Heat shock protein 90 is responsible for hyperdynamic circulation in portal hypertensive rats

doi:10.3748/wjg.v9.i11.2544

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Nov 15, 2003 (publication date) through Apr 26, 2024

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World Journal of Gastroenterology

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1007-9327

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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA

Basic Research

World J Gastroenterol. Nov 15, 2003; 9(11): 2544-2547
Published online Nov 15, 2003. doi: 10.3748/wjg.v9.i11.2544

Heat shock protein 90 is responsible for hyperdynamic circulation in portal hypertensive rats

Jian-Hua Ai, Zhen Yang, Fa-Zu Qiu, Tong Zhu

Jian-Hua Ai, Zhen Yang, Fa-Zu Qiu, Center for Hepatic Surgery, Tongji Hospital, Tongji Medical College, Huazhong Science and Technological University Wuhan 430030, Hubei Province, China

Tong Zhu, Institute of Organ Transplantation, Tongji Hospital, Tongji Medical College, Huazhong Science and Technological University, Wuhan 430030, Hubei Province, China

Author contributions: All authors contributed equally to the work.

Supported by the National Natural Science Foundation of China, No.30170920

Correspondence to: Dr. Jian-Hua Ai, International Cooperation Laboratory on Signal Transduction, Eastern Hepatobiliary Surgery Institute, Second Military Medical University, Shanghai 200438, China. aijh_2000@yahoo.com

Telephone: +86-21-25070846

Received: May 10, 2003
Revised: May 20, 2003
Accepted: June 4, 2003
Published online: November 15, 2003

Abstract

AIM: To examine the participation of HSP90 in portal hypertensive rat mesentery in vitro.

METHODS: immunohistochemistry and Western-blot were used to examine the expression of HSP90 in mesenteric vasculature. HSP90 mRNA was detected by RT-PCR, and the role of HSP90 in hyperdynamic circulation was examined by in vitro mesenteric perfusion studies.

RESULTS: HSP90 was overexpressed in endothelium of mesentery vasculature in animals with experimental portal hypertension induced by partial portal vein ligation (PVL) compared with normal animals. Geldanamycin (GA), a special inhibitor of HSP90 signaling, attenuated ACh-dependent vasodilation but did not affect vasodilation in response to sodium nitroprusside in normal rats. In PVL animals, the perfused mesentery was hyporesponsive to vasoconstrictor methoxamine. GA significantly potentiated methoxamine-induced vasoconstrictor after PVL.

CONCLUSION: HSP90 plays a key role in NO-dependent hyperdynamic circulation in portal hypertension and provides a novel method for future treatment of portal hypertension.

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