Long non-coding RNA MEG3 promotes fibrosis and inflammatory response in diabetic nephropathy via miR-181a/Egr-1/TLR4 axis | Zendy

Fangfang Zha | Zendy; Xiaolu Qu | Zendy; Bo Tang | Zendy; Ji Li | Zendy; Yakun Wang | Zendy; Pengxi Zheng | Zendy; Tingting Ji | Zendy; Chun Zhu | Zendy; Shoujun Bai | Zendy

Open Access

Long non-coding RNA MEG3 promotes fibrosis and inflammatory response in diabetic nephropathy via miR-181a/Egr-1/TLR4 axis

Author(s) -

Fangfang Zha,

Xiaolu Qu,

Bo Tang,

Ji Li,

Yakun Wang,

Pengxi Zheng,

Tingting Ji,

Chun Zhu,

Shoujun Bai

Publication year - 2019

Publication title -

aging

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.473

H-Index - 90

ISSN - 1945-4589

DOI - 10.18632/aging.102011

Subject(s) - meg3 , fibrosis , long non coding rna , in vivo , downregulation and upregulation , diabetic nephropathy , tlr4 , rna , in vitro , cancer research , competing endogenous rna , inflammation , chemistry , microbiology and biotechnology , biology , signal transduction , gene , medicine , diabetes mellitus , immunology , endocrinology , biochemistry , genetics

Long non-coding RNAs (lncRNAs) play vital roles in diabetic nephropathy (DN). This research aimed to study the potential role and underlying molecular mechanisms of long non-coding RNA MEG3 in DN. We found that MEG3 was upregulated in DN in vivo and in vitro and could enhance cell fibrosis and inflammatory response in DN. MEG3 functioned as an endogenous sponge for miR-181a in mesangial cells (MCs) via direct targeting and in an Ago2-dependent manner. MiR-181a inhibition promoted MC fibrosis and inflammatory response. In addition, Egr-1 was confirmed as a target gene of miR-181a. Further investigations verified that MEG3 promotes fibrosis and inflammatory response via the miR-181a/Egr-1/TLR4 axis in vitro and in vivo. These results provide new insights into the regulation between MEG3 and the miR-181a/Egr-1/TLR4 signaling pathway during DN progression.

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