| Literature DB >> 33301422 |
Wenqing Li1, Robert Shenkar2, Mathew R Detter3, Thomas Moore2, Christian Benavides3, Rhonda Lightle2, Romuald Girard2, Nicholas Hobson2, Ying Cao2, Yan Li2,4, Erin Griffin3, Carol Gallione3, Joseph M Zabramski5, Mark H Ginsberg1, Douglas A Marchuk3, Issam A Awad2.
Abstract
Propranolol, a pleiotropic β-adrenergic blocker, has been anecdotally reported to reduce cerebral cavernous malformations (CCMs) in humans. However, propranolol has not been rigorously evaluated in animal models, nor has its mechanism of action in CCM been defined. We report that propranolol or its S(-) enantiomer dramatically reduced embryonic venous cavernomas in ccm2 mosaic zebrafish, whereas R-(+)-propranolol, lacking β antagonism, had no effect. Silencing of the β1, but not β2, adrenergic receptor mimicked the beneficial effects of propranolol in a zebrafish CCM model, as did the β1-selective antagonist metoprolol. Thus, propranolol ameliorated cavernous malformations by β1 adrenergic antagonism in zebrafish. Oral propranolol significantly reduced lesion burden in 2 chronic murine models of the exceptionally aggressive Pdcd10/Ccm3 form of CCM. Propranolol or other β1-selective antagonists may be beneficial in CCM disease.Entities:
Keywords: Mouse models; Stroke; Vascular Biology; endothelial cells
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Year: 2021 PMID: 33301422 PMCID: PMC7843213 DOI: 10.1172/JCI144893
Source DB: PubMed Journal: J Clin Invest ISSN: 0021-9738 Impact factor: 19.456