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Research Article Free access | 10.1172/JCI1324

Distribution of heme oxygenase isoforms in rat liver. Topographic basis for carbon monoxide-mediated microvascular relaxation.

N Goda, K Suzuki, M Naito, S Takeoka, E Tsuchida, Y Ishimura, T Tamatani, and M Suematsu

Department of Biochemistry, School of Medicine, Keio University, Tokyo 160, Japan.

Find articles by Goda, N. in: PubMed | Google Scholar

Department of Biochemistry, School of Medicine, Keio University, Tokyo 160, Japan.

Find articles by Suzuki, K. in: PubMed | Google Scholar

Department of Biochemistry, School of Medicine, Keio University, Tokyo 160, Japan.

Find articles by Naito, M. in: PubMed | Google Scholar

Department of Biochemistry, School of Medicine, Keio University, Tokyo 160, Japan.

Find articles by Takeoka, S. in: PubMed | Google Scholar

Department of Biochemistry, School of Medicine, Keio University, Tokyo 160, Japan.

Find articles by Tsuchida, E. in: PubMed | Google Scholar

Department of Biochemistry, School of Medicine, Keio University, Tokyo 160, Japan.

Find articles by Ishimura, Y. in: PubMed | Google Scholar

Department of Biochemistry, School of Medicine, Keio University, Tokyo 160, Japan.

Find articles by Tamatani, T. in: PubMed | Google Scholar

Department of Biochemistry, School of Medicine, Keio University, Tokyo 160, Japan.

Find articles by Suematsu, M. in: PubMed | Google Scholar

Published February 1, 1998 - More info

Published in Volume 101, Issue 3 on February 1, 1998
J Clin Invest. 1998;101(3):604–612. https://doi.org/10.1172/JCI1324.
© 1998 The American Society for Clinical Investigation
Published February 1, 1998 - Version history
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Abstract

Carbon monoxide (CO) derived from heme oxygenase has recently been shown to play a role in controlling hepatobiliary function, but intrahepatic distribution of the enzyme is unknown. We examined distribution of two kinds of the heme oxygenase isoforms (HO-1 and HO-2) in rat liver immunohistochemically using monoclonal antibodies. The results showed that distribution of the two isoforms had distinct topographic patterns: HO-1, an inducible isoform, was observed only in Kupffer cells, while HO-2, a constitutive form, distributed to parenchymal cells, but not to Kupffer cells. Both isoforms were undetectable in hepatic stellate cells and sinusoidal endothelial cells. Of the two isoforms, HO-2 in the parenchymal cell rather than HO-1 in the Kupffer cell, appears to play a major role in regulation of microvascular tone. In the perfused liver, administration of HbO2, a CO-trapping reagent that can diffuse across the fenestrated endothelium into the space of Disse, elicited a marked sinusoidal constriction, while administration of a liposome-encapsulated Hb that cannot enter the space had no effect on the microvascular tone. These results suggest that CO evolved by HO-2 in the parenchymal cells, and, released to the extrasinusoidal space, served as the physiological relaxant for hepatic sinusoids.

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