ArticleCell stress & chaperones2003
Overexpression of heat shock proteins differentially modulates protein kinase C expression in rat neonatal cardiomyocytes.
Article in Cell stress & chaperones, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 12 citations in OpenAlex.
- Protein kinase C-α interaction with iHSP70 in mitochondria promotes recovery of mitochondrial function after injury in renal proximal tubular cells.American journal of physiology. Renal physiology · 2013Article
- Protein kinase Cepsilon mediates salutary effects on electrical coupling induced by ischemic preconditioning.Heart rhythm · 2007Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Previous studies have suggested that protein kinase C (PKC) is involved in heat shock protein (Hsp)-mediated cardioprotection. Therefore, we wanted to determine whether overexpression of Hsps modulates PKC expression, which will give us further insight into understanding the mechanism by which Hsps and PKC interact to protect cells from stress-induced injury. Specifically, we overexpressed the inducible form of Hsp70 (Hsp70i) or Hsp90 in rat neonatal cardiomyocytes and evaluated PKCdelta or PKCepsilon expression by immunoblotting and immunofluorescent confocal microscopy. Western analysis showed that overexpression of Hsp70i or Hsp90 decreased PKCepsilon expression. However, overexpression of Hsp70i or Hsp90 did not modify PKCdelta expression over control levels. Overexpression of constitutively active PKCdelta or PKCepsilon increased Hsp70i expression over control levels. The data suggest that overexpression of Hsps differentially modulates expression of PKC isoforms in rat neonatal cardiomyocytes. Furthermore, PKC may directly play a role in Hsp-mediated cardioprotection by upregulating Hsp70i expression.
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Registered trials
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