Role and mechanism of microRNA-21 in H2O2-induced apoptosis in bone marrow mesenchymal stem cells

Hao, Yuehan; Han, Yaxin; Zhang, Wei; Liu, Cong; Shi, Yiting; Tu, Guanjun

doi:10.1016/j.jocn.2015.07.029

Cited by 25 publications

(21 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Based on our observations, ethanol negatively regulates bone formation and BMSC osteogenic differentiation via PTEN activation. Previous studies by other scientists have indicated that PTEN may contribute to antiapoptosis, proliferation, and differentiation mechanisms in BMSCs [49]. Davis HM et al demonstrated that the role of PTEN signaling in osteocyte apoptosis, osteoclast formation/ recruitment and skeletal aging [50].…”

Section: Discussionmentioning

confidence: 99%

Diminished membrane recruitment of Akt is instrumental in alcohol‐associated osteopenia via the PTEN/Akt/GSK‐3β/β‐catenin axis

et al. 2019

View full text Add to dashboard Cite

Alcohol is considered a leading risk factor for osteopenia. Our previous research indicated that the Akt/GSK‐3β/β‐catenin pathway plays a critical role in the ethanol‐induced antiosteogenic effect in bone mesenchymal stem cells (BMSCs). PI3K/Akt is negatively regulated by the phosphatase and tensin homolog (PTEN) phosphatase. In this study, we found that ethanol increased PTEN expression in the BMSCs and bone tissue of ethanol‐treated Sprague–Dawley rats. PTEN upregulation impaired Akt recruitment to the plasma membrane and suppressed Akt phosphorylation at Ser473, thereby inhibiting Akt/GSK3β/β‐catenin signaling and the expression of COL1 and OCN in BMSCs in vitro and in vivo. The results of in vivo assays indicated that PTEN inhibition protected bone tissue against ethanol. Interestingly, our data revealed that following ethanol stimulation, PTEN and PTEN pseudogene 1 (PTENP1) mRNA expression was increased in a time‐dependent manner, resulting in an increased PTEN protein level. In addition, ethanol upregulated PTEN expression and decreased PTEN phosphorylation (p‐PTEN), indicating an increase in functional PTEN levels. In summary, the ethanol‐mediated transcriptional and post‐transcriptional regulation of PTEN impaired downstream Akt/GSK3β/β‐catenin signaling and BMSC osteogenic differentiation. Therefore, we propose that Akt/GSK3β/β‐catenin activation via PTEN inhibition may be a potential therapeutic approach for preventing the development of alcohol‐induced osteopenia.

show abstract

Section: Discussionmentioning

confidence: 99%

Diminished membrane recruitment of Akt is instrumental in alcohol‐associated osteopenia via the PTEN/Akt/GSK‐3β/β‐catenin axis

et al. 2019

View full text Add to dashboard Cite

show abstract

“…The PI3K/Akt pathway has an anti-apoptotic effect via the phosphorylation of downstream protein Bad and the activation of B-cell lymphoma 2 (Bcl-2) (22). Previous studies demonstrated that activation of the PI3K/Akt pathway regulates the H 2 O 2 -induced apoptosis of rat BMSCs (rBMSCs) (23)(24)(25)(26)(27). The current study hypothesized that the antagonistic effect of ginsenoside Rg1 against the apoptosis of BMSCs induced by oxidative stress may be associated with the activation of the PI3K/Akt pathway.…”

Section: Introductionmentioning

confidence: 99%

Rg1 protects rat bone marrow stem cells against hydrogen peroxide-induced cell apoptosis through the PI3K/Akt pathway

