ArticleJournal of molecular and cellular cardiology2010
VAMP-1, VAMP-2, and syntaxin-4 regulate ANP release from cardiac myocytes.
Article in Journal of molecular and cellular cardiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 31 citations in OpenAlex.
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- Pivotal role of mTORC2 and involvement of ribosomal protein S6 in cardioprotective signaling.Circulation research · 2014Article
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- Cardiomyocyte-secreted acetylcholine is required for maintenance of homeostasis in the heart.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013Article
- Non-neuronal cholinergic machinery present in cardiomyocytes offsets hypertrophic signals.Journal of molecular and cellular cardiology · 2012Article
- Nuclear miRNA regulates the mitochondrial genome in the heart.Circulation research · 2012Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
ANP is a peptide released by cardiac myocytes that regulates blood pressure and natriuresis. However, the molecular mechanisms controlling ANP release from cardiac myocytes are not defined. We now identify three components of the exocytic machinery that regulate ANP release from atrial myocytes. We found that cardiac myocytes express N-ethylmaleimide sensitive factor (NSF), soluble NSF attachment protein (α-SNAP), and SNAP receptors (SNAREs). Additionally we found that specific SNARE molecules, VAMP-1 and VAMP-2, both co-sediment and co-localize with ANP. Also, one SNARE molecule, syntaxin-4, partially co-sediments and partially co-localizes with ANP. Furthermore, these three SNAREs, syntaxin-4 and VAMP-1 and VAMP-2, form a SNARE complex inside cardiac myocytes. Finally, knockdown of VAMP-1, VAMP-2, or syntaxin-4 blocks regulated release of ANP. In contrast, silencing of VAMP-3 did not have an effect on ANP release. Our data suggest that three specific SNAREs regulate cardiac myocyte exocytosis of ANP. Pathways that modify the exocytic machinery may influence natriuresis and blood pressure.
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Registered trials
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