Abstract

At birth, both the arteries and veins in the lungs must relax so that blood can flow freely to the lungs and they can function normally and get the baby to """"""""pink up"""""""". If the lung arteries do not relax, the resistance for blood to flow into the lungs remains high and blood is diverted away from the lungs leading to the baby remaining blue after birth. If the veins in the lungs do not relax, the lungs can get very wet. By understanding why the lung arteries behave abnormally following chronic oxygen deprivation of the fetus, and why the lung veins function a bit better, we hope to find means of prevention and treatment of Pulmonary Hypertension of the Newborn, a condition that can lead to death of the newborn. ? ? ?

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Project (R01)
Project #
2R01HL075187-05A1
Application #
7475293
Study Section
Special Emphasis Panel (ZRG1-RES-B (04))
Program Officer
Moore, Timothy M
Project Start
2003-09-22
Project End
2012-08-31
Budget Start
2008-09-15
Budget End
2009-08-31
Support Year
5
Fiscal Year
2008
Total Cost
$489,518
Indirect Cost

  Institution

Name
University of Illinois at Chicago
Department
Pediatrics
Type
Schools of Medicine
DUNS #
098987217
City
Chicago
State
IL
Country
United States
Zip Code
60612

  Publications

Sun, Miranda; Ramchandran, Ramaswamy; Chen, Jiwang et al. (2016) Smooth Muscle Insulin-Like Growth Factor-1 Mediates Hypoxia-Induced Pulmonary Hypertension in Neonatal Mice. Am J Respir Cell Mol Biol 55:779-791
Zhou, Guofei; Chen, Tianji; Raj, J Usha (2015) MicroRNAs in pulmonary arterial hypertension. Am J Respir Cell Mol Biol 52:139-51
Yang, Qiwei; Sun, Miranda; Ramchandran, Ramaswamy et al. (2015) IGF-1 signaling in neonatal hypoxia-induced pulmonary hypertension: Role of epigenetic regulation. Vascul Pharmacol 73:20-31
Chen, Tianji; Zhou, Guofei; Zhou, Qiyuan et al. (2015) Loss of microRNA-17?92 in smooth muscle cells attenuates experimental pulmonary hypertension via induction of PDZ and LIM domain 5. Am J Respir Crit Care Med 191:678-92
Ramchandran, Ramaswamy; Raghavan, Aarti; Geenen, David et al. (2014) PKG-1? leucine zipper domain defect increases pulmonary vascular tone: implications in hypoxic pulmonary hypertension. Am J Physiol Lung Cell Mol Physiol 307:L537-44
Yang, Q; Dahl, M J; Albertine, K H et al. (2013) Role of histone deacetylases in regulation of phenotype of ovine newborn pulmonary arterial smooth muscle cells. Cell Prolif 46:654-64
Ibe, Joyce Christina F; Zhou, Qiyuan; Chen, Tianji et al. (2013) Adenosine monophosphate-activated protein kinase is required for pulmonary artery smooth muscle cell survival and the development of hypoxic pulmonary hypertension. Am J Respir Cell Mol Biol 49:609-18
Lu, Ziyan; Tian, Yufeng; Salwen, Helen R et al. (2013) Histone-lysine methyltransferase EHMT2 is involved in proliferation, apoptosis, cell invasion, and DNA methylation of human neuroblastoma cells. Anticancer Drugs 24:484-93
Ye, Liping; Liu, Juan; Liu, Huixia et al. (2013) Sulfhydryl-dependent dimerization of soluble guanylyl cyclase modulates the relaxation of porcine pulmonary arteries to nitric oxide. Pflugers Arch 465:333-41
Kang, Kang; Peng, Xiao; Zhang, Xiaoying et al. (2013) MicroRNA-124 suppresses the transactivation of nuclear factor of activated T cells by targeting multiple genes and inhibits the proliferation of pulmonary artery smooth muscle cells. J Biol Chem 288:25414-27

Showing the most recent 10 out of 37 publications