Intracellular calcium changes induced by the endozepine triakontatetraneuropeptide in human polymorphonuclear leukocytes
- PDF / 701,375 Bytes
- 8 Pages / 610 x 792 pts Page_size
- 10 Downloads / 146 Views
BioMed Central
Open Access
Research
Intracellular calcium changes induced by the endozepine triakontatetraneuropeptide in human polymorphonuclear leukocytes: role of protein kinase C and effect of calcium channel blockers Franca Marino1, Marco Cosentino*1, Marco Ferrari1, Simona Cattaneo1, Giuseppina Frigo1, Anna M Fietta2, Sergio Lecchini1 and Gian Mario Frigo3 Address: 1Department of Clinical Medicine, Section of Experimental and Clinical Pharmacology, University of Insubria, Varese, Italy, 2Department of Hematological, Pneumological and Cardiovascular Sciences, University of Pavia, Pavia, Italy and 3Department of Internal Medicine and Therapeutics, Section of Pharmacology and Toxicology, University of Pavia, Pavia, Italy Email: Franca Marino - [email protected]; Marco Cosentino* - [email protected]; Marco Ferrari - [email protected]; Simona Cattaneo - [email protected]; Giuseppina Frigo - [email protected]; Anna M Fietta - [email protected]; Sergio Lecchini - [email protected]; Gian Mario Frigo - [email protected] * Corresponding author
Published: 30 June 2004 Cell Communication and Signaling 2004, 2:6
doi:10.1186/1478-811X-2-6
Received: 24 January 2004 Accepted: 30 June 2004
This article is available from: http://www.biosignaling.com/content/2/1/6 © 2004 Marino et al; licensee BioMed Central Ltd. This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original URL.
polymorphonuclear channels. leukocytestriakontatetraneuropeptideintracellular Ca++interleukin-8protein kinase CCa++ channel blockersT-type Ca++-
Abstract Background: The endozepine triakontatetraneuropeptide (TTN) induces intracellular calcium ([Ca++]i) changes followed by activation in human polymorphonuclear leukocytes (PMNs). The present study was undertaken to investigate the role of protein kinase (PK) C in the modulation of the response to TTN by human PMNs, and to examine the pharmacology of TTN-induced Ca++ entry through the plasma membrane of these cells. Results: The PKC activator 12-O-tetradecanoylphorbol-13-acetate (PMA) concentrationdependently inhibited TTN-induced [Ca++]i rise, and this effect was reverted by the PKC inhibitors rottlerin (partially) and Ro 32-0432 (completely). PMA also inhibited TTN-induced IL-8 mRNA expression. In the absence of PMA, however, rottlerin (but not Ro 32-0432) per se partially inhibited TTN-induced [Ca++]i rise. The response of [Ca++]i to TTN was also sensitive to mibefradil and flunarizine (T-type Ca++-channel blockers), but not to nifedipine, verapamil (L-type) or ωconotoxin GVIA (N-type). In agreement with this observation, PCR analysis showed the expression in human PMNs of the mRNA for all the α1 subunits of T-type Ca++ channels (namely, α1G, α1H, and α1I). Conclusions: In human PMNs TTN activates PKC-modulated pathways leading to Ca++ entry possibly through T-type Ca++ channels.
Introduction Triakontatet
Data Loading...
