ISSN:
1573-2568
Keywords:
COLITIS
;
CHANNEL
;
CALCIUM
;
INFLAMMATORY BOWEL DISEASE
;
DIARRHEA
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Abstract Colitis in experimental animals or idiopathicinflammatory bowel disease, such as ulcerative colitisor Crohn's disease in humans, is associated with reducedmuscle contraction. This is predicted to be due to disturbance of Ca2+homeostasis in the inflamed muscle cell. However, theunderlying molecular mechanism remains to be elucidated.Since the catalytic α-1 subunit of the L-typeCa2+ channel regulates Ca2+ influx, levels of the α-1mRNA and protein were examined. Colitis induced byintrarectal administration of trinitrobenzenesulfonicacid was monitored by measuring the myeloperoxidaseactivity and histology. The levels of mRNA and protein wereestimated using RT-PCR and immunoblotting.Myeloperoxidase activity increased in the inflamedcolon, and the lamina propria and muscle layers showedinfiltration of inflammatory cells and loss of crypts. Twoalternatively spliced α-1 mRNA isoforms weredetected in the colonic muscle. The ratio of unsplicedto spliced mRNA isoforms remained unaltered in inflamed muscle. In contrast, the level of correspondingprotein isozymes decreased in the colitic animals. Thuscolitis-induced reduction in the α-1 protein mayaccount for the reduced colonic contractility seen in colitis.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1023/A:1026694406446
