ArticleAmerican journal of physiology. Heart and circulatory physiology2009
Kinetics of the translocation and phosphorylation of alphaB-crystallin in mouse heart mitochondria during ex vivo ischemia.
Article in American journal of physiology. Heart and circulatory physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
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- Insight into the biochemical and cell biological function of an intrinsically unstructured heat shock protein, Hsp12 of Ustilago maydis.Molecular plant pathology · 2023Article
- The interaction of heat shock proteins with cellular membranes: a historical perspective.Cell stress & chaperones · 2021Review
- HspB5 protects mouse neural stem/progenitor cells from paraquat toxicity.American journal of stem cells · 2020Article
- The small heat shock proteins, HSPB1 and HSPB5, interact differently with lipid membranes.Cell stress & chaperones · 2019Article
- Review
- Phosphorylation and degradation of αB-crystallin during enterovirus infection facilitates viral replication and induces viral pathogenesis.Oncotarget · 2017Article
- A comparison of phosphospecific affinity reagents reveals the utility of recombinant Forkhead-associated domains in recognizing phosphothreonine-containing peptides.New biotechnology · 2016Article
- Therapeutic potential of α-crystallin.Biochimica et biophysica acta · 2016Review
- Dysfunctional survival-signaling and stress-intolerance in aged murine and human myocardium.Experimental gerontology · 2014Article
- Effects of hyperbaric oxygen preconditioning on cardiac stress markers after simulated diving.Physiological reports · 2013Article
- O-GlcNAcylation of αB-crystallin regulates its stress-induced translocation and cytoprotection.Molecular and cellular biochemistry · 2013Article
- Novel roles for α-crystallins in retinal function and disease.Progress in retinal and eye research · 2012Review
- Small heat shock proteins in redox metabolism: implications for cardiovascular diseases.The international journal of biochemistry & cell biology · 2012Review
- αB-crystallin/sHSP protects cytochrome c and mitochondrial function against oxidative stress in lens and retinal cells.Biochimica et biophysica acta · 2012Article
- Study of αB-crystallin expression in Gerbil BCAO model of transient global cerebral ischemia.Oxidative medicine and cellular longevity · 2012Article
- Location matters: clarifying the concept of nuclear and cytosolic CaMKII subtypes.Circulation research · 2011Article
- Proteomic analysis reveals perturbed energy metabolism and elevated oxidative stress in hearts of rats with inborn low aerobic capacity.Proteomics · 2011Article
- SR-targeted CaMKII inhibition improves SR Ca²+ handling, but accelerates cardiac remodeling in mice overexpressing CaMKIIδC.Journal of molecular and cellular cardiology · 2011Article
- Constitutively active calcineurin induces cardiac endoplasmic reticulum stress and protects against apoptosis that is mediated by alpha-crystallin-B.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
alphaB-crystallin (alphaBC) is a small heat shock protein expressed at high levels in the myocardium where it protects from ischemia-reperfusion damage. Ischemia-reperfusion activates p38 MAP kinase, leading to the phosphorylation of alphaBC on serine 59 (P-alphaBC-S59), enhancing its ability to protect myocardial cells from damage. In the heart, ischemia-reperfusion also causes the translocation of alphaBC from the cytosol to other cellular locations, one of which was recently shown to be mitochondria. However, it is not known whether alphaBC translocates to mitochondria during ischemia-reperfusion, nor is it known whether alphaBC phosphorylation takes place before or after translocation. In the present study, analyses of mitochondrial fractions isolated from mouse hearts subjected to various times of ex vivo ischemia-reperfusion showed that alphaBC translocation to mitochondria was maximal after 20 min of ischemia and then declined steadily during reperfusion. Phosphorylation of mitochondrial alphaBC was maximal after 30 min of ischemia, suggesting that at least in part it occurred after alphaBC association with mitochondria. Consistent with this was the finding that translocation of activated p38 to mitochondria was maximal after only 10 min of ischemia. The overexpression of alphaBC-AAE, which mimics alphaBC phosphorylated on serine 59, has been shown to stabilize mitochondrial membrane potential and to inhibit apoptosis. In the present study, infection of neonatal rat cardiac myocytes with adenovirus-encoded alphaBC-AAE decreased peroxide-induced mitochondrial cytochrome c release. These results suggest that during ischemia alphaBC translocates to mitochondria, where it is phosphorylated and contributes to modulating mitochondrial damage upon reperfusion.
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