Novel lncRNA Erbb4-IR Promotes Diabetic Kidney Injury in <i>db/db</i> Mice by Targeting miR-29b

Sun, Si; Tang, Patrick Ming‐Kuen; Feng, Min; Xiao, Jun; Huang, Xiao Ru; Li, Ping; Ma, Rong; Lan, Hui‐Yao

doi:10.2337/db17-0816

Cited by 140 publications

(182 citation statements)

References 36 publications

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“…The lncRNAs ENSRNOG00000037522 and LINC01619 have been reported to participate in podocyte injury in DN [34,35]. Further, Erbb4-IR is reportedly a Smad3-dependent lncRNA that promotes renal fibrosis in type 2 DN [36]. The lncRNA Gm4419 has been reported to regulate inflammation in DN [13].…”

Section: Discussionmentioning

confidence: 99%

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The Long Noncoding RNA 150Rik Promotes Mesangial Cell Proliferation via miR-451/IGF1R/p38 MAPK Signaling in Diabetic Nephropathy

Zhang¹,

Sun²,

Peng³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Diabetic nephropathy (DN) as the primary cause of end-stage kidney disease is a common complication of diabetes. However, the initiating molecular events triggering DN are unknown. Recently, long noncoding RNAs (lncRNAs) have been shown to play important roles in DN. Methods: The expression level of lncRNA 1500026H17Rik (150Rik for short) was measured by qRT-PCR (quantitative real-time PCR). Cell proliferation ability was detected by 5-Ethynyl-2’-deoxyuridine (EdU). The relationship between 150Rik and microRNA 451 (miR-451) was examined by luciferase assay and RNA immunoprecipitation (RIP) assay. Finally, the effect of 150Rik on cell proliferation through the miR-451/insulin-like growth factor 1 receptor (IGF1R)/mitogen-activated protein kinases (p38MAPK) pathway was detected by EdU, flow cytometry analysis, western blot. Results: We found that 150Rik, an evolutionarily conserved lncRNA, was significantly upregulated in renal tissue of db/db DN mice and in mesangial cells (MCs) cultured under a high glucose condition. Further, overexpression or knockdown of 150Rik was found to regulate cell proliferation in MCs. Moreover, 150Rik was found to interact with miR-451 in both a direct and argonaute-2 (Ago2)-dependent manner. Results also revealed that overexpression of 150Rik inhibited cell proliferation through the miR-451/IGF1R/p38MAPK pathway in MCs under the high glucose condition, while knockdown of 150Rik increased cell proliferation via the miR-451/IGF1R/p38MAPK pathway. Conclusion: Taken together, these results provide new insight into the association between 150Rik and the miR-451/IGF1R/p38MAPK signaling pathway during DN progression.

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Section: Discussionmentioning

confidence: 99%

“…Studies have also shown that lncRNAs are involved in various diseases, including DN [28][29][30][31]. Two lncRNAs, ENSMUST00000147869 and CYP4B1-PS1-001, have recently been reported to regulate MCs proliferation and fibrosis induced by DN [29,32].…”

Section: Discussionmentioning

confidence: 99%

The Long Noncoding RNA 150Rik Promotes Mesangial Cell Proliferation via miR-451/IGF1R/p38 MAPK Signaling in Diabetic Nephropathy

Zhang¹,

Sun²,

Peng³

et al. 2018

Cell Physiol Biochem

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“…Our recent study demonstrated that the origin of a novel lncRNA could be identified by a combination of fluorescent in situ hybridization (FISH) and immunohistochemistry (IHC) staining on diabetic injured kidney section (Sun et al . ) (Fig. ).…”

Section: Introductionmentioning

confidence: 93%

“…More importantly, silencing of renal Erbb4‐IR significantly inhibited the expression of collagen I in both diabetic‐ and obstructive‐injured kidneys in vivo (Sun et al . ; Feng et al . ).…”

Section: Introductionmentioning

confidence: 99%

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Transforming growth factor‐β signalling in renal fibrosis: from Smads to non‐coding RNAs

Tang

Zhang

Mak

et al. 2018

The Journal of Physiology

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Transforming growth factor-β (TGF-β) is the key player in tissue fibrosis. However, antifibrotic therapy targeting this multifunctional protein may interfere with other physiological processes to cause side effects. Thus, precise therapeutic targets need to be identified by further understanding the underlying mechanisms of TGF-β1 signalling during fibrogenesis. Equilibrium of Smad signalling is crucial for TGF-β-mediated renal fibrosis, where Smad3 is pathogenic but Smad2 and Smad7 are protective. The activation of TGF-β1/Smad signalling triggers extracellular matrix deposition, and local myofibroblast generation and activation. Mechanistic studies have shown that TGF-β/Smad3 transits the microRNA profile from antifibrotic to profibrotic and therefore promotes renal fibrosis via regulating non-coding RNAs at transcriptional levels. More importantly, disease-specific Smad3-dependent long non-coding RNAs have been recently uncovered from mouse kidney disease models and may represent novel precision therapeutic targets for chronic kidney disease. In this review, mechanisms of TGF-β-driven renal fibrosis via non-coding RNAs and their translational capacities will be discussed in detail.

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miR‐185 affected the EMT, cell viability, and proliferation via DNMT1/MEG3 pathway in TGF‐β1‐induced renal fibrosis

Xue

et al. 2019

Cell Biology International

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Kidney fibrosis is usually the final manifestation of a wide variety of renal diseases. Recent years, research reported that lncRNAs played important roles in a variety of human diseases. However, the role and underlying mechanisms of lncRNAs in kidney fibrosis were complicated and largely unclear. In our study, we constructed the cell model of renal fibrosis in HK2 cells using TGF-β1 and found that lncRNA MEG3 was down-regulated in TGF-β1-induced renal fibrosis. We then found that overexpressed MEG3 inhibited the TGF-β1-induced promotion of EMT, cell viability and proliferation. Furthermore, we demonstrated that DNMT1 regulated the MEG3 expression via altering the CpGs methylation level of MEG3 promoter in TGF-β1-induced renal fibrosis. In addition, we further revealed that miR-185 could regulated the DNMT1 expression and thus, modulating the MEG3 in TGF-β1-induced renal fibrosis. Ultimately, our study illustrated that the modulation of the miR-185/ DNMT1/ MEG3 pathway exerted important roles in TGF-β1-induced renal fibrosis. In summary, our finding displayed a novel regulatory mechanism for TGF-β1-induced renal fibrosis, which provided a new potential therapeutic target for renal fibrosis.

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Novel lncRNA Erbb4-IR Promotes Diabetic Kidney Injury in db/db Mice by Targeting miR-29b

Cited by 140 publications

References 36 publications

The Long Noncoding RNA 150Rik Promotes Mesangial Cell Proliferation via miR-451/IGF1R/p38 MAPK Signaling in Diabetic Nephropathy

The Long Noncoding RNA 150Rik Promotes Mesangial Cell Proliferation via miR-451/IGF1R/p38 MAPK Signaling in Diabetic Nephropathy

Transforming growth factor‐β signalling in renal fibrosis: from Smads to non‐coding RNAs

miR‐185 affected the EMT, cell viability, and proliferation via DNMT1/MEG3 pathway in TGF‐β1‐induced renal fibrosis

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