ArticleMolecular and cellular biochemistry2010
The role of the rat sarcoplasmic reticulum Ca2+-ATPase promoter in myocardial ischemia-preconditioning.
Article in Molecular and cellular biochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed, 4 citations in OpenAlex.
- Alarin regulates RyR2 and SERCA2 to improve cardiac function in heart failure with preserved ejection fraction.European journal of histochemistry : EJH · 2024Article
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Authors and funding
2 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intracellular calcium ion concentration ([Ca2+]i) is a key regulator of ischemia-reperfusion injury (IRI) and ischemic preconditioning (IPC), with myocardial sarcoplasmic reticulum Ca2+-ATPase (SERCA2a) acting as the major regulatory protein in the control of [Ca2+]i. In this study, we examined the effect of the SERCA2a promoter in IRI and IPC. The SERCA2a promoter fragment was acquired using PCR and molecular cloning technology, and was inserted into a luciferase reporter gene vector to construct reporter gene plasmids. Primary cultured neonatal rat cardiomyocytes were treated by analog ischemic treatment to produce in vitro models of IRI and IPC. Using an in vitro gene transfer assay, SERCA2a transcriptional activity was measured under conditions of IRI and IPC. Results from this study showed that (1) short duration analog ischemia treatment (analog IPC) results in a significant decrease in transcriptional activity, (2) analog IRI caused a dramatic depression in SERCA2a gene expression in transcription initiation levels, and (3) analog IPC attenuated IRI-induced transcriptional depression, even though IPC itself significantly depressed transcriptional activity. In conclusion, the SERCA2a promoter plays a significant role in IRI and IPC, with IPC able to precondition the SERCA2a promoter against the deleterious effects of IRI-induced injury.
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