|  Help  |  About  |  Contact Us

Publication : Expression of adhesion molecular proteins in the cochlear lateral wall of normal and PARP-1 mutant mice.

First Author  Shi X Year  2007
Journal  Hear Res Volume  224
Issue  1-2 Pages  1-14
PubMed ID  17184942 Mgi Jnum  J:117701
Mgi Id  MGI:3697273 Doi  10.1016/j.heares.2006.10.011
Citation  Shi X, et al. (2007) Expression of adhesion molecular proteins in the cochlear lateral wall of normal and PARP-1 mutant mice. Hear Res 224(1-2):1-14
abstractText  Sound can damage peripheral cochlear function through a number of mechanisms, and emerging evidence suggests that inflammation may be one of them. Using immunohistochemistry and poly (ADP-ribose) polymerase-1 (PARP-1) mutant mice, we tested whether PARP-1 contributes to loud-sound induced cochlear lateral wall damage by triggering inflammatory effects, including upregulating intercellular adhesion molecule-1 (ICAM-1), P-selectin and platelet-endothelial cell-adhesion molecule-1 (PECAM-1). In control conditions, we found that there was no detectable poly-ADP-ribose (PAR) in the marginal cells and microvessels. ICAM-1 was expressed only at low levels in the vessels of the stria vascularis and the spiral ligament. P-selectin and PECAM-1 were barely detected and only in the vessels of the spiral ligament. Following loud-sound exposure, PAR was detected in numbers of marginal cells and some vessels of the spiral ligament. Also, an elevated expression of ICAM-1 was demonstrated in some vessels of the stria vascularis and spiral ligament. Increased expression of P-selectin and PECAM-1 were mainly located in the vessels of the spiral ligament, while increased populations of non-migrated and migrated leukocytes were observed in the area of the spiral ligament. However, neither increased expression of adhesion proteins nor increased population of leukocytes, were observed in the PARP-1 knockout mouse. We thus conclude that loud-sound stress activates the expression of adhesion molecular proteins in the lateral wall and that PARP-1 modulates inflammation-linked protein expression and leukocyte migration.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

2 Authors

3 Bio Entities

0 Expression