LncRNA TTN-AS1 exacerbates extracellular matrix accumulation via miR-493-3p/FOXP2 axis in diabetic nephropathy

被引：3

作者：

Jia, Lin ^{[1
]}

Wang, Wenzhe ^{[1
]}

Liu, Hui ^{[1
]}

Zhu, Fan ^{[1
]}

Huang, Yunfang ^{[1
]}

机构：

[1] Huazhong Univ Sci & Technol, Cent Hosp Wuhan, Tongji Med Coll, Dept Nephrol, Wuhan 430014, Hubei, Peoples R China

来源：

JOURNAL OF GENETICS | 2022年 / 102卷 / 01期

关键词：

TTN-AS1; miR-493-3p; FOXP2; ECM accumulation; diabetic nephropathy; RENAL FIBROSIS; NONCODING RNAS; THERAPEUTICS; CELLS;

D O I：

10.1007/s12041-022-01397-4

中图分类号：

Q3 [遗传学];

学科分类号：

071007 ; 090102 ;

摘要：

Diabetic nephropathy (DN), a common cause of chronic renal failure and end-stage renal disease, leads to a high mortality. However, the role of TTN-AS1 in extracellular matrix (ECM) accumulation during DN remains unclear. In our study, TTN-AS1 exhibited high expression in high glucose-treated mesangial cells, and TTN-AS1 silencing alleviated high glucose-induced ECM accumulation in mesangial cells. Additionally, animal study revealed that TTN-AS1 was upregulated in renal tissues of DN rats, and TTN-AS1 knockdown mitigated renal injury of DN rats. Mechanistically, TTN-AS1 was validated to bind to miR-493-3p, and miR-493-3p targeted forkhead box P2 (FOXP2) 3 ' untranslated region in mesangial cells. TTN-AS1 interacted with miR-493-3p to upregulate FOXP2 in vitro and in vivo. Moreover, FOXP2 overexpression counteracted the effects of TTN-AS1 silencing on the ECM accumulation. In conclusion, TTN-AS1 exacerbated ECM accumulation via the miR-493-3p/FOXP2 axis during DN development. This research may provide a potential new direction for DN treatment.

引用

页数：13

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