ArticlePloS one2015
Heat shock protein 22 (Hsp22) regulates oxidative phosphorylation upon its mitochondrial translocation with the inducible nitric oxide synthase in mammalian heart.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 23 citations in OpenAlex.
- Protein S-nitrosylation in the heart: Mechanisms, physiological roles, and pathological remodeling.Redox biology · 2026Review
- Role of heat shock proteins and analysis of gene expression in response to high temperatures in date palm (Phoenix dactylifera).Genes & genomics · 2025Article
- Heat shock protein 22: A new direction for cardiovascular disease (Review).Molecular medicine reports · 2025Review
- The Protective Role of Heat Shock Proteins against Stresses in Animal Breeding.International journal of molecular sciences · 2024Review
- PINK1 and Parkin Ameliorate the Loss of Motor Activity and Mitochondrial Dysfunction Induced by Peripheral Neuropathy-Associated HSPB8 Mutants inBiomedicines · 2023Article
- Heat Shock Protein 22 in Physiological and Pathological Hearts: Small Molecule, Large Potentials.Cells · 2021Review
- Insights of heat shock protein 22 in the cardiac protection against ischemic oxidative stress.Redox biology · 2020Review
- Structural and functional properties of proteins interacting with small heat shock proteins.Cell stress & chaperones · 2020Review
- Characterization of Hspb8 in Zebrafish.Cells · 2020Article
- Neuromuscular Diseases Due to Chaperone Mutations: A Review and Some New Results.International journal of molecular sciences · 2020Review
- Role of heat shock protein 22 in the protective effect of geranylgeranylacetone in response to oxidized-LDL.Drug design, development and therapy · 2019Article
- The Different Expression Patterns of HSP22, a Late Embryogenesis Abundant-like Protein, in Hypertrophic H9C2 Cells Induced by NaCl and Angiotensin II.Electrolyte & blood pressure : E & BP · 2018Article
- A knock-in/knock-out mouse model of HSPB8-associated distal hereditary motor neuropathy and myopathy reveals toxic gain-of-function of mutant Hspb8.Acta neuropathologica · 2018Article
- The valosin-containing protein is a novel repressor of cardiomyocyte hypertrophy induced by pressure overload.Aging cell · 2017Article
- The valosin-containing protein is a novel mediator of mitochondrial respiration and cell survival in the heart in vivo.Scientific reports · 2017Article
- Tat-HSP22 inhibits oxidative stress-induced hippocampal neuronal cell death by regulation of the mitochondrial pathway.Molecular brain · 2017Article
- Lactobacillus fermentum Suo Attenuates HCl/Ethanol Induced Gastric Injury in Mice through Its Antioxidant Effects.Nutrients · 2016Article
- Shuidouchi (Fermented Soybean) Fermented in Different Vessels Attenuates HCl/Ethanol-Induced Gastric Mucosal Injury.Molecules (Basel, Switzerland) · 2015Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
objectivesStress-inducible heat shock protein 22 (Hsp22) confers protection against ischemia through induction of the inducible isoform of nitric oxide synthase (iNOS). Hsp22 overexpression in vivo stimulates cardiac mitochondrial respiration, whereas Hsp22 deletion in vivo significantly reduces respiration. We hypothesized that Hsp22-mediated regulation of mitochondrial function is dependent upon its mitochondrial translocation together with iNOS. METHODS AND
resultsAdenoviruses harboring either the full coding sequence of Hsp22 (Ad-WT-Hsp22) or a mutant lacking a N-terminal 20 amino acid putative mitochondrial localization sequence (Ad-N20-Hsp22) were generated, and infected in rat neonatal cardiomyocytes. Compared to β-Gal control, WT-Hsp22 accumulated in mitochondria by 2.5 fold (P<0.05) and increased oxygen consumption rates by 2-fold (P<0.01). This latter effect was abolished upon addition of the selective iNOS inhibitor, 1400 W. Ad-WT-Hsp22 significantly increased global iNOS expression by about 2.5-fold (P<0.01), and also increased iNOS mitochondrial localization by 4.5 fold vs. β-gal (P<0.05). Upon comparable overexpression, the N20-Hsp22 mutant did not show significant mitochondrial translocation or stimulation of mitochondrial respiration. Moreover, although N20-Hsp22 did increase global iNOS expression by 4.6-fold, it did not promote iNOS mitochondrial translocation.
conclusionTranslocation of both Hsp22 and iNOS to the mitochondria is necessary for Hsp22-mediated stimulation of oxidative phosphorylation.
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