Vascular remodeling is the process of structural alteration and cell rearrangement of blood vessels in response to injury and is the cause of many of the world's most afflicted cardiovascular conditions, including pulmonary arterial hypertension (PAH). Many studies have focused on the effects of vascular endothelial cells and smooth muscle cells (SMCs) during vascular remodeling, but pericytes, an indispensable cell population residing largely in capillaries, are ignored in this maladaptive process. Here, we report that hypoxia-inducible factor 2α (HIF2α) expression is increased in the lung tissues of PAH patients, and HIF2α overexpressed pericytes result in greater contractility and an impaired endothelial-pericyte interaction.
View Article and Find Full Text PDFIncreased production of fetal hemoglobin (HbF) can ameliorate the severity of sickle cell disease and β-thalassemia. BCL11A represses the genes encoding HbF and regulates human hemoglobin switching through variation in its expression during development. However, the mechanisms underlying the developmental expression of BCL11A remain mysterious.
View Article and Find Full Text PDFIntroduction: Cell-free plasma hemoglobin is associated with poor outcome in patients with sepsis. Extracellular hemoglobin and secondarily released heme amplify inflammation in the presence of microbial TLR ligands and/or endogenous mediators. Hemopexin, a plasma protein that binds heme with extraordinary affinity, blocks these effects and has been proposed as a possible treatment approach to decrease inflammation in critically ill patients.
View Article and Find Full Text PDFJ Cardiovasc Pharmacol
November 2010
Pulmonary hypertension (PH) is a life-threatening disease with unclear vascular mechanisms. We tested whether PH involves abnormal pulmonary vasoconstriction and impaired vasodilation. Male Sprague-Dawley rats were exposed to hypoxia (9% O(2)) for 2 weeks or injected with single dose of monocrotaline (MCT, 60 mg/kg s.
View Article and Find Full Text PDFAm J Perinatol
August 2009
Intrauterine closure of the fetal ductus arteriosus is a rare but serious condition. It can lead to congestive heart failure, fetal hydrops, and fetal death. No intrauterine intervention is currently available to treat this condition.
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