Essay on Degradation of the Liver by Matrix Metalloproteinases

Essay on Degradation of the Liver by Matrix Metalloproteinases

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Matrix metalloproteinases (MMPs) are the enzymes responsible for matrix degradation in the liver [38]. These are calcium-dependent enzymes that specifically degrade collagens and noncollagenous substrates. MMPs are divided into 5 categories according to their substrate [39]:

1) interstitial collagenases (MMP-1, -8, -13),
2) gelatinases (MMP-2,-9, and fibroblast activation protein),
3) stromelysins (MMP-3, -7, -10, -11),
4) membrane type (MMP-14, -15, -16, -17, -24, -25), and
5) metalloelastase (MMP-12).

The degradation of normal extracellular matrix (ECM) is a key event in the process of liver fibrosis as it allows its replacement with scar matrix. Activated HSCs secrete large amounts of MMP-2 and MMP-9, which degrade the collagen type IV of normal ECM [40]. They also express large amounts of MMP-1 mRNA, the principal MMP which degrades scar matrix (predominantly collagen type I), however little active enzyme is detectable in fibrotic liver [40]. Tissue inhibitors of matrix metalloproteinases (TIMPs) are the main regulators (inhibitors) of MMP activity. HSCs produce large amounts of TIMP-1 and TIMP-2 and these prevent the degradation of the interstitial collagens of scar matrix by MMP-1[41]. TIMP-1 also promotes HSC survival [42, 43].

Loss of Retinoids
A characteristic feature of stellate cell activation is the loss of retinoid (Vitamin A) droplets from the perinuclear region. The exact role that this plays in the transition from the quiescent to activated phenotype remains unclear.

1.2.2 Alternative Sources of Myofibroblasts
Recently it has been recognized that myofibroblasts are derived from a number of sources other than the quiescent HSC population. These sources include portal fibroblasts, circulating fibrocytes an...


... middle of paper ...


... role in fibrosis of other organs, particularly the lungs, is well documented [65]. Kisseleva and colleagues [66] transplanted bone marrow from mice expressing GFP under the control of the α1(I) collagen promoter into wild type animals. These mice then underwent bile duct ligation. Bone marrow-derived collagen-producing GFP+ cells were detected in the liver of chimeric mice and these did not express αSMA or desmin, markers typical of hepatic stellate cells. However, only 1% of these cells expressed CD34 – a typical phenotypic characteristic of fibrocytes.

Although the studies discussed here provide convincing evidence for the extra-hepatic origin of myofibroblasts, it is clear that the role of the bone marrow and circulating cells in liver fibrosis is complex and at best, poorly understood and their overall contribution to hepatic fibrogenesis may be limited.

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