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Extracellular matrix degradation and the role of hepatic stellate cells

Extracellular matrix degradation and the role of hepatic stellate cells
Extracellular matrix degradation and the role of hepatic stellate cells
Following liver injury, hepatic stellate cells (HSCs) become activated and express a combination of matrix metalloproteinases (MMPs) and their specific tissue inhibitors (TIMPs). In the early phases of liver injury (and primary cell culture), HSCs transiently express MMP-3, MMP-13, and uroplasminogen activator (uPA) and exhibit a matrix-degrading phenotype. In the later stages of liver injury and HSC activation, the pattern changes and the cells express a combination of MMPs that have the ability to degrade normal liver matrix, while inhibiting degradation of the fibrillar collagens that accumulate in liver fibrosis. This pattern is characterized by the combination of pro-MMP-2 and membrane type 1 (MT1)-MMP expression, which drive pericellular generation of active MMP-2 and local degradation of normal liver matrix. In addition there is a marked increase in expression of TIMP-1 leading to a more global inhibition of degradation of fibrillar liver collagens by interstitial collagenases (MMP-1/MMP-13). These pathways play a significant role in the progression of liver fibrosis. Following cessation of liver injury, the pattern reverses and TIMP-1 in particular is rapidly downregulated. This phase is characterized by increasing activity of collagenases, degradation of liver matrix, and regression of liver fibrosis.
cirrhosis, liver fibrosis, matrix degradation, matrix metalloproteinases, tissue inhibitor of metalloproteinases
0272-8087
373-384
Benyon, R. Christopher
6efa9278-56e6-47ec-9854-78afd98dd4c9
Arthur, Michael J.P.
d61d056b-6470-4afc-bafb-7a20be9cc413
Benyon, R. Christopher
6efa9278-56e6-47ec-9854-78afd98dd4c9
Arthur, Michael J.P.
d61d056b-6470-4afc-bafb-7a20be9cc413

Benyon, R. Christopher and Arthur, Michael J.P. (2001) Extracellular matrix degradation and the role of hepatic stellate cells. Seminars in Liver Disease, 21 (3), 373-384. (doi:10.1055/s-2001-17552).

Record type: Article

Abstract

Following liver injury, hepatic stellate cells (HSCs) become activated and express a combination of matrix metalloproteinases (MMPs) and their specific tissue inhibitors (TIMPs). In the early phases of liver injury (and primary cell culture), HSCs transiently express MMP-3, MMP-13, and uroplasminogen activator (uPA) and exhibit a matrix-degrading phenotype. In the later stages of liver injury and HSC activation, the pattern changes and the cells express a combination of MMPs that have the ability to degrade normal liver matrix, while inhibiting degradation of the fibrillar collagens that accumulate in liver fibrosis. This pattern is characterized by the combination of pro-MMP-2 and membrane type 1 (MT1)-MMP expression, which drive pericellular generation of active MMP-2 and local degradation of normal liver matrix. In addition there is a marked increase in expression of TIMP-1 leading to a more global inhibition of degradation of fibrillar liver collagens by interstitial collagenases (MMP-1/MMP-13). These pathways play a significant role in the progression of liver fibrosis. Following cessation of liver injury, the pattern reverses and TIMP-1 in particular is rapidly downregulated. This phase is characterized by increasing activity of collagenases, degradation of liver matrix, and regression of liver fibrosis.

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More information

Published date: 2001
Keywords: cirrhosis, liver fibrosis, matrix degradation, matrix metalloproteinases, tissue inhibitor of metalloproteinases

Identifiers

Local EPrints ID: 26936
URI: https://eprints.soton.ac.uk/id/eprint/26936
ISSN: 0272-8087
PURE UUID: 991bb3eb-e752-484c-b361-28b02d19cbdc

Catalogue record

Date deposited: 25 Apr 2006
Last modified: 17 Jul 2017 16:05

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