Key result
LncRNA NONHSAG053901 overexpression promotes mesangial cell inflammation and fibrosis via Egr-1/TGF-β pathways.
Why the study?
The role and mechanism of lncRNA NONHSAG053901 in the pathogenesis of diabetic nephropathy were not well understood.
lncRNA NONHSAG053901 promotes diabetic nephropathy by stimulating Egr-1/TGF-β-mediated renal inflammation, highlighting a potential molecular target for DN.
Hypothesis-generating for lncRNA NONHSAG053901 as a target in diabetic nephropathy; leaves open translation to human disease or therapy.
Diabetic nephropathy (DN) is an important factor leading to end-stage kidney disease that affects diabetes mellitus patients globally. Our previous transcriptome sequencing has identified a large group of differentially expressed long noncoding RNA (lncRNA) in early development of DN. On basis of this, we aimed to investigate the function of lncRNA NONHSAG053901 in DN pathogenesis. In this study, we revealed that the expression of NONHSAG053901 was drastically elevated in both DN mouse model and mesangial cells (MCs). It was found that overexpression of NONHSAG053901 remarkably promoted inflammation, fibrosis and proliferation in MCs. Consistently, further investigations suggested that the stimulation of NONHSAG053901 on proinflammatory cytokines via direct binding to early growth response protein 1 (Egr-1). Interaction between Egr-1 and transforming growth factor β (TGF-β) could augment TGF-β function in DN inflammation. Furthermore, the effects of NONHSAG053901 on stimulation of proinflammatory cytokines were abolished by knockdown of Egr-1. These results together suggested that NONHSAG053901 promoted proinflammatory cytokines via stimulating Egr-1/TGF-β mediated renal inflammation.
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Peng et al. (2019) studied Diabetic nephropathy. lncRNA NONHSAG053901 was evaluated on Inflammation, fibrosis and proliferation in mesangial cells. Overexpression of lncRNA NONHSAG053901 promoted inflammation, fibrosis, and proliferation in mesangial cells via stimulating Egr-1/TGF-β-mediated renal inflammation.
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