期刊
PANCREAS
卷 38, 期 8, 页码 930-935出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/MPA.0b013e3181b8476a
关键词
amylase secretion; genetic deletion; trypsinogen
资金
- National Institutes of Health [R21 DK69702, RO1 DK33850, DK54021]
- USC-UCLA Research Center for Alcoholic Liver and Pancreatic Injury [5 P60 AA11999]
- Veterans Administration Merit and Senior Career Development Award
Objectives: To define the role of protein kinase C delta (PKC delta) in acinar cell responses to the hormone cholecystokinin-8 (CCK) using isoform-specific inhibitors and a previously unreported genetic deletion model. Methods: Pancreatic acinar cells were isolated from (1) rat, and pretreated with a PKC delta-specific inhibitor or (2) PKC delta-deficient and wild type mice. Isolated cells were stimulated with CCK (0.001-100 nmol/L) and cell responses were measured. Results: The PKC delta inhibitor did not affect stimulated amylase secretion from rat pancreatic acinar cells. Cholecystokinin-8 stimulation induced a typical biphasic dose-response curve for amylase secretion in acinar cells isolated from both PKC delta(-/-) and wild type mice, with maximal stimulation at 10-pmol/L CCK. Cholecystokinin-8 (100 nmol/L) induced zymogen and nuclear factor kappa B activation in both PKC delta(-/-) and wild type mice, although it was up to 50% less in PKC delta(-/-). Conclusions: In contrast to previous studies, this study has used specific and complementary approaches to examine PKC delta-mediated acinar cell responses. We could not confirm that it mediates amylase release but corroborated its role in the early stages of acute pancreatitis.
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