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Amyloid β protein deposition in cerebral vessels, a characteristic of Alzheimer's disease, is a risk factor for intracerebral hemorrhage. Amyloid β protein directly modulates human platelet function; however, the exact mechanism of action is unclear. Therefore, we investigated the effects of amyloid β protein on human platelet activation using an aggregometer with laser scattering. Amyloid β protein decreased platelet aggregation induced by thrombin receptor-activating protein, but not by collagen and ADP. Amyloid β protein also suppressed platelet aggregation induced by SCP0237 and A3227. Platelet-derived growth factor-AB secretion and phosphorylated-heat shock protein 27 release by thrombin receptor-activating protein were inhibited by amyloid β protein. Additionally, thrombin receptor-activating protein-induced phosphorylation of JNK and p38 MAP kinase was reduced by amyloid β protein. Collectively, our results strongly suggest that amyloid β protein negatively regulates protease-activated receptor-elicited human platelet activation. These findings may indicate a cause of intracerebral hemorrhage due to amyloid β protein. [ABSTRACT FROM AUTHOR]

Tumor cells overexpress low-density lipoprotein (LDL) receptors (LDL-r). Hence, LDL is proposed as a targeting shuttle of anticancer drugs. Therefore, the objective of this study was to synthesize a dual inhibitor of heat shock protein 27 (HSP27) and human epidermal growth factor receptor 2 (HER2) conjugated with cholesterol and encapsulated into LDL for selective targeting of ovarian cancer cells. In the present study, the anticancer agent and its cholesterol conjugate were successfully prepared and characterized physically for color, shape, and melting point. Moreover, the compounds were chemically characterized for 1H NMR and 13C NMR spectra using FTIR and LCMS/MS. Our results revealed that the prepared anticancer agent and its cholesterol conjugate elicited dual HSP27 and HER2 inhibition, as confirmed using western blotting. The anticancer agent (compound D) entered cells and targeted the HSP27 function, thereby reducing HER2 expression. However, a cholesterol-conjugated anticancer agent (compound F) had high cellular uptake and inhibited the growth of SKOV3 cells after encapsulation into LDL. The obtained results concluded that the design of an LDL-encapsulated cholesterol-conjugated HSP27-HER2 dual inhibitor may be a promising approach to realize specific targeted achieve killing of ovarian cancer. [ABSTRACT FROM AUTHOR]

Background: Heat shock proteins (HSPs) are a class of highly conserved proteins responsible for various functions critical to cell survival. Pharmacological induction of HSPs has been implicated in the regulation of neuronal loss and functional deficits in peripheral and central nervous system injuries. Accordingly, the present study was conducted to investigate the effect of trehalose on spinal expression of HSP27, HSP70 and caspase-3 genes following traumatic spinal cord injury (SCI) in rats. Methods: Male rats weighing 250-300 g underwent laminectomy and were divided into four groups including sham, SCI (received SCI), vehicle (received SCI and phosphate buffer saline intrathecally) and trehalose (received 10 mM trehalose intrathecally following SCI). On days 1, 3 and 7 after injury, HSP27, HSP70 and caspase-3 genes transcripts were quantified in spinal cord tissues via a real-time PCR technique. In addition, locomotor function was assessed using the Basso, Beattie and Bresnahan (BBB) rating scale. Results: SCI induced the expression of HSP27, HSP70 and caspase-3 genes and BBB score at all time points. Trehalose treatment upregulated HSP27, HSP70 genes expression at 1 day after SCI. Interestingly, a significant reduction in the expression of HSP27 and HSP70 genes was observed on days 3 and 7 following trauma compared with the vehicle group (p < 0.01). Caspase-3 gene showed a decrease in expression in the trehalose-treated group at all times. In addition, neurological function revealed an improvement after treatment with trehalose. Conclusion: This study suggests that the neuroprotective effect of trehalose is mediated via regulation of HSP27 and HSP70, which are involved in cytoprotection and functional recovery following SCI. [ABSTRACT FROM AUTHOR]

