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The Rho subfamily of GTPase belongs to the Ras superfamily of small GTP binding protein, it is a nucleotide dependent protein, which plays a "molecular switch" function in the signal transduction process and control of numerous signaling pathways. Rho protein has many biological effects on cytoskeleton or target proteins as a signal converter in signal transduction, such as the regulation of membrane transport function, cell migration, cell adhesion, and cell proliferation. It also plays a very important role in the infection and immune inflammation of the body. Rho protein is widely distributed in related immune cells, such as T cells, B cells, NK cells and so on. When the body is infected by microorganism, the immune inflammatory reaction will be regulated through a series of signal transduction mechanism, and Rho GTPases signal transduction mechanism is one of the important signal pathways. In this paper, we conclude that Rho GTPases how to regulate the body's immune response through its signal pathway, and ultimately affect the body's immune response.

Objective: To investigate the effect of clostridium difficile toxin A(TcdA) on the Rho GTPases and the cytoskeleton in K562 cells., Methods: K562 cells were cultured in vitro with different concentration of TcdA.The effect of TcdA proliferation of cells was detected by MTT method after the K562 cells were stimulated with TcdA for 24,48 and 72h; the expression of cdc42, RhoA, Rac1 mRNA was assessed by RT-PCR; the changes of the microtubule, the microfilament were observed by confocal laser scanning microscopy., Results: The proliferation of K562 cells was inhibited after exposure to TcdA for 24, 48 and 72h, and the inhibitory rate was 47.67% in the treatment for 48 h. the cdc42，RhoA and Rac1 mRNA expressions in the experimental groups decreased after treated with TcdA(P<0.05), which positively correlated with concentration of TcdA. Also, the microfilament decreased ,which was observed by confocal laser scanning microscopy., Conclusion: TcdA inhibites K562 cell proliferation and induces apoptosis, TcdA can change the cytoskeleton structure through the cytoskeletal protein genes cdc42 and RhoA, Rac1 mRNA expression,. It is related with cell microfilament content decreasing.

Copyright of Journal of Sichuan University (Medical Science Edition) is the property of Editorial Board of Journal of Sichuan University (Medical Sciences) 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 study the expressions and activities of Rho GTPases in hypoxia and its relationship with tumor angiogenesis., Methods: Three tumor cell lines were used in this study: gastric cancer cell lines AGS, SGC7901 and hepatocellular carcinoma cell line HepG2. Expression level of Rac1 mRNA was detected by semi-quantitative RT-PCR. Activity of Rac1 was determined by pull-down assay and expression of HIF-1alpha, VEGF, p53 and PTEN protein was detected by Westernblot., Results: The expression level of Rac1 mRNA was significantly increased in hypoxia compared to normoxia. Pull-down assay showed that hypoxia-induced activity of Rac1 was elevated in a time-dependent manner and climaxed at 3 hours. The expressions of HIF-1alpha and VEGF protein were up-regulated, while those of PTEN and p53 protein were down-regulated., Conclusion: These results indicate that hypoxia enhances Rac1 expression which might be involved in tumor angiogenesis by reacting with hypoxia-responsive genes.

