This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kuo, F C Articles by Darnell, J E Search for Related Content PubMed PubMed Citation Articles by Kuo, F C Articles by Darnell, J E, Jr

Evidence that interaction of hepatocytes with the collecting (hepatic) veins triggers position-specific transcription of the glutamine synthetase and ornithine aminotransferase genes in the mouse liver.

Rockefeller University, New York, New York 10021.

ABSTRACT

We previously demonstrated that glutamine synthetase (GS) and ornithine aminotransferase (OAT) mRNAs are expressed in the mouse liver acinus preferentially in pericentral hepatocytes, that is, those immediately surrounding terminal central veins (A.L. Bennett, K.E. Paulson, R.E. Miller, and J.E. Darnell, Jr., J. Cell Biol. 105:1073-1085, 1987, and F.C. Kuo, W.L. Hwu, D. Valle, and J.E. Darnell, Jr., Proc. Natl. Acad. Sci. USA, in press). We now show that hepatocytes surrounding large collecting hepatic veins but not portal veins also express these two mRNAs. The pericentral hepatocytes are the most distal hepatocytes with respect to acinar blood flow, whereas this is not necessarily the case for hepatocytes next to the large collecting hepatic veins. This result implies that it is contact with some hepatic venous element which signals positional expression. In an effort to induce conditions that change relationships between hepatocytes and blood vessels, regenerating liver was studied. After surgical removal of two-thirds or more of the liver, there was no noticeable change in GS or OAT expression in the remaining liver tissue during regeneration. However, treatment with carbon tetrachloride (CCl4), which specifically kills pericentral hepatocytes, completely removed GS- and OAT-containing cells and promptly halted hepatic transcription of GS. Repair of CCl4 damage is associated with invasion of inflammatory and scavenging cells, which remove dead hepatocytes to allow regrowth. Only when hepatocytes resumed contact with pericentral veins were the pretreatment levels of OAT and GS mRNA and high levels of GS transcription restored.

This article has been cited by other articles:

• Bode, J. G., Peters–Regehr, T., Kubitz, R., Häussinger, D. (2000). Expression of Glutamine Synthetase in Macrophages. J. Histochem. Cytochem. 48: 415-422 [Abstract] [Full Text]  
• Gupta, S., Rajvanshi, P., Sokhi, R. P., Vaidya, S., Irani, A. N., Gorla, G. R. (1999). Position-specific Gene Expression in the Liver Lobule Is Directed by the Microenvironment and Not by the Previous Cell Differentiation State. J. Biol. Chem. 274: 2157-2165 [Abstract] [Full Text]  
• Sabourin, J.-C., Kern, A.-S., Grégori, C., Porteu, A., Cywiner, C., Châtelet, F.ço.-P., Kahn, A., Pichard, A.-L. (1996). An Intronic Enhancer Essential for Tissue-specific Expression of the Aldolase B Transgenes. J. Biol. Chem. 271: 3469-3473 [Abstract] [Full Text]