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http://hdl.handle.net/1942/30790
Title: | Nitric Oxide Donors Augment Interleukin-1β-Induced Vascular Endothelial Growth Factor in Airway Smooth Muscle Cells | Authors: | Sharma, H.S. Alagappan, V.K.T. WIDYASTUTI, Anna Mooi, W.J. de Boer, W.I. |
Issue Date: | 2013 | Publisher: | HUMANA PRESS INC |
Source: | Cell Biochemistry and Biophysics, Cell Biochemistry and Biophysics, 67 (2) , p. 247 -254 | Abstract: | Angiogenesis and microvascular leakage are features of chronic inflammatory diseases of which molecular mechanisms are poorly understood. We investigated the effects of interleukin-1 beta (IL-1 beta) on the expression and secretion of vascular endothelial growth factor (VEGF) and placenta growth factor (PlGF) in porcine airway smooth muscle cells (PASMC) in relation to a nitric oxide (NO) pathway. Serum-deprived (48 h) PASMC were stimulated with IL-1 beta alone or with NO donor, l-arginine and/or NO synthase inhibitor l-NAME for 4 and 24 h. IL-1 beta did not affect PlGF release, but augmented VEGF release (2.4-fold) after 24 h. VEGF release was inhibited by l-NAME (531.8 +/- A 52 pg/ml), but restored and further elevated by l-arginine (1,529 +/- A 287 pg/ml). IL-1 beta up-regulated VEGF mRNA (1.8-fold) and this response was attenuated by l-NAME (1.1-fold) and augmented by l-arginine (3.8-fold) at 4 h. Restoration of a NO pathway by l-arginine in l-NAME-treated cells resulted in elevated VEGF mRNA levels (2.2-fold). [H-3]Thymidine incorporation assay revealed enhanced porcine pulmonary artery endothelial cell proliferation in response to IL-1 beta, VEGF and PlGF, and this mitogenic effect was not influenced via the NO pathway. Our results suggest that a NO pathway modulates VEGF synthesis during inflammation contributing to bronchial angiogenesis and vascular leakage. | Keywords: | Airway smooth muscle;Angiogenesis;VEGF;Nitric oxide;Interleukin-1 beta | Document URI: | http://hdl.handle.net/1942/30790 | Link to publication/dataset: | http://www.scopus.com/inward/record.url?eid=2-s2.0-84886584460&partnerID=MN8TOARS | DOI: | 10.1007/s12013-013-9773-7 | ISI #: | WOS:000326282900004 | Rights: | Springer Science+Business Media New York 2013 | Category: | A1 | Type: | Journal Contribution |
Appears in Collections: | Research publications |
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