Objective To investigate the role of Rho kinase (ROCK) in the protective effects of hydrogen on intestinal epithelial barrier function in sepsis. Methods Caco-2 cells were cultured routinely, and divided into 6 groups randomly (n= 3): control group (C group), hydrogen-rich medium group (H group), lipopolysaccharide (LPS)-treatment group (L group), hydrogen+ LPS-treatment group (HL group), Rho kinase inhibitor (Y-37632) treatment group (Y group) and Rho kinase inhibitor Y-27632+LPS-treatment group (YL group). H group was treated with 0.6 mmol/L hydrogen-rich media. The concentration of LPS and Y-27632 were 50 mg/L and 25 μmol/L separately. After the Caco-2 monolayer model was established, the transepithelial electrical resistance (TEER) values were measured regularly. When the TEER value reached 800 Ω·cm2, the treatment was administered. Then TEER values were measured at 6 h, 12 h and 24 h, and FITC-dextran permeability was detected at 24 h. Cells were seeded on 6-well plates. After cell density reached 80%-90%, treatments were given randomly. The real time-polymerase chain reaction (RT-PCR) was conducted to assess mRNA levels of ZO-1 and ROCK mRNA. ZO- 1 and ROCK protein expression levels were detected by Western blot assay. Results Compared with C group, TEER values were elevated in 12 h and 24 h in H group (P < 0.05). There were no statistical significances in FITC-dextran permeability, protein expression levels of ZO-1 and ROCK between C group and H group (P > 0.05). TEER values were elevated at 6 h, 12 h and 24 h in Y group (P < 0.05). There was no significant difference in FITC-dextran permeability between C group and Y group (P > 0.05). The mRNA expression of ZO-1 increased and mRNA expression of ROCK decreased in Y group (P < 0.05). The TEER values reduced at 6 h, 12 h and 24 h in L group. The FITC-dextran permeability increased significantly, mRNA and protein expressions of ZO-1 significantly decreased, mRNA and protein expressions of ROCK significantly increased in L group (all P < 0.05). Compared with L group, TEER values increased significantly at 6 h, 12 h and 24 h in YL group, FITC- dextran permeability decreased, mRNA expressions of ZO- 1 increased, mRNA expressions of ROCK decreased in YL group (P < 0.05). Compared with L group, TEER values increased at 6 h, 12 h and 24 h in HL group, FITCdextran permeability reduced markedly, protein expressions of ZO-1 increased at each time point, protein expressions of ROCK decreased at each time point in HL group (P < 0.05). Conclusion Hydrogen can protect intestinal barrier function against sepsis, ameliorate the integrity and permeability of intestinal epithelium and increase the expressions of intercellular tight junction proteins. The suppression of Rho kinase over-expression induced by LPS may be involved in these protective effects of hydrogen. [ABSTRACT FROM AUTHOR]

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AIM: To investigate the effects of γ-synuclein on autophagy and apoptosis of colon cancer cells induced by endoplasmic reticulum stress, as well as the protective effect on the cells. METHODS: Gene expression profile chip analysis was performed to compare the cDNA expression profiles between human colon cancer HCT116 cells with γ-synuclein knockdown and HCT116 cells with control siRNA, and to identify potential molecules related to autophagy and apoptosis. In colon cancer cell lines, the functional effects of γ-synuclein on autophagy and apoptosis induced by thapsigargin (TG), an endoplasmic reticulum stress-inducing agent, were systematically explored by conducting immunofluorescence staining, Western blot, CCK-8 assay, flow cytometry, and transmission electron microscopy. Western blot was used to detect the expression of γ-synuclein protein, autophagy-related proteins [microtubule-associated protein 1 light chain 3 (LC3), beclin-1, autophagy-related protein 5 (ATG5) and ATG7], and apoptosis-related proteins [poly (ADP-ribose) polymerase (PARP), pro-caspase-3, and pro-caspase-9]. To further analyze the mechanism of γ-synuclein in regulating autophagy and apoptosis, extracellular signal-regulated kinase (ERIK) inhibitor PD98059, ERII inhibitor SP600125 and c-Jun N-terminal kinase (JNII) activator anisomycin were applied separately to test HCT116 cells transfected with 7-synuclein siRNA. Subsequently, autophagy proteins, apoptosis proteins, and ERK and JNII pathway-related proteins were detected by Western blot. RESULTS: The TG-induced autophagy of colon cancer cells mainly occurred at the early stage (0~24 h), and apoptosis mainly occurred at the late stage (36~48 h). Endoplasmic reticulum stress up-regulated the expression of γ-synuclein in colon cancer cells, which was associated with enhanced autophagy. γ-Synuclein promoted autophagy by activating ERK and JNII pathways at the early stage (0~24 h), and inhibited apoptosis by blocking JNII pathways at the late stage (24~48 h) to protect HCT116 cells. In our model, γ-synuclein was observed to play a critical role in the transition from endoplasmic reticulum stress-induced autophagy to apoptosis. CONCLUSION: In the context of endoplasmic reticulum stress, 7-synuclein promotes autophagy and inhibits apoptosis by regulating ERK and JNII signaling pathways, thus protecting colon cancer cells. This provides a potential idea for anti-tumor therapy. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research 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.)

