ArticlePloS one2018
17β-Estradiol and/or estrogen receptor alpha signaling blocks protein phosphatase 1 mediated ISO induced cardiac hypertrophy.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- GSNOR deletion differentially alters age-related cardiac function in a sex-dependent manner.American journal of physiology. Heart and circulatory physiology · 2026Article
- Network pharmacology combined with experimental analysis to explore the mechanism of the XinShuaiNing formula on heart failure.3 Biotech · 2025Article
- The role of A-kinase anchoring proteins in cardiovascular diseases and recent advances.Frontiers in cell and developmental biology · 2025Review
- 17β-estradiol biosensors based on different bioreceptors and their applications.Frontiers in bioengineering and biotechnology · 2024Review
- Serum testosterone level correlates with left ventricular hypertrophy in older women.Frontiers in endocrinology · 2022Article
- The Effect of Estrogen on Intracellular CaJACC. Basic to translational science · 2020Article
- Cardiac CaMKIIEvidence-based complementary and alternative medicine : eCAM · 2020Article
- MicroRNA changes of bone marrow-derived mesenchymal stem cells differentiated into neuronal-like cells by Schwann cell-conditioned medium.Neural regeneration research · 2019Article
- Inhibitor 1 of Protein Phosphatase 1 Regulates CaOxidative medicine and cellular longevity · 2019Article
- Brain aromatase modulates cardiac functions in embryonic zebrafish.International journal of veterinary science and medicine · 2019Article
- The Role of 17β-Estradiol and Estrogen Receptors in Regulation of CaFrontiers in endocrinology · 2019Review
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Earlier studies have shown that estrogen possess protective function against the development of pathological cardiac hypertrophy. However, the molecular mechanisms of estrogens (E2) protective effect are poorly understood. Additionally, abnormal activation of β-adrenergic signaling have been implicated in the development of pathological cardiac remodeling. However, the role of serine/threonine protein phosphatase 1 (PP1) in pathological cardiac remodeling under the influence of β-adrenergic signaling have been sparsely investigated. In this study, we assessed the downstream effects of abnormal activation of PP1 upon isoproterenol (ISO) induced pathological cardiac changes. We found that pre-treatment of 17β-estradiol (E2), tet-on estrogen receptor-α, or both significantly inhibited ISO-induced increase in cell size, hypertrophy marker gene expression and cytosolic calcium accumulation in H9c2 cells. Additionally, treatment with estrogen receptor inhibitor (ICI) reversed those effects, implicating role of E2 in inhibiting pathological cardiac remodeling. However, specific inhibition of ERα using melatonin, reduced ISO-induced PP1c expression and enhanced the level of ser-16 phosphorylated phospholamban (PLB), responsible for regulation of sarcoplasmic reticulum Ca2+-ATPase (SERCA) activity. Furthermore, hypertrophic effect caused by overexpression of PP1cα was reduced by treatment with specific inhibitor of ERα. Collectively, we found that estrogen and estrogen receptor-α have protective effect against pathological cardiac changes by suppressing PP1 expression and its downstream signaling pathway, which further needs to be elucidated.
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