PMID: 7541947Jun 1, 1995Paper

VIP inhibits basal and histamine-stimulated proliferation of human airway smooth muscle cells

The American Journal of Physiology
K MarunoS I Said

Abstract

Airway smooth muscle (ASM) cell proliferation contributes to increased airway resistance in bronchial asthma. We have examined the modulation of ASM proliferation by vasoactive intestinal peptide (VIP), a cotransmitter of airway relaxation. Human ASM cells were grown in culture as a monolayer. VIP (1.0 nM-1.0 microM) inhibited proliferation in a dose-dependent manner by up to 82% on day 2, but the related peptide glucagon had no effect. Histamine (100 nM-100 microM) increased cell counts by 66%, but in the presence of VIP, cell counts and [3H]thymidine incorporation were reduced by up to 55%. Adenosine 3',5'-cyclic monophosphate (cAMP)-promoting agents, including 3-isobutyl-1-methylxanthine, forskolin, and 8-bromo-adenosine 3',5'-cyclic monophosphate, alone and especially combined with VIP, reduced cell counts and [3H]thymidine incorporation, in correlation with cAMP levels. KT-5720 (1.0 nM-1.0 microM), a selective inhibitor of cAMP-dependent protein kinase A (PKA), abolished the inhibitory effect of VIP. The results show that VIP selectively and potently inhibits human ASM cell growth and multiplication, and nullifies the mitogenic effect of histamine, by a PKA-mediated mechanism. A deficiency of VIP may lead to ASM hyperplasi...Continue Reading

Citations

Jun 20, 2006·American Journal of Physiology. Lung Cellular and Molecular Physiology·Anthony M SzemaSami I Said
Feb 9, 2000·American Journal of Physiology. Cell Physiology·I Rubinstein
Oct 1, 2003·Respiratory Physiology & Neurobiology·Limei Zhou, Marc B Hershenson
Aug 26, 2021·Journal of Experimental Pharmacology·Ronald Zolty

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