The colorectal cancer (CRC) is one of the most common malignant tumors of digestive system, and has a complex process of development and progression. Its development is a complex and multistep process so the occurrence of CRC may influence organism immune and cause change of immunity. There are lots of researches demonstrating the immune system’s reaction during the occurrence or development of the malignancy. Peripheral blood mononuclear cell (PBMC) is an ideal sample to study the immune functions, which is main part of the immune system and easily available. In this study, a novel MS method, data independent acquision (DIA) was utilized, which has high specificity and coverage, to perform protein quantitation and find out differentially expressed proteins between the peripheral blood mononuclear cells (PBMC) of CRC and benign intestines disease. Based on the quantified results, 113 differentially expressed proteins (p<0.05) were identified, including 23 up-regulated proteins and 90 down-regulated proteins. The gene ontology (GO) and reactome pathway enrichment analyses of the up-regulated proteins and the down-regulated proteins were performed separately. GO analysis results showed that down regulated proteins were significantly enriched in platelet degranulation, regulated exocytosis, exocytosis, vesicle-mediated transport and secretion by cell and secretion biological processes (BP). For molecular function (MF) analysis, the down-regulated proteins were enriched in cell adhesion molecule binding, cadherin binding involved in cell-cell adhesion, protein binding involved in cell-cell adhesion, protein binding involved in cell adhesion, cadherin binding. And GO cell component (CC) analysis showed that the downregulated proteins were significantly enriched in the membrane-bounded vesicle, extracellular exosome, extracellular vesicle, extracellular organelle, extracellular region part, extracellular region, while up-regulated proteins were not enriched in any cell component. The reactome pathway analysis showed the down regulated proteins were enriched in Platelet degranulation. MAP2K and MAPK activation, P130Cas linkage to MAPK signaling for integrins, GRB2; SOS provides linkage to MAPK signaling for integrins. integrin alphallb beta3 signaling, common pathway of fibrin clot formation, integrin cell surface interactions, RHO GTPases activate PAKs, RHO GTPases activate PKNs pathway. The up-regulated proteins were enriched in SRP-dependent cotranslational protein targeting to membrane pathways. Especially, the up-regulated protein Galectin 1 and the downregulated ones Dok-2, AIINAK1 are expected to be biomarkers of CRC in PBMC, which are closely related to immune function. They all involve in kinds of immune activities of macrophage, T cell and dendritic cell and are expected to be biomarkers of CRC in PBMC. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research 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.)

Ras-related C3 botulinum toxin substrate 1 (RAC1) is a crucial member of the Ras GTPase super-family, exerting an overriding role in cell behaviors such as motility, proliferation and adhesion, and is involved in regulating vascular permeability and cellular barrier function. Recently, the significance of RAC1 in the etiology and progression of various pulmonary disorders has garnered increasing attention, which sheds light on lung disease study. In this review, we introduce the characteristics of RAC1 systematically and recapitulate its effects and molecular mechanisms in the context of lung tumors, chronic obstructive pulmonary disease, lung injury and pulmonary arterial hypertension, hoping to provide new insights for future pulmonary disease treatment. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research 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.)

