MiR‐214 is an important regulator of the musculoskeletal metabolism and disease

Sun, Youqiang; Kuek, Vincent; Wang, Kun; Tickner, Jennifer; Yuan, Yu; Chen, Leilei; Zeng, Zhilin; Shao, Min; He, Wei; Xu, Jiake

doi:10.1002/jcp.26856

Cited by 53 publications

(46 citation statements)

References 213 publications

(361 reference statements)

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“…MiR-214-3p is involved in many pathological and physiological processes, such as cell growth, migration, proliferation, invasion, apoptosis, and fibrosis. 51,52 Our previous study also demonstrated that miR-214-3p plays an important role in regulating cardiac pyroptosis by binding to the caspase-1 during diabetic cardiomyopathy progression. 28 Moreover, consistent with the present study, our previous report has documented that the level of miR-214-3p is significantly decreased in patients with DM, 53 which is in agreement with the published data by other groups, 54,55 suggesting the possible implication of our findings in humans.…”

Section: Discussionmentioning

confidence: 90%

Melatonin exerts neuroprotective effects by inhibiting neuronal pyroptosis and autophagy in STZ‐induced diabetic mice

Che

Yang

et al. 2020

FASEB j.

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Diabetes mellitus (DM) patients are at a higher risk of developing brain injury characterized by neuronal death. Melatonin, a hormone produced by the pineal gland, exerts neuroprotective effects against brain damage. However, the effect of melatonin on diabetes‐induced brain injury has not been elucidated. This study was to evaluate the role of melatonin against neuronal death in DM and to elucidate the underlying mechanisms. Herein, we found that melatonin administration significantly alleviated the neuronal death in both streptozotocin (STZ)‐induced diabetic mice and high glucose (HG)‐treated neuronal cells. Melatonin inhibited neuronal pyroptosis and excessive autophagy, as evidenced by decreased levels of NLRP3, cleaved caspase‐1, GSDMD‐N, IL‐1β, LC3, Beclin1, and ATG12 both in vivo and in vitro. MicroRNA‐214‐3p (miR‐214‐3p) was decreased in DM mice and HG‐treated cells, and such a downregulation was corrected by melatonin, which was accompanied by repression of caspase‐1 and ATG12. Furthermore, downregulation of miR‐214‐3p abrogated the anti‐pyroptotic and anti‐autophagic actions of melatonin in vitro. Our results indicate that melatonin exhibits a neuroprotective effect by inhibiting neuronal pyroptosis and excessive autophagy through modulating the miR‐214‐3p/caspase‐1 and miR‐214‐3p/ATG12 axes, respectively, and it might be a potential agent for the treatment of brain damage in the setting of DM.

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Section: Discussionmentioning

confidence: 90%

Melatonin exerts neuroprotective effects by inhibiting neuronal pyroptosis and autophagy in STZ‐induced diabetic mice

Che

Yang

et al. 2020

FASEB j.

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“…Chromatin immunoprecipitation (ChIP) enables the analysis of interactions between proteins and DNA in chromosomal fragments and the identification of the binding sites of transcription factors and other proteins [ 180 , 187 ]. Additionally, four web-based miRNA databases, miRBase ( http://www.mirbase.org ), TargetScan ( http://www.targetscan.org ), PicTar ( http://www.pictar.mdc-berlin.de ), and miRanda ( http://www.microRNA.org ), are essential for bioinformatics analysis [ 108 ]. Assays of pit formation, actin ring formation, cell migration, macrophage commitment, and apoptosis are also widely used to evaluate the functions and generation of osteoclasts [ 86 , 98 , 115 , 129 , 147 , 153 ].…”

Section: Discussionmentioning

confidence: 99%

Involvement of Noncoding RNAs in the Differentiation of Osteoclasts

Zhao

Jia

Zheng

et al. 2020

Stem Cells International

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As the most important bone-resorbing cells, osteoclasts play fundamental roles in bone remodeling and skeletal health. Much effort has been focused on identifying the regulators of osteoclast metabolism. Noncoding RNAs (ncRNAs) reportedly regulate osteoclast formation, differentiation, survival, and bone-resorbing activity to participate in bone physiology and pathology. The present review intends to provide a general framework for how ncRNAs and their targets regulate osteoclast differentiation and the important events of osteoclastogenesis they are involved in, including osteoclast precursor generation, early differentiation, mononuclear osteoclast fusion, and multinucleated osteoclast function and survival. This framework is beneficial for understanding bone biology and for identifying the potential biomarkers or therapeutic targets of bone diseases. The review also summarizes the results of in vivo experiments and classic experiment methods for osteoclast-related researches.

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“…Our ndings illustrated that miR-214 was downregulated in hyperoxia-induced BPD neonatal rats. MiR-214, a member of microRNA precursors, plays a pivotal role in the pathogenesis of multiple human disorders, including cardiovascular diseases and cancers [24,25]. The expression of miR-214 increased by TWIST1 promotes the epithelial-to-mesenchymal transition and metastasis in lung adenocarcinoma [26].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-214 Prevents Pulmonary Angiogenesis and Alveolarization in Rat Models with Bronchopulmonary Dysplasia via PlGF-Dependent STAT3 Signaling Pathway

Zhiqun

Hong

et al. 2020

Preprint

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Background: In recent years, the roles of microRNAs (miRNAs) in pulmonary diseases have been widely studied and researched. However, the molecular mechanism by which miR-214 affects bronchopulmonary dysplasia (BPD) remains elusive and merits further exploration. Hence, this study aims to clarify the function of miR-214 in pulmonary angiogenesis and alveolarization in preterm infants with BPD. Methods: BPD neonatal rat model was induced by hyperoxia, and pulmonary epithelial cells were isolated from rats and exposed to hyperoxia. Gain- or loss-of-function experiments were performed in BPD neonatal rats and hyperoxic pulmonary epithelial cells. MiR-214 and PlGF expression in BPD neonatal rats, and eNOS, Bcl-2, c-myc, Survivin, α-SMA and E-cadherin expression in hyperoxic pulmonary epithelial cells were detected using RT-qPCR and western blot analysis. The interaction between PlGF and miR-214 was identified using dual luciferase reporter gene assay and RIP assay. ELISA was adopted to assess IL-1β, TNF-a, IL-6, ICAM-1 and Flt-1 expression in rats. Results: Decreased miR-214 expression and elevated PlGF expression were evident in the lung tissues of neonatal rats with BPD. PlGF was a target of miR-214, and miR-214 downregulated PlGF to inactivate the STAT3 signaling pathway. miR-214 overexpression or PlGF silencing decreased apoptosis of hyperoxic pulmonary epithelial cells and declined pulmonary angiogenesis and alveolarization in BPD neonatal rats. Conclusions: Collectively, miR-214 can protects against pulmonary angiogenesis and alveolarization in preterm infants with BPD by suppressing PlGF and blocking STAT3 signaling pathway.

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MiR‐214 is an important regulator of the musculoskeletal metabolism and disease

Cited by 53 publications

References 213 publications

Melatonin exerts neuroprotective effects by inhibiting neuronal pyroptosis and autophagy in STZ‐induced diabetic mice

Melatonin exerts neuroprotective effects by inhibiting neuronal pyroptosis and autophagy in STZ‐induced diabetic mice

Involvement of Noncoding RNAs in the Differentiation of Osteoclasts

MicroRNA-214 Prevents Pulmonary Angiogenesis and Alveolarization in Rat Models with Bronchopulmonary Dysplasia via PlGF-Dependent STAT3 Signaling Pathway

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