| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Articles in PresS, published online ahead of print October 24, 2001
Am J Physiol Gastrointest Liver Physiol, 10.1152/ajpgi.00241.2001
Submitted on June 7, 2001
Accepted on October 22, 2001
1 Department of Medicine, Rhode Island Hospital and Brown University School of Medicine, Providence, RI, USA
2 Avda Universidad s/n Nursing School, 10071 Caceres, Spain
* To whom correspondence should be addressed. E-mail: Zuo-Liang_Xiao_MD{at}brown.edu.
Reactive oxygen species (ROS) have been implicated in the pathogenesis of muscle dysfunction in acute inflammatory processes. The aim of these studies was to determine the effects of ROS on gallbladder muscle function in vitro. Single muscle cells were obtained by enzymatic digestion. 70 µM H2O2 caused maximal contraction of up to 14% and blocked the response to CCK-8, ACh and KCl. It did not affect the contraction induced by GTP
S, DAG and IP3 that circumvent membrane receptors. The contraction induced by H2O2 was inhibited by AACOCF3 (cPLA2 inhibitor), indomethacin (cyclooxygenase inhibitor), chelerythrine (PKC inhibitor) or PD98059 (MAPK inhibitor). H2O2 also reduced the CCK receptor binding capacity from 0.36 ± 0.05 pmol/mg protein (controls) to 0.17 ± 0.03 pmol/mg protein. The level of lipid peroxidation as well as the PGE2 content was significantly increased after H2O2 pretreatment. Unlike SOD, the free radical scavenger catalase prevented the H2O2 induced contraction and its inhibition of the CCK-8 induced contraction. It is concluded that ROS cause damage to the plasma membrane of the gallbladder muscle and cause contraction through the generation of PGE2 induced by cPLA2-cyclooxygenase and probably mediated by the PKC-MAPK pathway.
This article has been cited by other articles:
|
|
 |
|
  P. Cong, Z.-L. Xiao, P. Biancani, and J. Behar Reactive oxygen species are messengers in maintenance of human and guinea pig gallbladder tonic contraction Am J Physiol Gastrointest Liver Physiol, December 1, 2007; 293(6): G1244 - G1251. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Z. Xiao, F. Schmitz, V. E. Pricolo, P. Biancani, and J. Behar Role of caveolae in the pathogenesis of cholesterol-induced gallbladder muscle hypomotility Am J Physiol Gastrointest Liver Physiol, June 1, 2007; 292(6): G1641 - G1649. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Z.-L. Xiao, J. Amaral, P. Biancani, and J. Behar Impaired cytoprotective function of muscle in human gallbladders with cholesterol stones Am J Physiol Gastrointest Liver Physiol, March 1, 2005; 288(3): G525 - G532. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Z.-L. Xiao, P. Biancani, and J. Behar Role of PGE2 on gallbladder muscle cytoprotection of guinea pigs Am J Physiol Gastrointest Liver Physiol, January 1, 2004; 286(1): G82 - G88. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. P. L. Guarino, Z.-L. Xiao, P. Biancani, and J. Behar PAF-like lipids- and PAF-induced gallbladder muscle contraction is mediated by different pathways in guinea pigs Am J Physiol Gastrointest Liver Physiol, December 1, 2003; 285(6): G1189 - G1197. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Rattan, R. N. Puri, and Y.-P. Fan Involvement of Rho and Rho-Associated Kinase in Sphincteric Smooth Muscle Contraction by Angiotensin II Experimental Biology and Medicine, September 1, 2003; 228(8): 972 - 981. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
