MiR-142-3p Enhances Cell Viability and Inhibits Apoptosis by Targeting CDKN1B and TIMP3 Following Sciatic Nerve Injury

Wu, Dongmei; Wen, Xin; Han, Xin‐Rui; Wang, Shan; Wang, Yongjian; Shen, Min; Fan, Shao‐Hua; Zhuang, Juan; Zhang, Zi-Feng; Shan, Qun; Li, Meng‐Qiu; Sun, Chunhui; Lü, Jun; Zheng, Yuxin

doi:10.1159/000489626

Cited by 17 publications

(14 citation statements)

References 34 publications

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“…For example, Bao et al found that miR-142-3p promoted endothelial cell proliferation via Bcl-2-associated transcription factor 1 [41]. In addition, Wu et al found that miR-142-3p promoted the neuronal cell cycle and inhibited apoptosis after peripheral nerve injury [42]. Thus, further investigation, especially the appropriate animal model studies, of microRNAs involved in the regulation of cell growth should be performed to clarify these issues.…”

Section: Discussionmentioning

confidence: 99%

Metformin inhibits high glucose-induced smooth muscle cell proliferation and migration

Zhou

Ran

et al. 2020

Aging

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We investigated the protective effects and mechanism of action of metformin on high glucose-induced smooth muscle cell proliferation and migration. Vascular smooth muscle cells (VSMCs) were subjected to a series of concentrations (0-10 mM) of metformin. CCK-8, wound healing, and transwell assays were performed. Correlations between metformin concentration and high-mobility group box 1 (HMGB1) and miR-142-3p levels were assessed. In addition, miR-142-3p mimic and siRNA were used to investigate VSMC migration in the presence or absence of metformin. In the high-glucose condition, metformin decreased cell growth and inhibited cell migration. HMGB1 gene expression correlated negatively with metformin concentration, whereas miR-142-3p expression correlated positively with metformin concentration. In addition, mimic-induced miR-142-3p elevation resulted in decreased HMGB1 and LC3II levels and elevated p62 levels in the high-glucose condition, whereas miR-142-3p knockdown had the reverse effects, and metformin abolished those effects. Metformin inhibits high glucose-induced VSMC hyperproliferation and increased migration by inducing miR-142-3p-mediated inhibition of HMGB1 expression via the HMGB1-autophagy related pathway.

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Section: Discussionmentioning

confidence: 99%

Metformin inhibits high glucose-induced smooth muscle cell proliferation and migration

Zhou

Ran

et al. 2020

Aging

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“…Numerous investigations have shown that miRNAs play a vital role in PNI and peripheral nerve repair; for instance, the expression of miRNAs in dorsal root ganglia (DRG) tissues after sciatic nerve injury in rats was significantly changed ( Li et al, 2012 ). miR-142-3p can target CDKN1B and TIMP3 to enhance the viability of rat DRG neurons and inhibit apoptosis after sciatic nerve injury ( Wu D.M. et al, 2018 ).…”

Section: Discussionmentioning

confidence: 99%

Electroacupuncture Promoted Nerve Repair After Peripheral Nerve Injury by Regulating miR-1b and Its Target Brain-Derived Neurotrophic Factor

et al. 2020

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Growing evidence indicates that electroacupuncture (EA) has a definite effect on the treatment of peripheral nerve injury (PNI), but its mechanism is not completely clear. MicroRNAs (miRNAs) are involved in the regulation of a variety of biological processes, and EA may enhance PNI repair by regulating miRNAs. In this study, the rat sciatic nerve injury model was treated with EA for 4 weeks. Acupoints Huantiao (GB30) and Zusanli (ST36) were stimulated by EA 20 min once a day, 6 days a week for 4 weeks. We found that EA treatment downregulated the expression of miR-1b in the local injured nerve. In vitro experiments showed that overexpression of miR-1b inhibited the expression of brain-derived neurotrophic factor (BDNF) in rat Schwann cell (SC) line, while BDNF knockdown inhibited the proliferation, migration, and promoted apoptosis of SCs. Subsequently, the rat model of sciatic nerve injury was treated by EA treatment and injection of agomir-1b or antagomir-1b. The nerve conduction velocity ratio (NCV), sciatic functional index (SFI), and S100 immunofluorescence staining were examined and showed that compared with the model group, NCV, SFI, proliferation of SC, and expression of BDNF in the injured nerves of rats treated with EA or EA + anti-miR-1b were elevated, while EA + miR-1b was reduced, indicating that EA promoted sciatic nerve function recovery and SC proliferation through downregulating miR-1b. To summarize, EA may promote the proliferation, migration of SC, and nerve repair after PNI by regulating miR-1b, which targets BDNF.

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“…MiRNA participates in biological processes in human organism mainly by regulating the expression of its target genes [30,31]. Dong-Mei Wu et al shown that miR-142-3p can partially promote the neuronal cell cycle and inhibit cell apoptosis by inhibiting CDKN1B and TIMP3 expressions [32]. In this study, the miR-221-3p mimic down-regulated CDKN1B level, while miR-221-3p inhibitor up-regulated CDKN1B level.…”

Section: Discussionmentioning

confidence: 46%

Study on the ameliorating effect of miR-221-3p on the nerve cells injury induced by sevoflurane

Wang

Tian

et al. 2020

International Journal of Neuroscience

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Purpose: Sevoflurane is a widely used anesthetics, however, it has been reported that sevoflurane has neurotoxic effects. Studies have shown that miR-221-3p can ameliorate neuron damage. This study was to investigate whether miR-221-3p could reduce the neurotoxic effect of sevoflurane on nerve cells. Materials and methods: The rat hippocampal neuron cells were treated with sevoflurane or cultured normally. And we constructed neuron cells that overexpressed or low expression of miR-221-3p in the presence or absence of sevoflurane. The cells were transfected with CDKN1B or siCDKN1B, and co-transfected with miR-221-3p mimic and CDKN1B or miR-221-3p inhibitor and siCDKN1B. Cell viability and apoptosis were detected by CCK-8 and flow cytometer. Target gene of miR-221-3p were predicted by TargetScan and luciferase reporter assay. The expressions of related genes were detected by western blotting and quantitative real-time polymerase chain reaction. Results: Sevoflurane decreased miR-221-3p level and increased CDKN1B level, inhibited cell viability and promoted apoptosis. Overexpress of miR-221-3p decreased CDKN1B level, up-regulated cell viability and inhibited apoptosis, and reversed the effects of sevoflurane on cell viability and apoptosis, while the effects low expression of miR-221-3p was contrary. CDKN1B was the target gene of miR-221-3p, which inhibited cell viability and promoted apoptosis, and reversed the effects of miR-221-3p mimic, whereas siCDKN1B did the opposite effects. Conclusions: Sevoflurane can cause nerve cell injury, and miR-221-3p may promote cell activity and inhibit apoptosis by inhibiting CDKN1B expression, thereby ameliorating cell injury induced by sevoflurane.

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MiR-142-3p Enhances Cell Viability and Inhibits Apoptosis by Targeting CDKN1B and TIMP3 Following Sciatic Nerve Injury

Cited by 17 publications

References 34 publications

Metformin inhibits high glucose-induced smooth muscle cell proliferation and migration

Metformin inhibits high glucose-induced smooth muscle cell proliferation and migration

Electroacupuncture Promoted Nerve Repair After Peripheral Nerve Injury by Regulating miR-1b and Its Target Brain-Derived Neurotrophic Factor

Study on the ameliorating effect of miR-221-3p on the nerve cells injury induced by sevoflurane

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