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Clusterin altered cerulein-induced activation of NF-κB in AR4-2J cells
NF-κB is among the key regulators of the transcription of stress proteins as well as the control of apoptosis. Pancreas-specific targeted disruption of the p65-subunit of NF-κB in the exocrine IOX2 dramatically aggravates experimental pancreatitis (H. Algul and R.M. Schmid, personal communication). However, an overwhelming NF-κB response may also be deleterious and must be controlled.
Targeted disruption of clusterin aggravated experimental pancreatitis
To confirm our in vitro data we were investigated effects of targeted disruption of the clusterin gene in inflamed pancreas in vivo. Experimental pancreatitis was performed using the cerulein-model [39]. Clusterin knockout mice developed a more severe pancreatitis than controls, reflected by significantly more elevated amylase and lipase serum levels 8 h after induction of pancreatitis ( Table 2) as well as enhanced inflammation characterized by interstitial infiltrates of macrophages and granulocytes ( Table 3A and Fig. 4A and B).
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