8), tumor necrosis factor alpha (TNF-α) and transformation growth factor beta1 (TGF-β1) in lung tissue. The correlation of caveolin-1 expression with IL-8, TNF-αand TGF-β1 expression were analyzed. Results: Compared with the control group, the lung adaptation of rats in experimental group decreased, lung elastic resistance and airway resistance increased, the content of IL-8, TNF-αand TGF-β1 in lung tissue were significantly increased, the expression of caveolin-1 in the lung tissue was significantly decreased (P<0.05). There was negative correlation of the caveolin-1 expression with IL-8, TNF-α, TGF-β1 contents in the lung tissue. Conclusions: The expression of Caveolin-1 in the lung tissue of rats with COPD was significantly decreased, Caveolin-1 might promote the release of inflammatory cytokines and airway remodeling, further participated in the development of COPD. [ABSTRACT FROM AUTHOR]

Objective To explore the dynamic expression of caveolin-1 in rat hippocampus after diffuse axonal injury (DAI) and its role in activation of astroglia. Methods Western blot was used to determine the expression of caveolin-1 in the hippocampus after DAI; immunohistochemistry staining was used to determine the dynamic expression of GFAP in the hippocampus of rats after DAI. The expression and co-localization of caveolin-1 and GFAP in rats after DAI were evaluated by immunofluorescence staining at different time points. Results The expression of caveolin-1 significantly decreased after DAI, and continued to decline from day 1 to day 7 (P<0.05). Immunohistochemistry staining indicated that GFAP-positive cells significantly increased from day 1 to day 3, and slightly decreased at day 7 (P<0.05). The co-localization of caveolin-1 and GFAP revealed that the number of both caveolin-1- and GFAP-positive cells gradually increased. Conclusion Caveolin-1 expression significantly decreased with the increase of GFAP expression in the hippocampus of rats after DAI. Caveolin-1 may be involved in the dynamic expression of GFAP and play an important role in the activation of astroglia after DAI. [ABSTRACT FROM AUTHOR]

PURPOSE: To investigate the changes and the significance of caveolin-1 gene and protein in tongue squamous cell carcinoma(TSCC). METHODS: Immunohistochemical staining and in situ hybridization were used to detect the changes of caveolin-1 gene and the protein in 92 TSCCs and their adjacent normal tissues. The data were analyzed with SPSS10.0 software package. RESULTS: The expressions of caveolin-1 gene(24.6 ± 1.8) and its protein(471.2 ± 68.1) in TSCC were lower than those of the control group (167.2 ± 20.5, 964.5 ± 77.2), respectively. The difference was significant (P<0.01). The expression of caveolin-1 protein in well-differentiated TSCC(5.6 ± 1.4) was higher than that in moderately and poorly differentiated TSCC (1.3 ± 0.8); The expression of caveolin-1 protein in stage I -II patients(6.1 ± 2.0) was higher than that in stage III-IV patients (2.4 ± 0.7), and the difference was significant (P<0.01). There was no significant relationship between the expression of caveolin-1 protein and cervical lymph node metastasis(P>0.05). CONCLUSIONS: The level of caveolin-1 gene and the expression of the protein decrease in TSCC and the level of protein has a significant relationship with the clinical stage and the pathological grade, rather than the cervical lymph node metastasis. [ABSTRACT FROM AUTHOR]

Objective: To explore relationship between postoperative serum caveolin-1 contents after open reduction and internal fixation and delayed healing of tibial fracture patients., Methods: From April 2018 to June 2020, 134 tibial fracture patients underwent open reduction and internal fixation were included, and divided into delayed healing group and normal healing group according to fracture healing condition. Contents of serum caveolin-1 protein before operation, 1, 4, 8, 12 weeks after operation between two groups were compared. Influencing factors of delayed healing was analyzed by Logistic regression model, and predictive value of serum caveolin-1 protein on delayed healing was analyzed by receiver operating characteristic(ROC) curve., Results: Fracture healing was evaluated at 4 months after fracture, 93 patients healed well and 41 patients delayed heal. At 1, 4, 8 and 12 weeks, content of serum caveolin-1 protein in delayed healing group was lower than that of normal healing group( P <0.05). There were statistical difference in smoking, diabetes, open fracture and Gutlio Ⅲ fracture between delayed healing group and normal healing group( P <0.05). Smoking, diabetes, open fracture, Gustlio Ⅲ fracture, decrease of serum caveolin-1 protein at 4 and 8 weeks after operation were risk factor of delayed healing by Logistic analysis( P <0.05). By ROC curve analysis, content of serum caveolin-1 protein had predictive value for delayed fracture, the best cut-off values were 12.45 ng/ml and 12.52 ng/ml respectively, corresponding sensitivity were 45.34%, 43.90%, and specificity were 80.65% and 87.10% ( P <0.05)., Conclusion: Decrease of serum caveolin-1 protein content at 4 and 8 weeks after open reduction and internal fixation for tibia fracture patients were related with delayed healing. Detection of serum caveolin-1 protein content at 4 and 8 weeks after operation has predictive value for delayed healing.

