Abstract
keratins in K8-/mice during pancreatitis. Methods: Proteir,./RNA analysis of actin, tubulin, keratin and vimentin was done by immunoblotting, microscopy, PCR, and nuclear runoff assays Mice were injected with caemlein hourly 7x (one series of injections) followed by histdogic/binchemical analysis 2-d later, or were re-injected after the 2-d recovery with a 2nd series of injections then analyzed 2-d later. Results: Basally, K8-/pancreata have normal histology and express similar levels of actin but have a 2-fold increase in tubulin as compared wltfi wdd-type (WT) mice After the 1st acute pancreatitis in WT and K8 +/mice, actin/ tubulin remain unchanged while keratins increase ~3-fold In contrast, K8-/pancreata increase their actln mid mbufin RNA/protein ~2-fold, after one serie~ of injections, vs WT and +/pancreata The actm/tubufin increase becomes even more pronounced (3x) in KS-Imice alter the 2nd pancreatitis, and increases ~l.5-fold in w r and +/mice. Ductal but not acmar K7/K18/K19/K20 also increase more prominently in K84vs control mice after injury'. Histologically, KS-/pancreata are more protected from injury vs WT and +/pancreata. There is also a dramatic increase in vimentin in nonepithehal cells. Conclusion: Acttn/tubufin are over-expressed upon repeated pancreatic injury', while keratins are overexpressed upon limited injury,. Acrin/tubufin induction is far more significant in the absence of keratins and may serve a cytoprotective role. This is the first description of compensatory changes in actm/tubulin upon injury.
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