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Role of VPAC1 and VPAC2 in VIP mediated inhibition of pulmonary artery and aortic smooth muscle cell proliferation.
Author(s) -
St. Hilaire RoseClaire,
Kadowitz Philip J,
Jeter James R
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.lb26
Subject(s) - vasoactive intestinal peptide , receptor , gene knockdown , receptor antagonist , biology , endocrinology , medicine , pulmonary artery , cell growth , transfection , microbiology and biotechnology , antagonist , cell culture , neuropeptide , biochemistry , genetics
Vasoactive intestinal peptide (VIP) has been shown to inhibit the proliferation of both aortic and pulmonary artery smooth muscle cells. Two guanine nucleotide binding protein (G‐protein)‐coupled receptors VIP/PACAP receptor 1(VPAC1) and VIP/PACAP receptor 2 (VPAC2) have been shown to mediate the biological effects of VIP. In this report we examine the distribution and role of these receptors in aortic and pulmonary artery smooth muscle cells as well as in tissue sections. Western blot analysis and immunohistochemistry showed that both VIP receptors are expressed in whole tissues sections as well as in cultured aortic and pulmonary artery smooth muscle cells. Transfection of cells with VIP did not result in a significant change in the expression of either VPAC1 or VPAC2 suggesting that VIP does not appear to regulate the expression of these receptors. In addition the use of a receptor antagonist for VPAC1 did not show a statistically significant release from VIP induced inhibition of cell proliferation. Treatment with a potent VIP receptor antagonist (VIP 6‐28) resulted in a statistically significant restoration of proliferation at a concentration of 300nM. Knockdown of VPAC2 gene expression using siRNA attenuated the antiproliferative effects of VIP. This suggests that VPAC2 may be receptor involved in the antiproliferative effects of VIP in both aortic and pulmonary artery smooth muscle cells.