Influence of vasoactive intestinal peptide on expression of pulmonary surfactant associated protein A in lung explants.
- Author:
Lian LI
1
;
Zi-qiang LUO
;
Gan-qiou WU
;
Xiu-hong SUN
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Epithelial Cells; drug effects; metabolism; In Vitro Techniques; Protein Kinase C; metabolism; Proto-Oncogene Proteins c-fos; metabolism; Pulmonary Alveoli; cytology; Pulmonary Surfactant-Associated Protein A; metabolism; Rats; Rats, Wistar; Signal Transduction; Vasoactive Intestinal Peptide; pharmacology
- From: Chinese Journal of Applied Physiology 2004;20(2):117-120
- CountryChina
- Language:Chinese
-
Abstract:
AIMTo study the influence of VIP on the expression of SP-A and its intracellular signal transduction pathway.
METHODSThe influence of VIP on the expression of SP-A was studied by immunohistochemistry and RT-PCR. The intracellular signal transduction pathway was further investigated by using receptor antagonist, protein kinase inhibitor and antisense oligonucleotides.
RESULTS(1) VIP(10(-8) mol/L) enhanced SP-A protein expression in alveolar type II cells (ATII) and increased the content of SP-A mRNA in lung tissue. (2) VIP receptor antagonist [D-P-C1-Phe (6)-Leu (17)]-VIP (10(-6) mol/L) could suppress the VIP-induced expression of SP-A protein and SP-A mRNA. (3) c-fos antisense oligonucleotides (9 x 10(-6) mol/L) could inhibit the VIP-induced expression of SP-A protein and SP-A mRNA. (4) Protein kinase C(PKC) inhibitor H7 (10(-5) mol/L) could also depress the V1P-induced SP-A protein and SP-A mRNA.
CONCLUSIONVIP can up-regulate the expression of SP-A through its receptor. PKC and c-fos protein play important roles in the intracellular signal transduction pathway through which VIP induces the expression of SP-A.
