Differential subcellular targeting of PKC-epsilon in response to pharmacological or ischemic stimuli in intestinal epithelia

American Journal of Physiology. Gastrointestinal and Liver Physiology
Joshua M V MammenJeffrey B Matthews

Abstract

Ischemia is the central pathogenic factor underlying a spectrum of intestinal disorders. The study of the cellular signaling responses to ischemic stress in nonepithelial cells has progressed substantially in the previous several years, but little is known about the response in epithelial cells. Unique features of the epithelial response to ischemic stress suggest differential regulation with regards to signaling. The PKC family of proteins has been implicated in ischemic stress in nonepithelial systems. The role of PKC isoforms in chemical ischemia in intestinal epithelial cells is evaluated in this study. Additionally, the phosphorylation of the F-actin cross-linking protein myristoylated alanine-rich C kinase substrate (MARCKS) is also studied. Chemical ischemia resulted in the transient activation of only the isoform PKC-epsilon as detected by translocation employing the subcellular fractionation technique. The pharmacological agonists phorbol 12-myristate 13-acetate and carbachol also led to the translocation of PKC-epsilon. By immunofluoresence, MARCKS is noted to be located at the lateral membrane under control conditions. In response to carbachol, MARCKS translocates to the cytosol, indicating its phosphorylation, which...Continue Reading

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Citations

Sep 22, 2011·Journal of Dental Research·D J CulpR L Evans
Feb 21, 2013·Hepatology : Official Journal of the American Association for the Study of Liver Diseases·Christopher M SchonhoffM Sawkat Anwer
Mar 31, 2006·American Journal of Physiology. Cell Physiology·Juan C IblaSean P Colgan

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