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Zhou T.-B.,Sun Yat Sen University | Zhao H.-L.,Guangxi Medical University | Fang S.-L.,Sun Yat Sen University | Drummen G.P.C.,Cellular Stress and Ageing Program
Journal of Receptors and Signal Transduction | Year: 2014

The association of transforming growth factor-β1 (TGFβ1) is an important signaling pathway factor involving extracellular matrix regulation, and its gene polymorphisms with the risk of rheumatoid arthritis (RA) is currently still fiercely debated. Therefore, this meta-analysis was performed to determine if TGFβ1 T869C, G915C, and C509T gene polymorphisms correlate with the risk of developing RA. Association reports were identified from PubMed, Cochrane Library and CBM-disc (China Biological Medicine Database) on 1 May 2013, and eligible studies were recruited and synthesized to identifying patterns among study results. T869C TT genotype in the overall population was associated with increased RA risk (OR=1.28, 95% CI: 1.02-1.60, p=0.03). In the sub-group analysis, T869C TT genotype was shown to be a risk factor for RA, and T869C C allele or CC genotype a protective factor against RA disease in Asians, but these associations were not found in Caucasians. Furthermore, TGFβ1 C509T TT genotype was distinctly associated with RA susceptibility, but the T allele and CC genotype were not. TGFβ1 G915C gene polymorphism was not associated with RA susceptibility. In conclusion, the TT genotype of TGFβ1 T869C was associated with RA risk in the overall population and Asians. Furthermore, CC genotype or C allele was determined to be protective factors with respect to the RA risk in the overall population and Asians. Nonetheless, additional studies are required to firmly establish a correlation between the aforementioned polymorphisms and RA risk. © 2014 Informa Healthcare USA, Inc. All rights reserved: reproduction in whole or part not permitted. Source


Zhou T.-B.,Sun Yat Sen University | Ou C.,Guangxi Medical University | Rong L.,Baylor College of Medicine | Drummen G.P.C.,Cellular Stress and Ageing Program
JRAAS - Journal of the Renin-Angiotensin-Aldosterone System | Year: 2014

Background and objective: All-trans retinoic acid (ATRA) exerts various effects on physiological processes such as cell growth, differentiation, apoptosis and inflammation. Prohibitins (PHB), including prohibitin 1 (PHB1) and prohibitin 2 (PHB2), are evolutionary conserved and pleiotropic proteins implicated in various cellular functions, including proliferation, tumor suppression, apoptosis, transcription, and mitochondrial protein folding. The renin-angiotensin- aldosterone system plays a pivotal role in the regulation of blood pressure and volume homeostasis. All these factors and systems have been implicated in renal interstitial fibrosis. Therefore, the objective of this study was to investigate the effect of ATRA treatment on the renin-angiotensin-aldosterone system and expression of prohibitins to further understand its role in the processes leading to renal interstitial fibrosis.Methods: The hypoxic and oxidative stress conditions in obstructive renal disease were simulated in a hypoxia/ reoxygenation model with renal tubular epithelial cells (RTEC) as a model system. Subsequently, the effect of ATRA on mRNA and protein expression levels was determined and correlations were established between factors involved in the renin-angiotensin-aldosterone system, the prohibitins, cellular redox status, renal interstitial fibrosis and ATRA treatment.Results: Correlation analysis showed that both PHB1 and PHB2 protein levels were negatively correlated with angiotensin I, ACE1, angiotensin II, TGF-β1, Col-IV, FN, ROS, and MDA (PHB1: r = -0.792, -0.834, -0.805, -0.795, -0.778, -0.798, -0.751, -0.682; PHB2: r = -0.872, -0.799, -0.838, -0.773, -0.769, -0.841, -0.794, -0.826; each p<0.05), but positively correlated with ACE2, SOD, and GSH (PHB1: r = 0.796, 0.879, 0.824; PHB2: r = 0.785, 0.914, 0.849; each p<0.05). ACE1 was positively correlated with angiotensin I, angiotensin II, TGF-β1, Col-IV, FN, ROS, and MDA, and negatively correlated with ACE2, SOD, and GSH (each p<0.05). ACE2 was negatively correlated with ACE1, angiotensin I, angiotensin II, TGF-β1, Col-IV, FN, ROS, and MDA, and positively correlated with SOD and GSH (each p<0.05).Conclusion: The results suggest that ATRA acts as a positive regulator of PHB1, PHB2 and ACE2, and as a negative regulator of ACE1, angiotensin I, and angiotensin II in a RTEC model system under hypoxia/reoxygenation conditions. © The Author(s) 2012. Source


