Cellular Localization of Calmodulin-dependent Protein Kinases I and II to A-cells and D-cells of the Endocrine PancreasLisa M. Matovcika,b, Angus C. Nairnd, and Fred S. Gorelickb,ca Departments of Surgery, VA CT Healthcare System and Yale University School of Medicine, New Haven, Connecticut b Cell Biology, VA CT Healthcare System and Yale University School of Medicine, New Haven, Connecticut c Medicine, VA CT Healthcare System and Yale University School of Medicine, New Haven, Connecticut d Laboratory of Molecular and Cellular Neurobiology, Rockefeller University, New York, New York Correspondence to: Lisa M. Matovcik, Surgical Service (112), VA CT Healthcare System, 950 Campbell Ave. West Haven, CT 06516. Ca2+/calmodulin-dependent protein kinases I and II, initially identified in brain on the basis of their ability to phosphorylate synapsin I, have been implicated in the regulation of Ca2+-dependent synaptic neurosecretion. Specific recombinant and synthetic peptide antibodies were used to examine the distribution of CaM kinases I and II in the rat pancreas and other tissues. The CaM kinase I antibodies detected a doublet of cytosolic proteins of ~38 and ~42 kD by immunoblot. CaM kinase I was observed in glucagon-containing A-cells at the periphery of the islet of Langerhans but had little or no overlap with pancreatic polypeptide or somatostatin cells. In contrast, CaM kinase II was localized to somatostatin-containing D-cells. CaM kinase I co-localized with glucagon secretory granules. CaM kinase II was not associated with the somatostatin granule but rather was enriched in areas of the cells that contained relatively little somatostatin. Because glucagon secretion is Ca2+-dependent, it is attractive to speculate that CaM kinase I may play a regulatory role in glucagon secretion. Glucagon and somatostatin cells both utilize intracellular Ca2+ for signaling. Therefore, specific CaM kinases may act as effectors of Ca2+ in these different cell types. (J Histochem Cytochem 46:519526, 1998) Key Words: Ca2+/calmodulin-dependent, protein kinase I, Ca2+/calmodulin-dependent, protein kinase II, cell signaling, calcium, exocytosis, glucagon, somatostatin, pancreas, parathyroid, neuroendocrine cells
This article has been cited by other articles:
|
|
||||||||||||||||||||||||||