ArticleAmerican journal of physiology. Heart and circulatory physiology2012
α-Crystallin B prevents apoptosis after H2O2 exposure in mouse neonatal cardiomyocytes.
Article in American journal of physiology. Heart and circulatory physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 74 citations in OpenAlex.
- Article
- Hypertrophic Cardiomyopathy-Associated CRYABInternational journal of molecular sciences · 2025Article
- Quantitative proteome analysis of LAP1-deficient human fibroblasts: A pilot approach for predicting the signaling pathways deregulated in LAP1-associated diseases.Biochemistry and biophysics reports · 2024Article
- A novel αB-crystallin R123W variant drives hypertrophic cardiomyopathy by promoting maladaptive calcium-dependent signal transduction.Frontiers in cardiovascular medicine · 2023Article
- Interplay between Nrf2 and αB-crystallin in the lens and heart of zebrafish under proteostatic stress.Frontiers in molecular biosciences · 2023Article
- Transcriptomics reveal stretched human pluripotent stem cell-derived cardiomyocytes as an advantageous hypertrophy model.Journal of molecular and cellular cardiology plus · 2022Article
- Article
- Alpha B-Crystallin in Muscle Disease Prevention: The Role of Physical Activity.Molecules (Basel, Switzerland) · 2022Review
- Therapeutic Potential of α-Crystallins in Retinal Neurodegenerative Diseases.Antioxidants (Basel, Switzerland) · 2021Review
- HSPB5 (αB-crystallin) confers protection against paraquat-induced oxidative stress at the organismal level in a tissue-dependent manner.Cell stress & chaperones · 2021Article
- Role of the Mitochondrial Protein Import Machinery and Protein Processing in Heart Disease.Frontiers in cardiovascular medicine · 2021Review
- Alpha B-Crystallin Overexpression Protects Oligodendrocyte Precursor Cells Against Oxidative Stress-Induced Apoptosis Through the Akt Pathway.Journal of molecular neuroscience : MN · 2020Article
- An Integrated Network Analysis of mRNA and Gene Expression Profiles in Parkinson's Disease.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- REEP5 depletion causes sarco-endoplasmic reticulum vacuolization and cardiac functional defects.Nature communications · 2020Article
- CRYAB promotes osteogenic differentiation of human bone marrow stem cells via stabilizing β-catenin and promoting the Wnt signalling.Cell proliferation · 2020Article
- HspB5 protects mouse neural stem/progenitor cells from paraquat toxicity.American journal of stem cells · 2020Article
- Peptidomics Analysis Reveals Peptide PDCryab1 Inhibits Doxorubicin-Induced Cardiotoxicity.Oxidative medicine and cellular longevity · 2020Article
- Oral delivery of xenon for cardiovascular protection.Scientific reports · 2019Article
- Moonlighting Proteins and Cardiopathy in the Spatial Response of MCF-7 Breast Cancer Cells to Tamoxifen.Proteomics. Clinical applications · 2019Article
- AKAP6 and phospholamban colocalize and interact in HEK-293T cells and primary murine cardiomyocytes.Physiological reports · 2019Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
α-Crystallin B (cryAB) is the most abundant small heat shock protein in cardiomyocytes (CMs) and has been shown to have potent antiapoptotic properties. Because the mechanism by which cryAB prevents apoptosis has not been fully characterized, we examined its protective effects at the cellular level by silencing cryAB in mouse neonatal CMs using lentivector-mediated transduction of short hairpin RNAs. Subcellular fractionation of whole hearts showed that cryAB is cytosolic under control conditions, and after H(2)O(2) exposure, it translocates to the mitochondria. Phosphorylated cryAB (PcryAB) is mainly associated with the mitochondria, and any residual cytosolic PcryAB translocates to the mitochondria after H(2)O(2) exposure. H(2)O(2) exposure caused increases in cryAB and PcryAB levels, and cryAB silencing resulted in increased levels of apoptosis after exposure to H(2)O(2). Coimmunoprecipitation assays revealed an apparent interaction of both cryAB and PcryAB with mitochondrial voltage-dependent anion channels (VDAC), translocase of outer mitochondrial membranes 20 kDa (TOM 20), caspase 3, and caspase 12 in mouse cardiac tissue. Our results are consistent with the conclusion that the cardioprotective effects of cryAB are mediated by its translocation from the cytosol to the mitochondria under conditions of oxidative stress and that cryAB interactions with VDAC, TOM 20, caspase 3, and caspase 12 may be part of its protective mechanism.
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