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Articles in PresS, published online ahead of print May 17, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00024.2002
Submitted on January 18, 2002
Accepted on May 1, 2002
1 Department of Medicine, University of Florida College of Medicine, Gainesville, Florida, USA
2 Research service, Malcom Randall VA Medical Center, Gainesville, Florida, USA; Department of Medicine, University of Florida College of Medicine, Gainesville, Florida, USA
3 Department of Medicine, University of Florida College of Medicine, Gainesville, Florida, USA; Research service, Malcom Randall VA Medical Center, Gainesville, Florida, USA
* To whom correspondence should be addressed. E-mail: Pateljm{at}medicine.ufl.edu.
Abstract
Li, Yong D., Edward R Block , and Jawaharlal M. Patel.. Activation of multiple signaling modules are critical in angiotensin IV-induced lung endothelial cell proliferation. Am. J. Physiol Lung Cell Mol. Physiol. 00: L000-L000, 2002.---Signaling events involving angiotensin IV (ANG-IV)-mediated pulmonary artery endothelial cell (PAEC) proliferation were examined. ANG-IV significantly increased upstream phosphoinositide (PI) 3-kinase (PI3K), PI-dependent kinase-1 (PDK-1), extracellular signal-related kinases (ERK-1/2), and protein kinase B-
/Akt (PKB-) activities as well as downstream p70 ribosomal S6 kinase (p70S6K) activities and/or phosphorylation of these proteins. ANG-IV also significantly increased 5-bromo-2'-deoxy-uridine (BrdU) incorporation into newly synthesized DNA in a concentration- and time-dependent manner. Pretreatment of cells with Wortmannin and LY294002, inhibitors of PI3K or rapamycin, an inhibitor of the mammalian target of rapamycin (mTOR) kinase and p70S6K, diminished the ANG-IV-mediated activation of PDK-1 and PKB-as well as phosphorylation of p70S6K. Although an inhibitor of ERK-1/2, PD98059, but not rapamycin, blocked ANG-IV-induced phosphorylation of ERK-1/2, both PD98059 and rapamycin independently caused partial reduction in ANG-IV-mediated cell proliferation. However, simultaneous treatment with PD98059 and rapamycin resulted in total inhibition of ANG-IV-induced cell proliferation. These results demonstrate that ANG-IV-induced DNA synthesis is regulated in a coordinated fashion involving multiple signaling modules in PAEC.
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