Novel long non-coding RNA lnc-URIDS delays diabetic wound healing by targeting Plod1
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posted on 2020-08-14, 17:24 authored by Ada AdminAda Admin, Mengdie Hu, Yuxi Wu, Chuan Yang, Xiaoyi Wang, Wei Wang, Liyan Zhou, Tingting Zeng, Jing Zhou, Chuan Wang, Guojuan Lao, Li Yan, Meng RenImpaired wound healing
is one of the main reasons that leads to diabetic foot ulcerations. However,
the exact mechanism of delayed wound healing in diabetes mellitus is not fully
understood. Long non-coding RNAs (lncRNAs) are widely involved in a variety of
biological processes and diseases, including diabetes and its associated complications.
Here, we identified a novel lncRNA MRAK052872, named lnc-URIDS
(lncRNA UpRegulated in Diabetic Skin), which
regulates wound healing in diabetes mellitus. Lnc-URIDS was highly
expressed in diabetic skin and dermal fibroblasts treated with advanced
glycation end products (AGEs). Lnc-URIDS knockdown promoted migration of dermal
fibroblasts under AGEs treatment in vitro and accelerated diabetic wound
healing in vivo. Mechanistically, lnc-URIDS
interacts with procollagen-lysine, 2-oxoglutarate 5-dioxygenase 1 (Plod1), a
critical enzyme responsible for collagen cross-linking. The binding of lnc-URIDS
to Plod1 results in a decreased protein stability of Plod1, which ultimately
leads to the dysregulation of collagen production and deposition and delays
wound healing. Collectively, this study identifies a novel lncRNA that
regulates diabetic wound healing by targeting Plod1. The findings of the present study offer some
insight into the potential mechanism for the delayed wound healing in diabetes
and provide a potential therapeutic target for diabetic foot.
Funding
This study was funded by National Natural Science Foundation of China (81870571, 81670764, 81900752) and Science and Technology Planning Project of Guangdong Province, China (2014A020212161, 20140202)
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