Lin Jia, Wenzhe Wang, Hui Liu, Fan Zhu, Yunfang Huang
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Abstract
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.
期刊介绍：
The journal retains its traditional interest in evolutionary research that is of relevance to geneticists, even if this is not explicitly genetical in nature. The journal covers all areas of genetics and evolution,including molecular genetics and molecular evolution.It publishes papers and review articles on current topics, commentaries and essayson ideas and trends in genetics and evolutionary biology, historical developments, debates and book reviews. From 2010 onwards, the journal has published a special category of papers termed ‘Online Resources’. These are brief reports on the development and the routine use of molecular markers for assessing genetic variability within and among species. Also published are reports outlining pedagogical approaches in genetics teaching.
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