To explore whether paeonol can play an anti-atherosclerotic role by regulating the expression of aortic caveolin-1 and affecting NF-κB pathway, so as to inhibit the inflammatory response of vascular endothelium in atherosclerotic rats. The atherosclerotic model of rats was induced by high-fat diet and vitamin D&#95;2. The primary culture of vascular endothelial cells(VECs) was carried out by tissue block pre-digestion and adherent method. The injury model of VECs was induced by lipopolysaccharide(LPS), and filipin, a small concave protein inhibitor, was added for control. HE staining was used to observe pathological changes of aorta. TNF-α, IL-6 and VCAM-1 were detected by ELISA. Western blot assay was used to detect the protein expression levels of caveolin-1 and p65 in aorta and VECs. The results showed that as compared with model group, paeonol significantly reduced aortic plaque area and lesion degree in rats, decreased the level of serum TNF-α, IL-6 and VCAM-1 in the rats and enhanced the relative expression level of caveolin-1, decreased p65 expression conversely(P&lt;0.05 or P&lt;0.01). In vitro, as compared to model group, paeonol obviously improved cell morphology, decreased the secretion of TNF-α, IL-6 and VCAM-1 in VECs, increased caveolin-1 expression, and decreased p65 protein expression(P&lt;0.05 or P&lt;0.01). Furthermore, filipin could reverse the effect of paeonol on expression of inflammatory factors and proteins(P&lt;0.05 or P&lt;0.01). According to the results, it was found that paeonol could play the role of anti-atherosclerosis by up-regulating the expression of caveolin-1 and inhibiting the activation of NF-κB pathway to reduce vascular inflammation in atherosclerotic rats.

CD36, the major scavenger receptor, is intimately involved in the uptake of oxLDL in macrophages. To further study the function of CD36 in macrophages, we constructed CD36 gene silence cell lines (J774A.1) by lentivirus-mediated RNA interference technique, and analyzed the effect of CD36 in caveolin-1 protein expression. At first, 5 shRNA fragments were designed and synthesized according to the coding sequence (CDS) region of CD36 gene. Next, the CD36-shRNA was inserted into lentiviral vector to yield pLKO.1-CD36-shRNA plasmid. After DNA sequencing, the pLKO.1-CD36-shRNA plasmid and psiCHECK-II-CD36 were co-transfected into the 293T cells to screen the efficient CD36-shRNA. The efficient CD36-shRNA plasmid and the helper plasmid were co-transfected into the 293T cells to package the lentivirus, and then infected the J774A.1 cells. After screening by puromycin, CD36 gene silence cell lines (J774A.1) was established. Western blotting and confocal fluorescence microscopy results showed that the CD36 silencing efficiency in the gene silence cell line was 90%. Accompanied by a decrease in CD36 protein on cell surface, oxLDL binding to CD36 was significantly inhibited, indicating that the CD36 gene silence cell line is successfully established. Finally, the oxLDL stimulation and inhibitor experiments results showed that the CD36 knockdown significantly suppresses the phosphorylation of JNK and ERK, thereby inhibiting the oxLDL-induced caveolin-1 protein expression, demonstrating that CD36 modulates the caveolin-1 protein expression through the JNK/ERK-mediated signaling transduction.

To aggressively proliferate and metastasize, cancer cells are in extreme need of energy supply and nutrients. Therefore, a promising cancer therapy strategy is developed to target its hallmark feature of metabolism. Recent findings revealed the regulatory role of caveolin-1 (Cav-1), a structural protein of caveolae, in cancer metabolism. And low Cav-1 expression in tumor stroma was proved to be a central player of cancer malignant phenotype. Here, we summarized the progressions of studies on Cav-1, mitochondria and cancer metabolism to indicate that the altered metabolism induced by Cav-1 and mitochondria association is a major cause of cancer malignant phenotype.

Objective: To investigate whether androgens can regulate the expression of eNOS in rat corpus cavernosum through AKT3, PIK3CA, CALM, and CAV1 and influence erectile function., Methods: Thirty-six 8-week-old male SD rats were randomly divided into groups A (4-week control), B (6-week control), C (4-week castration), D (6-week castration), E (4-week castration + testosterone replacement), and F (6-week castration + testosterone replacement). Both the testis and epididymis were removed from the rats in groups C, D, E and F, and on the second day after surgery, the animals of groups E and F were subcutaneously injected with testosterone propionate at 3 mg per kg of the body weight qd alt while all the others with isodose oil instead. At 4 weeks (for groups A, C and E) and 6 weeks (for groups B, D and F) after treatment, we detected the maximum intracavernous pressure (ICPmax), the mean carotid arterial pressure (MAP) and their ratio (ICPmax/MAP), measured the level of serum testosterone (T), and determined the expressions of eNOS, P-eNOS, AKT3, PIK3CA, CALM and CAV1 in the corpus cavernosum by Western blot and immunohistochemistry., Results: No statistically significant differences were observed in the body weight and MAP among different groups. The serum T level and ICPmax/MAP were remarkably lower in groups C and D than in the other four groups (P<0.01) as well as in groups E and F than in A and B (P<0.05) but exhibited no significant differences either between E and F or between A and B. Immunohistochemistry showed that eNOS and P-eNOS were mainly expressed in the vascular endothelial cell membrane and cavernous vascular lumen, while AKT3, PIK3CA, CALM and CAV1 chiefly in the vascular endothelial cell cytoplasm and membrane, with a few in the smooth muscle cells. Western blot analysis manifested that the expressions of eNOS, P-eNOS, AKT3, PIK3CA, CALM and CAV1 were markedly lower in groups C and D than in A, B, E and F (P<0.01) as well as in D than in C (P<0.05) but those in groups E and F did not showed any significant difference from those in A and B, nor E from F or A from B., Conclusions: Androgens can improve erectile function by upregulating the expressions of AKT3, PIK3CA, CALM and CAV1 protein molecules and activating eNOS after its phosphorylation, though the exact molecular mechanisms are yet to be further studied.