ArticleInternational journal of biological sciences2015
MicroRNA-1 participates in nitric oxide-induced apoptotic insults to MC3T3-E1 cells by targeting heat-shock protein-70.
Article in International journal of biological sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 31 citations in OpenAlex.
- Hypertension and Diabetes Cooperatively Drive HSP90 Activation, HSP70 Suppression, and Left Ventricular Interstitial Expansion: Relevance to Maladaptive Myocardial Remodeling.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026Article
- Review
- Exploring the Heat-Responsive miRNAs and their Target Gene Regulation in Ruditapes philippinarum Under Acute Heat Stress.Marine biotechnology (New York, N.Y.) · 2024Article
- The Role of Heat Shock Proteins in the Pathogenesis of Polycystic Ovarian Syndrome: A Review of the Literature.International journal of molecular sciences · 2023Review
- Insights into the expression of DNA (de)methylation genes responsive to nitric oxide signaling in potato resistance to late blight disease.Frontiers in plant science · 2022Article
- Apoptosis-promoting properties of miR-3074-5p in MC3T3-E1 cells under iron overload conditions.Cellular & molecular biology letters · 2021Article
- Ubiquitin‑proteasomes are the dominant mediators of the regulatory effect of microRNA‑1 on cardiac remodeling after myocardial infarction.International journal of molecular medicine · 2019Article
- Metformin Protects against HMolecular therapy. Nucleic acids · 2018Article
- Identification of miRNA, lncRNA and mRNA-associated ceRNA networks and potential biomarker for MELAS with mitochondrial DNA A3243G mutation.Scientific reports · 2017Article
- Cold Inducible RNA Binding Protein Is Involved in Chronic Hypoxia Induced Neuron Apoptosis by Down-Regulating HIF-1α Expression and Regulated By microRNA-23a.International journal of biological sciences · 2017Article
- Molecular Cloning and Induced Expression of Six Small Heat Shock Proteins Mediating Cold-Hardiness inFrontiers in physiology · 2017Article
- Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Our previous studies showed that nitric oxide (NO) could induce osteoblast apoptosis. MicroRNA-1 (miR-1), a skeletal- and cardiac muscle-specific small non-coding RNA, contributes to the regulation of multiple cell activities. In this study, we evaluated the roles of miR-1 in NO-induced insults to osteoblasts and the possible mechanisms. Exposure of mouse MC3T3-E1 cells to sodium nitroprusside (SNP) increased amounts of cellular NO and intracellular reactive oxygen species. Sequentially, SNP decreased cell survival but induced caspase-3 activation, DNA fragmentation, and cell apoptosis. In parallel, treatment with SNP induced miR-1 expression in a time-dependent manner. Application of miR-1 antisense inhibitors to osteoblasts caused significant inhibition of SNP-induced miR-1 expression. Knocking down miR-1 concurrently attenuated SNP-induced alterations in cell morphology and survival. Consecutively, SNP time-dependently inhibited heat-shock protein (HSP)-70 messenger (m)RNA and protein expressions. A bioinformatic search predicted the existence of miR-1-specific binding elements in the 3'-untranslational region of HSP-70 mRNA. Downregulation of miR-1 expression simultaneously lessened SNP-induced inhibition of HSP-70 mRNA and protein expressions. Consequently, SNP-induced modifications in the mitochondrial membrane potential, caspase-3 activation, DNA fragmentation, and apoptotic insults were significantly alleviated by miR-1 antisense inhibitors. Therefore, this study showed that miR-1 participates in NO-induced apoptotic insults through targeting HSP-70 gene expression.
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