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Kidney Week

Abstract: TH-PO881

The Role of LncRNA Meg3 in the Mitochondrial Dysfunction Induced by High Glucose in Podocytes

Session Information

Category: Diabetic Kidney Disease

  • 601 Diabetic Kidney Disease: Basic

Authors

  • Deng, Qiongxia, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, Guangdong, China
  • Cheng, Wang, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, Guangdong, China
Background

Podocytes have plenty of mitochondrial density to keep up with their high energy need. Mitochondrial dysfunction plays a key role in diabetic nephropathy(DN), which has been assumed related with Maternally expressed gene 3 (Meg3),a long noncoding RNA expressing in normal human tissues. While the exact mechanism of Meg3 on this pathophysiological process is poorly understood.

Methods

FISH+IF was used to detect the expression of Meg3 in podocytes of patients with DN. Podocytes were exposed or not to 30mM high glucose in vitro to study the effect of high glucose on Meg3 expression. In addition, the expression of Meg3 was regulated by CRISPR-Cas9 system and lentiviral vector to explore its function in mitochondrial dysfunction.

Results

Meg3 expression in podocytes of diabetic kidney tissue was higher than that in normal kidney tissue. In cultured human podocytes, the expression of Meg3 increased with the prolongation of high glucose exposure time. The results of PCR detection were consistent with those of Arraystar, suggesting that high glucose can up-regulate the expression of Meg3. Knocked out Meg3 can improve podocyte injury and mitochondrial dysfunction induced by high glucose. By contrast, the podocytes over-expression of Meg3 aggravated injury, expressing less Nephrin and Synaptopodin. Abnormal expression of proteins associated with mitochondrial fusion and fission caused dynamic imbalance of mitochondria, more fragmentation, lower mitochondrial membrane potential levels.

Conclusion

Our study demonstrates for the first time that Meg3 can be upregulated by high glucose, inducing a dynamic imbalance of mitochondria, leading to damage to podocytes. This finding will provide a potential treatment strategy to alleviate the development of DN.