ArticleAmerican journal of physiology. Heart and circulatory physiology2020
Deletion of cardiac polycystin 2/PC2 results in increased SR calcium release and blunted adrenergic reserve.
Article in American journal of physiology. Heart and circulatory physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 21 citations in OpenAlex.
- Effect of the gut microbiota metabolite phenylacetylglycine on cardiac CaBiophysical reports · 2026Article
- Investigating PKD2 deficiency-associated cardiomyopathies using hESC-cardiomyocytes and bioengineered 3D ventricular cardiac tissue strips.Cell death & disease · 2026Article
- Article
- Cardiovascular Complications in ADPKD.Kidney international reports · 2025Review
- The endoplasmic reticulum luminal CaPNAS nexus · 2025Article
- Cardiac Localized Polycystin-2 in the Natriuretic Peptide Signaling Pathway and Hypertension.Journal of the American Society of Nephrology : JASN · 2025Article
- Echocardiographic characteristics of autosomal dominant polycystic kidney disease.Scientific reports · 2024Article
- Protein carbonylation causes sarcoplasmic reticulum CaPflugers Archiv : European journal of physiology · 2024Article
- Utilization of the genetically encoded calcium indicator Salsa6F in cardiac applications.Cell calcium · 2024Article
- Cardiovascular perspectives of the TRP channel polycystin 2.The Journal of physiology · 2024Article
- Protein carbonylation causes sarcoplasmic reticulum Ca2+ overload by increasing intracellular Na+ level in ventricular myocytes.Research square · 2024Article
- Utilization of the genetically encoded calcium indicator Salsa6F in cardiac applications.bioRxiv : the preprint server for biology · 2023Article
- Cardiovascular Manifestations and Management in ADPKD.Kidney international reports · 2023Review
- Polycystin-2 (PC2) is a key determinant of in vitro myogenesis.American journal of physiology. Cell physiology · 2022Article
- Role of PKD2 in the endoplasmic reticulum calcium homeostasis.Frontiers in physiology · 2022Review
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Authors and funding
8 authors at 1 institution in 1 country.
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Abstract
Transient receptor potential proteins (TRPs) act as nonselective cation channels. Of the TRP channels, PC2 (also known as polycystin 2) is localized to the sarcoplasmic reticulum (SR); however, its contribution to calcium-induced calcium release and overall cardiac function in the heart is poorly understood. The goal of this study was to characterize the effect of cardiac-specific PC2 deletion in adult cardiomyocytes and in response to chronic β-adrenergic challenge. We used a temporally inducible model to specifically delete PC2 from cardiomyocytes (Pkd2 KO) and characterized calcium and contractile dynamics in single cells. We found enhanced intracellular calcium release after Pkd2 KO, and near super-resolution microscopy analysis suggested this was due to close localization of PC2 to the ryanodine receptor. At the organ level, speckle-tracking echocardiographical analysis showed increased dyssynchrony in the Pkd2 KO mice. In response to chronic adrenergic stimulus, cardiomyocytes from the Pkd2 KO had no reserve β-adrenergic calcium responses and significantly attenuated wall motion in the whole heart. Biochemically, without adrenergic stimulus, there was an overall increase in PKA phosphorylated targets in the Pkd2 KO mouse, which decreased following chronic adrenergic stimulus. Taken together, our results suggest that cardiac-specific PC2 limits SR calcium release by affecting the PKA phosphorylation status of the ryanodine receptor, and the effects of PC2 loss are exacerbated upon adrenergic challenge.
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