Purpose: It is known that the low-power irradiation of a high-output laser accelerates wound healing. However, there is little fundamental research on it, especially for cultured osteoblasts. The purpose of this study was to evaluate the effect of low-level irradiation of a hard laser on cultured osteoblasts, Materials and Methods: Osteoblasts cultured in collagen gel were irradiated using either a CO2 or a semiconductor laser. Expressions of OC, BSP, and HSP27 were examined at 3 days after irradiation and calcium volumes were measured after 1 week. Results: In the CO2 laser group, a significant difference was only observed with 2.6-W laser irradiation. There was no promoting effect of semiconductor laser irradiation. Additionally, the highest expression of HSP27 was shown with 2.6 W of CO2 laser irradiation. Conclusion: The CO2 laser at 2.6 W can increase the calcification of osteoblasts in three-dimensional cultures. The mechanism seems to be related to the cascade of HSP27. [ABSTRACT FROM AUTHOR]

Objective: We aimed to investigate the effects of angiotensin-(1-7) [Ang-(1-7)] on heat-shock protein 27 (HSP27) in a canine model of induced tachycardia.Methods: Eighteen dogs were randomized into three equal treatment groups: sham, pacing and pacing+Ang-(1-7) group. The dogs in the last two groups were subjected to 2weeks of rapid atrial pacing (500bpm). The effects of Ang-(1-7) on HSP27 were assessed by real-time polymerase chain reaction and western blot.Results: The expression levels of atrial HSP27 mRNA and protein were significantly (P<0.05) higher for the pacing group than the sham group and significantly (P<0.05) lower for the pacing+Ang-(1-7) group than the pacing group. There was no significant difference between the HSP27 expression levels in the right and left atria among all three groups.Conclusions: Our findings suggest that the overexpression of HSP27 may possibly be occurring as an adaptive response that allows atrial tissues to cope with rapid atrial pacing, and an inhibiting effect of Ang-(1-7) on atrial remodeling may be one of the mechanisms responsible for the attenuation of HSP27 up-regulation induced by rapid pacing. [ABSTRACT FROM AUTHOR]

Introduction Understanding protein expression profiles of apical periodontitis may contribute to the discovery of novel diagnostic or therapeutic molecular targets. Methods Periapical tissue samples ( n = 5) of patients with lesions characterized as nonhealing were submitted for proteomic analysis. Two differentially expressed proteins (heat shock protein 27 [HSP27] and serpin family B member 1 [SERPINB1]) were selected for characterization, localization by immunofluorescence, and association with known biomarkers of acute inflammatory response in human apical periodontitis ( n = 110) and healthy periodontal ligaments ( n = 26). Apical periodontitis samples were categorized as stable/inactive ( n = 70) or progressive/active ( n = 40) based on the ratio of expression of receptor activator of nuclear factor kappa-B ligand ( RANKL )/osteoprotegerin ( OPG ). Next, the expression of HSP27 , SERPINB1 , C-X-C motif Chemokine Receptor 1 ( CXCR1 ), matrix metalloproteinase 8 ( MMP8 ), myeloperoxidase ( MPO ), and cathepsin G ( CTSG ) messenger RNA was evaluated using real-time polymerase chain reaction. Data analysis was performed using the Shapiro-Wilk test, analysis of variance, and the Pearson test. P values <.05 were considered statistically significant. Results Proteomic analysis revealed 48 proteins as differentially expressed in apical periodontitis compared with a healthy periodontium, with 30 of these proteins found to be expressed in all 4 lesions. The expression of HSP27 and SERPINB1 was ∼2-fold higher in apical periodontitis. Next, an increased expression of HSP27 was detected in epithelial cells, whereas SERPINB1 expression was noted in neutrophils and epithelial cells. HSP27 and SERPINB1 transcripts were highly expressed in stable/inactive lesions ( P < .05). Significant negative correlations were found between the expression of HSP27 and SERPINB1 with biomarkers of acute inflammation including CXCR1 , MPO , and CTSG . Conclusions Our data suggest HSP27 and SERPINB1 as potential regulators of the inflammatory response in apical periodontitis. Additional functional studies should be performed to further characterize the role of these molecules during the development/progression of apical periodontitis. [ABSTRACT FROM AUTHOR]