Fan

2016

Molecular Medicine Reports

View full text Add to dashboard Cite

The aim of the present study was to investigate the protective mechanism of ginsenoside Rg1 against the apoptosis of rat bone marrow stem cells (rBMSCs) under oxidative stress, and to determine the association with the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) pathway. H2O2 was used to induce oxidative injury in rBMSCs. The cells in the H2O2 model group were treated with 800 µM H2O2 for 6 h to induce oxidative injury. The cells in the ginsenoside Rg1 group were treated with 10 µM ginsenoside Rg1 for 24 h, followed by H2O2 treatment. The cells in the Akt pathway blockage group were treated with 25 µM LY294002 for 1 h, followed by ginsenoside Rg1 + H2O2 treatment. The cell counting kit-8 assay was performed to determine cell viability. Cell apoptosis was detected by flow cytometry and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining. The results of flow cytometry and TUNEL staining indicated that the apoptotic rate of the H2O2 model group was significantly higher compared with that of the control group. Following the ginsenoside Rg1 pretreatment, the apoptotic rate was significantly reduced. In the Akt pathway blockage group, no significant alterations in the levels of cell apoptosis were observed compared with the H2O2 model group. Western blot analysis demonstrated that the ginsenoside Rg1 group had a significant downregulation of Bax and cleaved caspase‑3 and an upregulation of Bcl‑2 and phosphorylated Akt protein expression levels compared with the H2O2 model group and the Akt pathway blockage group. In conclusion, ginsenoside Rg1 had a protective effect against the H2O2‑induced oxidative stress of rBMSCs, and the specific mechanism may be associated with the activation of the PI3K/Akt pathway by ginsenoside Rg1.

show abstract

“…Second, miR-21 is proapoptotic as the DSS-treated miR-21 knockout mice had less intestinal epithelial cell apoptosis than controls [45]. Several studies have indicated a role for miR-21 in the protection of free radical-induced apoptosis that linked the pro-survival phenotype to the inhibition of phosphatase and tensin homology (PTEN) with subsequent elevation of PI3K-Akt-mTOR activity [46][47][48][49]. Additionally, miR-21 has been shown to prevent renal tubular apoptosis by directly reducing levels of Rab11 protein [50].…”

Section: Mir-21 Has An Essential Role In Ibd Development and Disease mentioning

confidence: 99%

MicroRNA in Inflammatory Bowel Disease

Fisher¹,

Ji²

2016

New Insights Into Inflammatory Bowel Disease

View full text Add to dashboard Cite

Idiopathic inlammatory bowel disease IBD is a complex set of disorders that predominantly includes ulcerative colitis and Crohn's disease. The pathogenesis of IBD is multifactorial including genetic, infectious, and immunologic factors. MicroRNAs belong to a class of noncoding small RNAs that postranscriptionally regulate gene expression, and they are an emerging class of genetic modiiers of IBD. Here, we focus on the use of unique microRNA expression paterns as biomarkers to classify and prognosticate disease severity in both mucosal tissue and serum from patients with either ulcerative colitis or Crohn's disease. Furthermore, we discuss speciic microRNAs with respect to their roles in IBD pathogenesis and ibrosis. We also discuss the role of microRNAs in IBD-associated carcinogenesis, including their role as biomarkers, tumor suppressors, and oncogenes. Finally, we discuss the emerging therapeutic applications of microRNA manipulation to lessen the efect of IBD and its sequelae. Recent discoveries of the diverse roles of microRNAs in IBD pathogenesis have the potential to provide new targeted therapeutics for personalized medicine.

show abstract

Role and mechanism of microRNA-21 in H2O2-induced apoptosis in bone marrow mesenchymal stem cells

Cited by 25 publications

References 33 publications

Diminished membrane recruitment of Akt is instrumental in alcohol‐associated osteopenia via the PTEN/Akt/GSK‐3β/β‐catenin axis

Diminished membrane recruitment of Akt is instrumental in alcohol‐associated osteopenia via the PTEN/Akt/GSK‐3β/β‐catenin axis

Rg1 protects rat bone marrow stem cells against hydrogen peroxide-induced cell apoptosis through the PI3K/Akt pathway

MicroRNA in Inflammatory Bowel Disease

Contact Info

Product

Resources

About