ArticlePloS one2013
Apoptosis of bone marrow mesenchymal stem cells caused by homocysteine via activating JNK signal.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 43 citations in OpenAlex.
- Astragalus polysaccharides inhibit arsenic trioxide-induced BMSCs damage through inhibition of Jnk and p38 signaling pathways.Chinese herbal medicines · 2026Article
- Recent advances in targeting cyanine dyes: hierarchical targeting mechanisms and theranostic integration for multi-disease precision therapy.Theranostics · 2026Review
- Exploring the effects of homocysteine metabolism in osteoporosis management in Indian adult females.International journal of molecular epidemiology and genetics · 2024Article
- Sodium selenite preserves rBM-MSCs' stemness, differentiation potential, and immunophenotype and protects them against oxidative stress via activation of the Nrf2 signaling pathway.BMC complementary medicine and therapies · 2023Article
- Resolving Geroplasticity to the Balance of Rejuvenins and Geriatrins.Aging and disease · 2022Article
- Article
- Effectiveness of mesenchymal stem cells cultured under hypoxia to increase the fertility rate in rats (Veterinary world · 2021Article
- Systems analysis of avascular necrosis of femoral head using integrative data analysis and literature mining delineates pathways associated with disease.Scientific reports · 2020Article
- Hyperhomocysteinemia inhibits tibial fracture healing in rats through PI3K/AKT signaling pathway.Experimental and therapeutic medicine · 2020Article
- miR-149-3p Regulates the Switch between Adipogenic and Osteogenic Differentiation of BMSCs by Targeting FTO.Molecular therapy. Nucleic acids · 2019Article
- Hydrogen sulfide attenuates homocysteine-induced osteoblast dysfunction by inhibiting mitochondrial toxicity.Journal of cellular physiology · 2019Article
- Comparison of biotechnological culture of hypoxia-conditioned rat mesenchymal stem cells with conventionalVeterinary world · 2019Article
- Restoration of skeletal muscle homeostasis by hydrogen sulfide during hyperhomocysteinemia-mediated oxidative/ER stress conditionCanadian journal of physiology and pharmacology · 2019Review
- The Effects of Homocysteine on the Skeleton.Current osteoporosis reports · 2018Review
- Challenges and opportunities for stem cell therapy in patients with chronic kidney disease.Kidney international · 2016Review
- Mitochondrial epigenetics in bone remodeling during hyperhomocysteinemia.Molecular and cellular biochemistry · 2014Review
- Regulatory role of the JNK-STAT1/3 signaling in neuronal differentiation of cultured mouse embryonic stem cells.Cellular and molecular neurobiology · 2014Article
- Article
- The beneficial effect of melatonin in brain endothelial cells against oxygen-glucose deprivation followed by reperfusion-induced injury.Oxidative medicine and cellular longevity · 2014Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bone marrow mesenchymal stem cells (BMSCs) are capable of homing to and repair damaged myocardial tissues. Apoptosis of BMSCs in response to various pathological stimuli leads to the attenuation of healing ability of BMSCs. Plenty of evidence has shown that elevated homocysteine level is a novel independent risk factor of cardiovascular diseases. The present study was aimed to investigate whether homocysteine may induce apoptosis of BMSCs and its underlying mechanisms. Here we uncovered that homocysteine significantly inhibited the cellular viability of BMSCs. Furthermore, TUNEL, AO/EB, Hoechst 333342 and Live/Death staining demonstrated the apoptotic morphological appearance of BMSCs after homocysteine treatment. A distinct increase of ROS level was also observed in homocysteine-treated BMSCs. The blockage of ROS by DMTU and NAC prevented the apoptosis of BMSCs induced by homocysteine, indicating ROS was involved in the apoptosis of BMSCs. Moreover, homocysteine also caused the depolarization of mitochondrial membrane potential of BMSCs. Furthermore, apoptotic appearance and mitochondrial membrane potential depolarization in homocysteine-treated BMSCs was significantly reversed by JNK inhibitor but not p38 MAPK and ERK inhibitors. Western blot also confirmed that p-JNK was significantly activated after exposing BMSCs to homocysteine. Homocysteine treatment caused a significant reduction of BMSCs-secreted VEGF and IGF-1 in the culture medium. Collectively, elevated homocysteine induced the apoptosis of BMSCs via ROS-induced the activation of JNK signal, which provides more insight into the molecular mechanisms of hyperhomocysteinemia-related cardiovascular diseases.
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