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SUMMARY:Bile acids and liver regeneration : the impact of TGR5?
DTSTART:20120828T143000
DTEND:20120828T153000
DTSTAMP:20260916T182546Z
UID:2f02dee9acf7c35fef2ca1df8bc3e0f3fa81ed6be148b42d9f53c255
CATEGORIES:Conferences - Seminars
DESCRIPTION:Thierry TORDJMANN\nMD\, PhD\, INSERM U757\, Université Paris 
 Sud\, Orsay\, France\n\nLiver regeneration is a vital process orchestrated
  by multiple pathways providing the different liver cell types with signal
 s initiating both proliferation and protection. This process involves a co
 mplex array of agonists and cellular interactions\, not only between hepat
 ocytes and other liver cells (autocrine\, paracrine interactions)\, but al
 so between the liver and the whole organism (endocrine\, neuroendocrine\, 
 nerves…). Apart from main growth factors\, cytokines and other agonists 
 extensively studied so far\, we have identified calcium-mobilizing agonist
 s which also contribute to the regeneration process (Gonzales et al.\, 201
 0\; Lagoudakis et al.\, 2010\; Doignon et al.\, 2011). In particular\, we 
 identified the hormone arginine vasopressin as a neuroendocrine agonist in
 volved in liver regeneration after partial hepatectomy (PH)\, in part in a
  bile acids and TGR5-dependent manner (Doignon et al.\, 2011). Bile acids 
 (BA) recently emerged as important players during liver regeneration\, alt
 hough a complete view of their involvement is lacking at the molecular\, c
 ellular\, and physiological levels. In both experimental models of liver r
 egeneration in rodents\, namely PH and CCl4 intoxication\, it has been wel
 l established (by us and by others)\, that BA flux to the remnant regenera
 ting liver\, and to the whole organism\, is rapidly enhanced\, with potent
 ially wide signaling consequences. FXR mediated BA effects have received m
 uch attention with respect to their roles during liver regeneration\; FXR 
 activation by BA indeed provides hepatocyte adaptive (protective) response
  to liver resection or injury\, through regulation of BA entry\, synthesis
  and export in hepatocytes\, while FXR-mediated activation of the transcri
 ption factor Fox M1b contributes to hepatocyte progression in the cell cyc
 le. Beside this body of information\, the involvement of the BA membrane r
 eceptor TGR5 has not received any published interest. We have began to stu
 dy liver regeneration in TGR5-KO mice and found that the lack of this BA r
 eceptor results in excessive hepatic BA overload culminating in extensive 
 hepatocyte necrosis after PH. The mechanisms involved are currently under 
 investigation.  
LOCATION:AI 1153 https://plan.epfl.ch/?room==AI%201153
STATUS:CONFIRMED
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