miR‐182‐5p overexpression inhibits chondrogenesis by down‐regulating PTHLH

Bai, Ming; Yin, He-Ping; Zhao, Jian; Yang, Li; Wu, Yimin

doi:10.1002/cbin.11047

Cited by 18 publications

(9 citation statements)

References 37 publications

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“…In the present study, to explore the pivotal anti‐inflammatory mechanism of miR‐182, an animal model of ALI was induced by the administration of LPS. We found that miR‐182 decreased in the lung of mice with ALI, which was content with previous results (Bai, Yin, Zhao, Li, & Wu, 2019). And the result of HE staining, MPO, D/W ratio, BALF and proinflammatory cytokines were proved successful establishment of an ALI model.…”

Section: Discussionsupporting

confidence: 92%

MicroRNA‐182 supplies negative feedback regulation to ameliorate lipopolysaccharide‐induced ALI in mice by targeting TLR4

Yang

Chen

Jiang

et al. 2020

Journal Cellular Physiology

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Acute lung injury (ALI), characterized by increased excessive pulmonary inflammation, is a pervasive inflammatory disease with clinically high incidence. MicroRNA (miRNAs) have been associated with the progression of multiple diseases and are regarded as novel regulators of inflammation. However, it remains largely unknown whether the miRNAsmediated regulatory mechanism has an effect on lipopolysaccharide (LPS)-induced inflammation in ALI. We discovered that miR-182 distinctly lessened expression in the lung tissue of mice with ALI and macrophages stimulated by LPS. We also found that overexpression of miR-182 significantly cut down the secretion of inflammatory cytokines, while this change was reversed by inhibition of miR-182. In addition, miR-182 suppressed the activation of NF-κB by targeting TLR4 expression. And it was confirmed that miR-182 directly regulated TLR4 expression at the posttranscriptional level by binding to the 3′-UTR of TLR4. Together, these data suggested that inhibition of TLR4 expression assuaged LPS-stimulated inflammation through negative feedback regulation of miR-182. K E Y W O R D Sacute lung injury, miR-182, NF-κB, TLR4

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Section: Discussionsupporting

confidence: 92%

MicroRNA‐182 supplies negative feedback regulation to ameliorate lipopolysaccharide‐induced ALI in mice by targeting TLR4

Yang

Chen

Jiang

et al. 2020

Journal Cellular Physiology

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“…Several miRNAs can regulate the development of IVDD [26][27][28] . Although miR-182-5p has been associated with a variety of human diseases 29,30 , this is the first study to identify miR-182-5p as a key factor in IVDD. We found that miR-182-5p could promote apoptosis and reduce mitophagy, and these effects were related to the regulation of circERCC2 on miR-182-5p/SIRT1 axis.…”

Section: Discussionmentioning

confidence: 90%

CircERCC2 ameliorated intervertebral disc degeneration by regulating mitophagy and apoptosis through miR-182-5p/SIRT1 axis

et al. 2019

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The molecular mechanism of intervertebral disc degeneration (IVDD) remains unclear. This study aimed to investigate the role of circular RNAs (circRNAs) in the pathogenesis of IVDD. We sued nucleus pulposus (NP) tissues of patients, tert-butyl hydroperoxide (TBHP) stimulated NP cells (NPCs), and IVDD rat model to explore the interaction between circERCC2 and miR-182-5p/SIRT1 axis. The results showed that downregulation of circERCC2 increased the level of miR-182-5p and decreased the level of SIRT1 in degenerative NP tissues in vivo as well as in TBHP-stimulated NPCs in vitro. Treatment of SIRT1-si activated apoptosis and inhibited mitophagy. Moreover, miR-182-5p-si could regulate the mitophagy and the apoptosis of NPCs by targeting SIRT1. The effects of circERCC2 on NPCs and IVDD rat model were mediated by miR-182-5p/SIRT1 axis. In conclusion, this study provides the first evidence that circERCC2 could ameliorate IVDD through miR-182-5p/SIRT1 axis by activating mitophagy and inhibiting apoptosis, and suggests that circERCC2 is a potentially effective therapeutic target for IVDD.

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“…MiR-92a-3p may be involved in regulating cartilage development by targeting WNT5A (Mao et al, 2018b). Conversely, miR-182-5p plays a negative role in BM-MSC chondrogenesis by downregulating parathyroid hormone-like hormone (PTHLH) (Bai et al, 2019). Table 1 summarizes the miRNAs, related to cartilage development, that have been studied in recent years.…”

Section: Cartilagementioning

confidence: 99%

Scaffold-Based Gene Therapeutics for Osteochondral Tissue Engineering

et al. 2020

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Significant progress in osteochondral tissue engineering has been made for biomaterials designed to deliver growth factors that promote tissue regeneration. However, due to diffusion characteristics of hydrogels, the accurate delivery of signaling molecules remains a challenge. In comparison to the direct delivery of growth factors, gene therapy can overcome these challenges by allowing the simultaneous delivery of growth factors and transcription factors, thereby enhancing the multifactorial processes of tissue formation. Scaffold-based gene therapy provides a promising approach for tissue engineering through transfecting cells to enhance the sustained expression of the protein of interest or through silencing target genes associated with bone and joint disease. Reports of the efficacy of gene therapy to regenerate bone/cartilage tissue regeneration are widespread, but reviews on osteochondral tissue engineering using scaffold-based gene therapy are sparse. Herein, we review the recent advances in gene therapy with a focus on tissue engineering scaffolds for osteochondral regeneration.

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miR‐182‐5p overexpression inhibits chondrogenesis by down‐regulating PTHLH

Abstract: miR-182-5p may play a negative role in chondrogenesis by down-regulating PTHLH.

Cited by 18 publications

References 37 publications

MicroRNA‐182 supplies negative feedback regulation to ameliorate lipopolysaccharide‐induced ALI in mice by targeting TLR4

MicroRNA‐182 supplies negative feedback regulation to ameliorate lipopolysaccharide‐induced ALI in mice by targeting TLR4

CircERCC2 ameliorated intervertebral disc degeneration by regulating mitophagy and apoptosis through miR-182-5p/SIRT1 axis

Scaffold-Based Gene Therapeutics for Osteochondral Tissue Engineering

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