Cyp2c44 gene disruption is associated with increased hematopoietic stem cells : implication in chronic hypoxia-induced pulmonary hypertension

Ryota Hashimoto, Sachindra Raj Joshi, Houli Jiang, Jorge H Capdevila, Ivan F Mcmurtry, Michal Laniado Schwartzman, Sachin A Gupte
American journal of physiology. Heart and circulatory physiology2017
We have recently demonstrated that disruption of t; we serendipitously found that Cyp2c44 gene disrupt; the objective of the present study was to investig; which catalyzed the oxidation of arachidonic acid ; increases the numbers of 1) HSCs (CD34?; CD117?; and CD133?; ); 2) proangiogenic (CD34?; CD133? and; CD34?; CD133?; ) cells; and 3) immunogenic/inflammatory; (CD34?; CD11b?; F4/80?; and F4/; 80?; ) macrophages in bone marrow and blood compared wi; wild-type mice. Among the various CYP2C44-derived ; only 15-HETE decreased CD117?; cell numbers when applied; to bone marrow cell cultures. Interestingly; CD133? and von Wille-; brand factor-positive cells; which are derived from proangiogenic stem cells; are increased in the bone marrow; blood; and lungs of mice exposed to chronic hypoxia and i; our results demonstrate that CYP2C44-derived 15-HE downregulating HSC proliferation and growth; because disruption of the Cyp2c44 gene increased HSCs that potentially contribute to chronic hypoxia-induced pulmonary arterial remodeling and occlusion.
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