Adverse effects of BMPR2 suppression in macrophages in animal models of pulmonary hypertension

Inflammatory cells contribute to irreversible damage in pulmonary arterial hypertension (PAH). We hypothesized that in PAH, dysfunctional BMPR2 signaling in macrophages contributes to pulmonary vascular injury and phenotypic changes via proinflammatory cytokine production. Studies were conducted in:...

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Bibliographic Details
Published in:Pulmonary circulation 2020-01, Vol.10 (1), p.1-11
Main Authors: West, James, Chen, Xinping, Yan, Ling, Gladson, Santhi, Loyd, James, Rizwan, Hamid, Talati, Megha
Format: Article
Language:English
Subjects:
animal models of pulmonary hypertension
BMPR2 mutation
Cytokines
Gene expression
Hypoxia
inflammatory cytokines
macrophages
pulmonary arterial hypertension
Pulmonary hypertension
Rodents
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Summary:Inflammatory cells contribute to irreversible damage in pulmonary arterial hypertension (PAH). We hypothesized that in PAH, dysfunctional BMPR2 signaling in macrophages contributes to pulmonary vascular injury and phenotypic changes via proinflammatory cytokine production. Studies were conducted in: (1) Rosa26-rtTA2 3 X TetO7-Bmpr2delx4 FVB/N mice (mutant Bmpr2 is universally expressed, BMPR2delx4 mice) given a weekly intra-tracheal liposomal clodronate injections for four weeks; and (2) LysM-Cre X floxed BMPR2 X floxed eGFP monocyte lineage-specific BMPR2 knockout (KO) mouse model (Bmpr2 gene expression knockdown in monocytic lineage cells) (BMPR2KO) following three weeks of sugen/hypoxia treatment. In the BMPR2delx4 mice, increased right ventricular systolic pressure (RVSP; P 
ISSN:2045-8940
2045-8932
2045-8940
DOI:10.1177/2045894019856483