Effect of Nitric Oxide on Mitogen-Activated Protein Kinases in Neonatal Pulmonary Vascular Smooth Muscle |
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Authors: | Email author" target="_blank">Scott?A?BarmanEmail author |
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Institution: | (1) Department of Pharmacology and Toxicology, Medical College of Georgia, Augusta, Georgia 30912, USA |
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Abstract: | Mitogen-activated protein kinases (MAPKs) belong to the group of serine/threonine kinases that are rapidly activated in response
to growth factor stimulation. In adult mammalian cells, the MAPK family includes extracellular signal-regulated kinases 1
and 2 (ERK1 and ERK2 or p44mapk and p42mapk), which translocate to the nucleus and integrate signals from second messengers leading to cellular proliferation or differentiation.
However, the specific role of MAPKs in neonatal pulmonary vascular smooth muscle is not well understood. Expression of p44mapk and p42mapk in primary cultured pulmonary vascular smooth muscle cells from neonatal (1–2 day old) rats was identified by Western immunoblot
analysis. Treatment with 10 nM endothelin-1 (ET-1), a potent vasoconstrictor with vascular mitogenic properties, induced phosphorylation
of both p44mapk and p42mapk , but treatment with the exogenous nitric oxide (NO) donor sodium nitroprusside inhibited both p44mapk and p42mapk phosphorylation by ET-1. The specific cGMP-dependent protein kinase (PKG) inhibitor KT5823, the nonspecific nitric oxide
synthase (NOS) inhibitor L-NAME, and the specific NOS 1 blocker NPLA all significantly enhanced both p44mapk and p42mapk phosphorylation by ET-1. Collectively, these data demonstrate the expression and phosphorylation of specific MAPKs in rat
neonatal pulmonary vascular smooth muscle and suggests that the NO signaling pathway modulates MAPK activation by ET-1. |
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Keywords: | Mitogen-activated protein kinase NOS isozymes Neonatal Pulmonary vascular smooth muscle Endothelin-1 |
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