Zhou T.-B.,Sun Yat Sen University | Jiang Z.-P.,Sun Yat Sen University | Qin Y.-H.,Guangxi Medical University | Drummen G.P.C.,Cellular Stress and Ageing Program
Nephrology | Year: 2014

Aim A possible association between the transforming growth factor-β1 (TGF-β1) T869C gene polymorphism and the risk of developing diabetic nephropathy (DN) remains unclear. This investigation was performed to assess if an association between the TGF-β1 T869C gene polymorphism and DN risk exists by using meta-analysis to combine comparable studies, thereby increasing sample size and statistical significance, and to identify patterns in various studies. Methods The association reports were identified from PubMed, Cochrane Library, and CBM-disc (China Biological Medicine Database) on 1 May 2013, and eligible studies were recruited and synthesized. Results Fifty reports were recruited into this meta-analysis for the association of the TGF-β1 T869C gene polymorphism with DN risk. The TT genotype in the overall population was shown to be associated with DN risk (odds ratio (OR) = 0.74, 95% confidence interval (CI): 0.56-0.98, P = 0.04). In the sub-group analysis, CC genotype was associated with DN risk in Asians, Caucasians, and Africans. However, the sample size for Caucasians and Africans was relatively small. Furthermore, T allele was distinctly associated with the risk of developing DN in the Asian population (OR = 0.76, 95% CI: 0.62-0.92, P = 0.005). Conclusions The TT genotype of TGF-β1 T869C in the overall population was associated with DN risk, whereas the CC genotype and T allele were distinctly associated with DN risk in the Asian population. Nonetheless, additional studies are required to firmly establish a correlation between the aforementioned polymorphism and DN risk. Summary at a Glance Previous studies have investigated a potential link between gene polymorphism of TGF-β1 and the risk of diabetic kidney disease but the data are not conclusive. In this study, the authors have used a meta-analytic approach to provide further data on the role of the TGF-β1 T869C gene polymorphism as a predictor of diabetic nephropathy. © 2013 Asian Pacific Society of Nephrology. Source


Zhou T.-B.,Sun Yat Sen University | Zhou T.-B.,Guangxi Medical University | Qin Y.-H.,Guangxi Medical University | Lei F.-Y.,Guangxi Medical University | And 2 more authors.
Molecular Biology Reports | Year: 2014

Prohibitins PHB1 and PHB2 are evolutionary conserved and pleiotropic proteins, which have been shown to be important factors in various cellular functions, including proliferation, tumour suppression, apoptosis, transcription, and mitochondrial protein folding. Recently, we demonstrated that down-regulation promoted renal interstitial fibrosis (RIF) in ureteral obstructed rats. Furthermore, the hypoxic conditions and oxidative stress have been implicated in obstruction-mediated renal disease. This study was performed to explore the association of PHBs with oxidative stress in a rat model of RIF. PHBs, the profibrotic transforming growth factor-β1 (TGF-β1), and the extracellular matrix proteins collagen-IV (Col-IV) and fibronectin (FN) were evaluated, as were markers of oxidative stress [total reactive oxygen species (ROS), malondialdehyde (MDA)] and antioxidative capacity (superoxide dismutase, glutathione), and apoptosis. Our results showed a progressive increase in oxidative stress and concomitant decrease in antioxidants over a period of 4 weeks ureteral obstruction. Concomitantly, profibrotic components increased and PHB expression decreased. Overall, both PHBs were negatively correlated with the extent of observed fibrosis, TGF-β1, Col-IV, FN, ROS, MDA, and apoptosis. © Springer Science+Business Media 2014. Source


Zhou T.-B.,Guangxi Medical University | Zhou T.-B.,Sun Yat Sen University | Qin Y.-H.,Guangxi Medical University | Lei F.-Y.,Guangxi Medical University | And 2 more authors.
PLoS ONE | Year: 2013

Prohibitin is an evolutionary conserved and pleiotropic protein that has been implicated in various cellular functions, including proliferation, tumour suppression, apoptosis, transcription, and mitochondrial protein folding. Both prohibitin over- and under-expression have been implicated in various diseases and cell types. We recently demonstrated that prohibitin down-regulation results in increased renal interstitial fibrosis (RIF). Here we investigated the role of oxidative stress and prohibitin expression in RIF in unilateral ureteral obstructed rats. Lentivirus-based delivery vectors were used to knockdown or over-express prohibitin. Our results show that increased prohibitin expression was negatively correlated with the RIF index, reactive oxygen species, malon dialdehyde, transforming growth factor β1, collagen IV, fibronectin, and cell apoptosis index. In conclusion, we postulate that prohibitin acts as a positive regulator of mechanisms that counteract oxidative stress and extracellular matrix accumulation and therefore has an antioxidative effect. © 2013 Zhou et al. Source

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