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AntagomiR directed against miR-20a restores functional BMPR2 signalling and prevents vascular remodelling in hypoxia-induced pulmonary hypertension
Author(s) -
Matthias Brock,
Víctor J. Samillan,
Michelle Trenkmann,
Colin C. Schwarzwald,
Silvia Ulrich,
Renate E. Gay,
Max Gassmann,
Louise Østergaard,
Steffen Gay,
Rudolf Speich,
Lars Huber
Publication year - 2012
Publication title -
european heart journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.336
H-Index - 293
eISSN - 1522-9645
pISSN - 0195-668X
DOI - 10.1093/eurheartj/ehs060
Subject(s) - bmpr2 , antagomir , medicine , vascular remodelling in the embryo , pulmonary hypertension , right ventricular hypertrophy , hypoxia (environmental) , in vivo , transfection , cardiology , biology , chemistry , bone morphogenetic protein , cell culture , genetics , organic chemistry , oxygen , gene , biochemistry , microbiology and biotechnology
Dysregulation of the bone morphogenetic protein receptor type 2 (BMPR2) is a hallmark feature that has been described in several forms of pulmonary hypertension. We recently identified the microRNA miR-20a within a highly conserved pathway as a regulator of the expression of BMPR2. To address the pathophysiological relevance of this pathway in vivo, we employed antagomiR-20a and investigated whether specific inhibition of miR-20a could restore functional levels of BMPR2 and, in turn, might prevent pulmonary arterial vascular remodelling.

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