The vasoactive intestinal peptide gene is a key modulator of pulmonary vascular remodeling and inflammation.

Publisher: New York Academy of Sciences Country of Publication: United States NLM ID: 7506858 Publication Model: Print Cited Medium: Internet ISSN: 1749-6632 (Electronic) Linking ISSN: 00778923 NLM ISO Abbreviation: Ann N Y Acad Sci Subsets: MEDLINE

Publication: 2006- : New York, NY : Malden, MA : New York Academy of Sciences ; Blackwell
Original Publication: New York, The Academy.

Hypertension, Pulmonary/*immunology ; Lung/*blood supply ; Lung/*metabolism ; Pneumonia/*metabolism ; Vasoactive Intestinal Peptide/*physiology; Animals ; Hypertension, Pulmonary/metabolism ; Hypertension, Pulmonary/pathology ; Mice ; Models, Animal ; Models, Biological ; NFATC Transcription Factors/metabolism ; Pulmonary Artery/metabolism ; Pulmonary Artery/pathology ; Rats ; Vasoactive Intestinal Peptide/genetics

Pulmonary vascular remodeling and inflammation often coexist in clinical and experimentally induced pulmonary arterial hypertension (PAH). In some instances, the pulmonary hypertension may be the primary, or at least the initial, problem, while inflammatory or autoimmune responses appear to initiate or dominate the picture in other cases. Based on studies in a model of PAH resulting from targeted deletion of the neuropeptide vasoactive intestinal peptide (VIP) gene, we propose that, at least in this experimental model, but possibly also in other situations, both vascular remodeling and inflammation may be mediated by one and the same mechanism: uncontrolled activation of calcineurin-NFAT (nuclear factor of activated T cells) signaling. If this hypothesis is validated, VIP would emerge as an endogenous modulator of pulmonary vascular remodeling and inflammation, through its suppression of NFAT activation.

0 (NFATC Transcription Factors)
37221-79-7 (Vasoactive Intestinal Peptide)

Date Created: 20081217 Date Completed: 20090219 Latest Revision: 20081216

20240829

10.1196/annals.1418.014

19076374