NDLI: Shear Stress Induces Hepatocyte PAI-1 Gene Expression Through Cooperative Sp1/Ets-1 Activation of Transcription

Content Provider	IEEE Xplore Digital Library
Author	Nakatsuka, H. Sokabe, T. Yamamoto, K. Ando, J.
Copyright Year	2006
Description	Author affiliation: Dept. of Biomed. Eng., Tokyo Univ. (Nakatsuka, H.; Sokabe, T.; Yamamoto, K.; Ando, J.)
Abstract	Partial hepatectomy causes hemodynamic changes which increases portal blood flow in the remaining lobe, where the expression of immediate-early genes, including plasminogen activator inhibitor-1 (PAI-1), is induced. We hypothesized that a hyperdynamic circulatory state occurring in the remaining lobe induces immediate-early gene expression. In this study, we investigated whether the mechanical force generated by flowing blood, shear stress, induces PAI-1 expression in hepatocytes. When cultured rat hepatocytes were exposed to flow, PAI-1 mRNA levels began to increase within 3 hours, peaked at levels significantly higher than the static control levels, and then gradually decreased. The flow-induced PAI-1 expression was shear-stress- rather than shear-rate-dependent, and accompanied by increased hepatocyte production of PAI-1 protein. Shear stress increased PAI-1 transcription, but did not affect PAI-1 mRNA stability. Functional analysis of the 2.1-kb PAI-1 5'-promoter indicated that a 278-bp segment containing transcription factors Sp1 and Ets-1 consensus sequences was critical to the shear-stress-dependent increase of PAI-1 transcription. Mutations of both the Sp1 and Ets-1 consensus sequences, but not of either one alone, markedly prevented basal PAI-1 transcription and abolished the response of the PAI-1 promoter to shear stress. Electrophoretic mobility shift assays and chromatin immunoprecipitation showed binding of Sp1 and Ets-1 to each consensus sequence under static conditions, which increased in response to shear stress. In conclusion, hepatocyte PAI-1 expression is flow-sensitive and transcriptionally regulated by shear stress via cooperative interactions between Sp1 and Ets-1
Starting Page	1
Ending Page	6
File Size	434526
Page Count	6
File Format	PDF
ISBN	1424407176
DOI	10.1109/MHS.2006.320328
Language	English
Publisher	Institute of Electrical and Electronics Engineers, Inc. (IEEE)
Publisher Date	2006-11-05
Publisher Place	Japan
Access Restriction	Subscribed
Rights Holder	Institute of Electrical and Electronics Engineers, Inc. (IEEE)
Subject Keyword	Stress Gene expression Hepatectomy Hemodynamics Portals Blood flow Production Proteins Stability Functional analysis
Content Type	Text
Resource Type	Article

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
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