Philip A.Gruppuso Our laboratory studies the control of hepatocyte proliferation during normal liver development. We do so based on the premise that understanding normal hepatocyte growth regulation will provide insight into abnormal growth (cancer) and the proliferative response of the liver's facultative stem cells to liver injury. We have concentrated on two main areas: developmental alterations in mitogenic signaling, and hepatocyte cell cycle control during development. Our model system is the rat. We use both in vitro (primary culture) and in vivo approaches.

We have arrived at a rather unexpected picture of how hepatocyte proliferation is regulated through late fetal and postnatal development. Our data indicate that the stimulation for rapid fetal hepatocyte growth is largely independent of the signal transduction pathways that stimulate the proliferation of adult rat hepatocytes. We have identified several novel mechanisms that support fetal hepatocyte growth. Furthermore, it appears that the transition to the quiescent adult hepatocyte phenotype involves active growth inhibition. Thus, our work has helped to establish the importance of normal and dysregulated hepatocyte growth inhibitory mechanisms to normal liver development and liver disease.

Awad, M. M., H. Enslen, J. M. Boylan, R. J. Davis and P. A. Gruppuso. Growth regulation via p38 mitogen-activated protein kinase in developing liver. J. Biol. Chem. 275:38716-38721, 2000.

Boylan, J.J., Anand, P. & Gruppuso, P.A. Ribosomal protein S6 phosphorylation and function during late gestation liver development in the rat. J. Biol. Chem. 276:44457-44463, 2001.

Anand, P., Boylan, J.M., Ou, Y. & Gruppuso, P.A. Insulin signaling during perinatal liver development in the rat. Am. J. Physiol. Endocrin. Metab. 283:E844-E852, 2002

Professor

M.D., University of Rochester, 1977

Rhode Island Hospital
Multiphasic Bldg., 2nd Floor

(401) 444-5504
Philip_Gruppuso@brown.edu

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