Browsing by Author "Zhang, Shukun"

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    High glucose-induced Matrilin-2 expression in mouse mesangial cells was mediated by transforming growth factor beta 1 (TGF-β1)
    (Elsevier, 2016-05) Zhang, Shukun; Zhang, Menglan; Huang, Hong; Zhou, Shiying; Du, Yanshneg; Yi, Xin; Luo, Junming; Department of Health Sciences, School of Health and Rehabilitation Sciences
    This study aimed at evaluating the effect of high glucose on the expression of extracellular matrix (ECM) protein Matrilin-2 and the mechanism underlying this effect by using a mouse mesangial cell line. Mouse mesangial cells (MMCs) were cultured in media containing normal (5 mM d-glucose) or high concentrations of glucose (30 mM d-glucose). The expression of Matrilin-2 was assessed by either RT-PCR or western blot. Additionally, transforming growth factor beta 1 (TGF-β1) inhibitors and TGF-β1 were used to determine whether glucose-regulated Matrilin-2 expression was mediated by the TGF-β1/Smad3 signaling pathway. Our data demonstrated that Matrilin-2 expression was markedly induced by high glucose and TGF-β1. High glucose-induced Matrilin-2 expression was inhibited by TGF-β1/Smad3 inhibitors, indicating that Matrilin-2 was markedly induced by high glucose and this induction was mediated by the TGF-β1/Smad3 pathway. Taken together, our results showed that high-glucose-induced Matrilin-2 expression that was mediated by the TGF-β1/Smad3 signaling pathway might play a role in Diabetic nephropathy (DN) pathogenesis and our finding provided a potential diagnostic and/or therapeutic target for DN.
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    The plasma level changes of VEGF and soluble VEGF receptor‐1 are associated with high‐altitude pulmonary edema
    (2018) Zhang, Shukun; Liu, Juanli; Jiang, Dongmei; Wuren, Tana; Ma, Siqing; Du, Yansheng; Wu, Shizheng; Neurology, School of Medicine
    Hypoxia‐induced plasma levels of VEGF and sFlt‐1 are responsible for increased vascular permeability occurred in both brain and pulmonary edema. Currently, it remains unclear the exact roles of VEGF and sFlt‐1 in High Altitude Pulmonary Edema (HAPE) pathogenesis. In this study, plasma levels of VEGF and sFlt‐1 from 10 HAPE and 10 non‐HAPE subjects were measured and compared. The results showed that plasma levels of both VEGF and sFlt‐1 in HAPE patients were significantly increased as compared to the non‐HAPE group. Interestingly, increased plasma levels of these two protein factors were markedly reduced after treatments. As compared to VEGF, sFlt‐1 was much more affected by hypoxia and treatments, suggesting this factor was a key factor contributed to HAPE pathogenesis. Importantly, the ratio of sFlt‐1 and VEGF in group of either non‐HAPE or HAPE after recovery was significantly lower than the ratio in HAPE patients prior to treatments. Our findings suggested that sFlt‐1 was a key factor that involved in HAPE pathogenesis and the sFlt‐1/VEGF ratio could be used as a sensitive diagnostic marker for HAPE.