Abstract
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Transgelin-2 as an Early Detection for Diabetic Nephropathy Through Inflammation, Periostin and E-cadherin by STAT3 Signaling Through ANXA2
by XiaoTing Duan, Cheng Chen, XiaoLi Liu, Fang Yang, TaoXia Wang, HuiJie Zhou, ShaoLong Zhao, GuiYing Li
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Background: Diabetic nephropathy (hereinafter referred to as DN) is one of the important causes of chronic renal failure, with great harm. We aimed to elucidate the role of transgelin-2, a key early detection for diabetic ne-phropathy.
Method: The serum samples of 12 DN patients and 12 normal volunteers were collected for this experiment. Mice of the model group were injected intraperitoneally with streptozotocin following a high fat diet. Mouse podocyte (MPC5) cells were induced with 20 mmol/L d-glucose.
Result: Transgelin-2 was highly expressed in DN patients with diabetic nephropathy both at the expression levels of mRNA and protein. Transgelin-2 expression was correlated with blood sugar in patients with DN. Transgelin-2 gene up-regulation enhanced inflammation and periostin levels, and reduced E-cadherin activity level in mice with DN. Over-expression of transgelin-2 increased inflammation and periostin levels, and reduced E-cadherin activity level in the in vitro model. Down-regulation of Transgelin-2 reduced inflammation and periostin levels and induced E-cadherin activity level in the in vitro model. Transgelin-2 induced ANXA2/ STAT3 signaling in a mouse model or an in vitro model. ANXA2 was one of the regulatory factors for the effects of transgelin-2 with inflammation, periostin, and E-cadherin in a model of DN.
Conclusions: Taken together, these findings demonstrated that transgelin-2 promoted inflammation and periostin levels, and suppressed E-cadherin levels in DN by STAT3 signaling through ANXA2.
DOI: 10.7754/Clin.Lab.2023.220926
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