ArticleMolecular and cellular biochemistry2008
Genistein potentiates protein kinase A activity in porcine coronary artery.
Article in Molecular and cellular biochemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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
3 citing papers in PubMed, 11 citations in OpenAlex.
- Genistein in the Treatment of Hypertension: A Review.Endocrine, metabolic & immune disorders drug targets · 2022Review
- The Vascular Effects of Isolated Isoflavones-A Focus on the Determinants of Blood Pressure Regulation.Biology · 2021Review
- Vascular effects of phytoestrogens and alternative menopausal hormone therapy in cardiovascular disease.Mini reviews in medicinal chemistry · 2012Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Soy consumption is associated with a lower risk of atherosclerotic disease in the oriental population. Genistein is a soy isoflavone bearing estrogenic properties. Previous experiments in our laboratory demonstrated the potentiation of endothelium-independent relaxation of coronary artery by both estrogen and genistein. The potentiating effects of both estrogen and genistein were mediated through the cAMP-signaling pathway. We hypothesize that genistein could enhance protein kinase A (PKA) activity in porcine coronary artery smooth muscle, thereby offering a mechanism for the potentiation of vascular relaxation by genistein. In our study, a high concentration of genistein (10(-4.5) M) significantly increased PKA activity in porcine coronary artery rings. While genistein at 10(-5.5) M and forskolin at 10(-7) M had no effect on PKA activity, the combination of the two compounds at the prescribed concentrations caused a significant increase in PKA activity. The increase in PKA activity by genistein was abolished by SQ 22536 (adenylate cyclase blocker), but not by NF 449 (Gs protein blocker) or ICI 182780 (estrogen receptor antagonist). Our results suggest that the action of genistein is mediated via adenylate cyclase, but does not appear to involve Gs protein or ICI 182780-sensitive estrogen receptor.
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Registered trials
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