Heat shock proteins (Hsps) 27 and 47 are involved in the control of apoptosis, cell migration, and collagen synthesis. There is some understanding of the immunolocalization of these proteins during the repair process in skin and gastrointestinal mucosa, but their expressions in normal and injured oral mucosa are unknown. The aim of this study was to analyze the immunolocalization and intensity of these proteins in oral ulcers induced in rats and to compare these expression levels with those reported in skin and gastric mucosa. Ulcers were induced on the ventral surface of the tongues of rats. The rats were then euthanized at 0, 24, 48, 72, and 120 h. Hsp27 expression remained low in the first hours of repair, but was higher at 72 h, mainly in the migrating epithelium. Expression of Hsp47 was high at 48 h, mainly in fibroblasts, cells of the vascular wall, and basal keratinocytes of migrating epithelium. In the control group, expressions of these proteins were low, which indicates that these Hsps are constitutive proteins in oral mucosa. Expression levels were similar to those reported in the healing of skin lesions and gastric ulcer, suggesting a common mechanism of Hsp activation in the repair of these tissues. [ABSTRACT FROM AUTHOR]

Abstract: Introduction: Transforming growth factor β1 (TGFβ1) regulates cellular functions including cell growth, differentiation, angiogenesis, migration, and metastasis. The TGFβ1 signal transduction pathways are mostly undefined in mouse dental papilla-derived MDPC-23 cells. In this study, we investigated TGFβ1-induced migration focusing on heat shock protein 27 (Hsp27) activation. Methods: Cellular responses mediated by TGFβ1 in MDPC-23 cells were measured by Western blot and MTT assays. Cell migration was determined by counting migrated cells using the chemotaxis cell migration assay. Results: TGFβ1 induced cell migration and increased the phosphorylation of Hsp27 and p38 MAPK in MDPC-23 cells. However, TGFβ1 did not affect Akt/NF-κB signaling to regulate the migration of MDPC-23 cells. Inhibiting p38 MAPK with SB203580 blocked TGFβ1-induced Hsp27 activation and cell migration. Conclusion: Hsp27 phosphorylation followed by p38 MAPK activation was required for TGFβ1-induced migration, and Hsp27 itself contributed to MDPC-23 cell migration. [Copyright &y& Elsevier]

Objective: To investigate and compare the effect of radio-frequency (RF) field exposure on expression of heat shock proteins (Hsps) in three human glioma cell lines (MO54, A172, and T98). Methods: Cells were exposed to sham or 1950 MHz continuous-wave for 1 h. Specific absorption rates (SARs) were 1 and 10 W/kg. Localization and expression of Hsp27 and phosphorylated Hsp27 ((78) Ser) (p-Hsp27) were examined by immunocytochemistry. Expression levels of Hsp27, p-Hs27, and Hsp70 were determined by Western blotting. Results: The Hsp27 was primarily located within the cytoplasm, p-Hsp27 in both cytoplasm and nuclei of MO54, A172, and T98 cells. RF field exposure did not affect the distribution or expression of Hsp27. In addition, Western blotting showed no significant differences in protein expression of Hsp27 or Hsp70 between sham- and RF field-exposed cells at a SAR of 1 W/kg and 10 W/kg for 1 h in three cells lines. Exposure to RF field at a SAR of 10 W/kg for 1 h slightly decreased the protein level of phosphorylated Hsp27 in MO54 cells. Conclusion: The 1950 MHz RF field has only little or no apparent effect on Hsp70 and Hsp27 expression in MO54, A172, and T98 cells. [Copyright &y& Elsevier]

Abstract: Dental pulp has various characteristics in the pulp chamber, but only a few biological evaluations about the effect of age on dental pulp tissue have been reported. The purpose of this study was to compare dental pulp from young and adult rats to characterize the homeostatic mechanism. Dental pulp cells (DPCs) were obtained from the first molar of rats, weighing 150 g each for the young group and 350 g each for the adult group. The expression of core-binding factor alpha-1 (Cbfa-1), vascular endothelial growth factor (VEGF), or heat shock protein (HSP) 27 messenger RNAs (mRNAs) by cultured pulp cells was determined by using a quantitative real-time PCR system after 3, 7, or 14 days. The expression of Cbfa-1 mRNA in the young group was higher than in the adult group. Expression of VEGF and HSP27 mRNAs in the adult group was higher than in the young group. The self-defense system in young DPCs is undertaken by calcification, but in adult DPCs it is carried out by the expression of self-defense proteins and the regeneration of vessels. [Copyright &y& Elsevier]

