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Am J Physiol Gastrointest Liver Physiol (December 14, 2006). doi:10.1152/ajpgi.00493.2006
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Submitted on October 23, 2006
Accepted on December 8, 2006

DELAYED LIVER REGENERATION IN MICE LACKING LIVER SERUM RESPONSE FACTOR

Maria-Ujue Latasa1, Dominique Couton1, Claude Charvet1, Aurélie Lafanechère1, Jacques-Emmanuel Guidotti1, Zhenlin Li2, David Tuil1, Dominique Daegelen3, Claudia Mitchell1, and Helene Gilgenkrantz4*

1 Genetics and Development, Cochin Institute, France; INSERM U567, Paris, France; CNRS UMR 8104, Paris, France; Université R. Descartes, Paris, France
2 CNRS UMR 7079, paris, France
3 Genetics and Development, Cochin Institute, paris, France; INSERM U567, paris, France; CNRS UMR 8104, paris, France; Université R. Descartes, paris, France
4 Genetics and Development, Cochin Institute, paris, France; INSERM U567, Paris, France; CNRS UMR 8104, Paris, France; Université R. Descartes, Paris, France

* To whom correspondence should be addressed. E-mail: gilgenkrantz{at}cochin.inserm.fr.

Various immediate early genes (IEGs) up-regulated during the early process of liver regeneration are transcriptional targets of the Serum Response Factor (SRF). We show here that the expression of SRF is rapidly induced in rodent liver after partial hepatectomy. Because the inactivation of the SRF gene in mice is embryonic lethal, the in vivo role of SRF in liver regeneration after partial hepatectomy was analyzed in mutant mice conditionally deleted for SRF in the liver. We demonstrate that SRF is not an essential factor for liver ontogenesis. However, adult mutant mice show impaired liver regeneration after partial hepatectomy, associated with a blunted up-regulation of various SRF target IEGs. In conclusion, our work suggests that SRF is an early-response transcription factor that may contribute to the initial phases of liver regneration through its activation of immediate early genes.




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