Gene expression of interstitial collagenase in both progressive and recovery phase of rat liver fibrosis induced by carbon tetrachloride

Loss of MMP 13 attenuates murine hepatic injury and fibrosis during cholestasis

“…Our results strongly support previous studies that demonstrated expression of MMP-13 in scar-associated macrophages and hepatocytes in CCl 4 -injured liver. [26][27][28] Other studies have shown that activated HSCs express MMP-13 in vivo 19 and in culture. 29,30 Cytokines, such as IL-1 and TGF-␤, stimulate MMP-13 production in cultured-HSCs, 30,31 which was also found in our study.…”

“…Although previous studies focused on MMP-13 expression during liver injury, alteration in expression of MMP-13 and the cellular source of MMP-13 during liver fibrogenesis are still in debate. 16,19 This study analyzed the expression pattern of MMP-13 in the liver after bile duct ligation (BDL) in mice. Moreover, we used the BDL model to examine the role of MMP-13 during liver fibrosis in MMP-13-deficient mice and their wild-type littermates.…”

Baculovirus-mediated interferon alleviates dimethylnitrosamine-induced liver cirrhosis symptoms in a murine model

“…23,24 MMP-2, which is stimulated by transforming growth factor-b (TGF-b), is necessary for the proliferation and infiltration of HSCs during the process of fibrosis formation. [25][26][27][28][29] Increased TIMP-1 expression promotes liver fibrosis progression by preventing the degradation of secreted collagens, and TIMP-1 expression decreases during the recovery phase. 30 In this study, MMP-13, MMP-2 and TIMP-1 expression levels were downregulated in mouse livers treated with baculovirus compared with saline-injected cirrhotic livers ( Figure 5).…”

Adenovirus-mediated gene transfer of interferon α improves dimethylnitrosamine-induced liver cirrhosis in rat model

“…However, the reversibility of hepatic fibrosis has been reported in these models. 24 Therefore, we employed a DMN-induced model, in which fibrosis and hepatic transaminase elevation do not spontaneously regress in rat LC. 16,18,22 This is the first preclinical study demonstrating the advantage and feasibility of IFN-a gene therapy for LC, and the efficacy and safety of the approach need to be reproduced in other LC models in different animals.…”

“…Interstitial collagenase (MMP-13) has been considered an essential enzyme for collagenolysis in liver fibrosis, and it was reported that expression of MMP-13 is elevated at peak fibrosis and drops rapidly in the recovery periods. 23,24 The MMP-2, which is stimulated by TGF-b, is necessary for proliferation and infiltration of hepatic stellate cells in the process of fibrosis formation. [25][26][27] The expression of TIMP-1 Adenovirus-mediated IFN gene therapy for LC in rat K Suzuki et al increases in the process of liver fibrosis to promote progression of liver fibrosis by preventing degradation of secreted collagens and decreases in the recovery phase.…”