Copyright of Biotechnology Bulletin is the property of Biotechnology Bulletin Editorial Office 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 investigate the role and mechanism of Rho-related GTP-binding protein F (RhoF)-mediated Th17 polarization in the development of severe acute pancreatitis (SAP). Methods RhoF transgenic mice were randomly divided into control group (n = 10), SAP group (n = 10) and SAP+Y-27632 group (n = 10), and WT mice were randomly divided into control group (n = 10), SAP group (n = 10) and SAP+Y-27632 group (n = 10). SAP models were established in all groups except the control group. The SAP+Y-27632 group was infused with Y-27632 via tail vein after model establishment. T cells in mouse blood samples were isolated for RhoF, p-MYPT1 protein detection and ROCK activity determination, and the percentage of lymphoid CD4+T cells producing IL-17 was analyzed by flow cytometry. Results The expression of RhoF and p-MYPT1 was increased in T cells in the SAP group compared with that in the control group (P < 0.01), and the level of RhoF was closely correlated with that of p-MYPT1 (P = 0.018). The expression of RhoF protein level in T cells of mice in the RhoF group increased by approximately 30% compared to that in the WT group, and the level of spontaneous IL-17 production by CD4+ T cells was significantly increased (P = 0.003). Compared with WT mice, the histological score of pancreatic injury, the expression of RhoF and p-MYPT1 in T cells, the number of IL-17+ T cells and serum IL-17 level in RhoF transgenic mice were significantly increased (P < 0.05). The histological score, RhoF and p-MYPT1 expression of T cells, IL-17+ T cell numbers and serum IL-17 level were significantly lower in the SAP+Y-27632 group than those in the SAP group (P < 0.05). Conclusion RhoF/ROCK signaling pathway-mediated polarization of Th17 cells is involved in the pathogenesis of SAP. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research 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.)

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Copyright of Journal of Clinical Hepatology / Linchuang Gandanbing Zazhi is the property of Journal of Clinical Hepatology 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 investigate the mechanisms of lysophosphatidic acid ( LPA ) in stimulating invasion and metastatic colonization of ovarian cancer cells. Methods The metastatic ability in vivo of ovarian cancer SK-OV3, HEY, OVCAR3 , and IGROVl cells was determined in tumor-bearing nude mouse models. Matrigel assay was used to detect the changes of response in vitro of ovarian cancer cells to LPA after Rac( - ) or Rac( + ) adenovirus treatment. LPA-induced Rho GTPase activation was detected by GST-fusion protein binding assay. Results The peritoneal metastatic colonization assay showed overt metastatic colonization in mice receiving SK-OV3 and HEY cell inoculation, indicating that they are invasive cells. Metastatic colonization was not detected in animals receiving 0VCAR3 and IGROVl cells, indicating that these cells are non-invasive cells. In the matrigel invasion assay, exposure to LPA led to a notably greater migratory response in metastatic SK-0V3 and HEY cells (Optical density; SK-0V3 cells; 0.594 ±0.023 vs. 1. 697 ±0.049, P <0.01; HEY cells; 0. 804 ± 0. 070 vs. 1. 851 ± 0. 095 , P < 0. 01). But LPA did little in the non-metastatic OVCAR3 and IGROVl cells (Optical density A: OVCAR3 cells; 0.336 ±0.017 vs. 0. 374 ± 0. 007, P > 0. 05; IGROVl cells; 0. 491 ± 0. 036 vs. 0. 479 ± 0. 061, P > 0. 05). LPA migratory responses of ovarian cancer cells were closely related to their metastatic colonization capabilities (r = 0.983, P<0.05). Rac( - ) blocked the LPA response of invasive SK-OV3 and HEY cells ( LPA-induced fold increase of cell migration: SK-OV3 cells: 2. 988 ±0.095 vs. 0.997 ±0. 100,P =0.01; HEY cells; 2.404 ±0.059 vs. 0.901 ±0.072, P=0.01). But Rac ( + ) confered the non-invasive cells with LPA response and invasion capability ( LPA-induced fold increase of cell migration; OVCAR3 cells; 1.072 ± 0.080 vs. 1.898 ±0. 078, P < 0.01; IGROVl cells; 1.002 ±0.044 vs. 2. 141 ±0.057, P < 0. 05). Among Rho GTPases, only Rac activation was different between ovarian cancer cell lines with different metastatic capability after LPA stimulation; Cdc42 could not be activated in both the invasive and noninvasive cell lines. RhoA could be activated in both the invasive and non-invasive cell lines. Rac could be activated by LPA in the invasive ovarian cancer cell lines. However, Rac could not be activated in the noninvasive cell lines. Conclusion Lysophosphalidic acid stimulates invasion and metastasis of ovarian cancer cells through Rac activation. [ABSTRACT FROM AUTHOR]

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