Abstract: We investigated the expression and biological significance of heat shock protein (HSP)-27 in patients with oral squamous cell carcinoma (SCC). The expression of HSP-27 was quantified immunohistochemically in specimens from 37 patients with oral SCC. Findings were correlated with lymph node metastases, effect of chemotherapy, and survival. The presence of HSP-27 was identified in 31 of the 37 specimens (84%). Expression was low in 4 patients (11%), intermediate in 13 (35%), and high in 14 (38%). There were significant differences in the therapeutic effect of chemotherapy (Oboshi–Shimosato''s grade) and prognosis in relation to expression of HSP-27. We found no correlation between the extent of expression of HSP-27 and stage or differentiation of the tumour. [Copyright &y& Elsevier]

Abstract: Background: Because congestive heart failure (CHF) is a complex syndrome with many different underlying mechanisms of worsening of heart function, it is important to recognize the global alternations in protein expression associated with the processes of CHF. Methods and Results: The purpose of our study was to use a proteomic approach to investigate global alternations in protein expression in tachycardia induced CHF dogs. We compared the 2-dimensional electrophoresis protein patterns of left ventricular samples from the normal with those from failing myocardium. Differentially expressed cardiac proteins showed approximately 500 cardiac protein spots. A total of 20 spots (14 increased, 6 decreased) was altered in CHF, whereas the more distinguishably increased spots in CHF were identified by using mass spectrometry as alpha B crystallin, heat shock protein (HSP) 27, and HSP20, which maintain both the morphologic and functional integrity of the cardiomyocytes and increase tolerance against various types of stress. Because phosphorylation is one of the most important posttranslational modifications, we evaluated whether or not the overexpressed small HSPs were phosphorylated in CHF. Phosphoprotein staining and Western blotting demonstrated that the phosphorylation of alpha B crystallin at serine (Ser)-59 site and of HSP27 at both Ser-78 and Ser-82 sites increased in CHF. Conclusion: Proteomics studies can provide new insights into molecular mechanisms in CHF and phosphorylated small HSPs may be involved in preventing cardiac dysfunction. [Copyright &y& Elsevier]

This study investigated the biochemical and histopathological alterations along with the immunoexpression pattern of heat shock protein 27 (Hsp27) within 6 h postmortem (PM) in skeletal muscle of boldenone (BOL)-treated rats. Forty-eight male rats were divided into two groups; a control group received sesame oil (0.25 mL/kg bwt), and BOL group received 5 mg/kg bwt BOL. Both treatments were intramuscularly injected once a week for eight weeks. Rats were euthanized by cervical dislocation, and the skeletal muscle specimens were collected at zero-time, 2, 4, and 6 h PM for biochemical and histopathological evaluations. The results revealed that BOL treatment significantly increased pH, MDA, ATP, ADP, glycogen, and hydroxyproline values. Still, it decreased the GPX, GST, and lactic acid levels, and Hsp27 immunoexpression compared to the control group. With increasing postmortem interval (PMI), whether control or BOL-treated, a significant reduction in pH value, markers of muscular antioxidant status, ATP, ADP, glycogen, hydroxyproline levels, as well as Hsp27 immunoexpression but a significant increase in lipid peroxidation and lactic acid content were recorded. Of note, the interaction between BOL treatment and PMI had a significant effect on ATP, ADP, lactic acid, hydroxyproline, GST, MDA, and TAC levels. Conclusively, these findings signify BOL exposure's modifying effect on the energy content, oxidative status, and histological architecture of skeletal muscles in the early PMI that reflected in delaying the onset of rigor mortis. For forensic practitioners, these findings should be highly considered at estimating PMI in athletic, AAS-treated patients, and fattening animals. [ABSTRACT FROM AUTHOR]