We are analyzing https://link.springer.com/article/10.1007/s10620-014-3167-6.

Title:
Caspase 3 Inactivation Protects Against Hepatic Cell Death and Ameliorates Fibrogenesis in a Diet-Induced NASH Model | Digestive Diseases and Sciences
Description:
Background/Aims Hepatocyte cell death is a key feature of nonalcoholic steatohepatitis (NASH). As the contribution of specific caspases remains unclear, our aim was to ascertain the effect of caspase 3 suppression on liver injury and fibrogenesis. Methods C57BL/6 wild-type (WT) and caspase 3 knock out (Casp3 −/−) mice were placed on a methionine- and choline-deficient (MCD) diet for 6 weeks to induce steatohepatitis and liver fibrosis. Thereafter, liver injury, liver fibrosis and hepatocellular apoptosis were quantified in liver sections. Additionally, expression of proteins associated with liver inflammation and fibrogenesis was analyzed. Results WT mice fed MCD diet showed marked activation of caspase 3 in hepatocytes, in conjunction with steatohepatitis and increased hepatic triglyceride levels, hepatocyte ballooning, inflammation and fibrosis. Casp3 −/− mice fed the MCD diet showed similar serum aminotransferase levels and NAFLD activity scores (NAS) compared with WT MCD-fed mice. However, Casp3 −/− mice on the MCD diet showed a marked reduction in expression of transcripts for profibrogenic genes, which translated into reduced hepatic collagen deposition. These changes were associated with decreased levels of apoptosis, and a significant reduction in the expression of cytokines involved in inflammatory signaling. Casp3 −/− mice on the MCD showed a reduction in expression of chemokine receptor 2 (CCR2) leading to ameliorated infiltration of inflammatory lymphocyte antigen 6 complex, locus C1 (Ly6c) positive monocytes. Conclusion These findings support a prominent role for hepatocyte caspase 3 activation in NASH-related apoptosis, fibrogenesis and fibrosis which in part is mediated via CCR2-dependent infiltration of Ly6c positive monocytes.
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article, pubmed, google, scholar, liver, cas, nonalcoholic, hepatic, steatohepatitis, feldstein, apoptosis, disease, fatty, fibrosis, central, caspase, hepatology, mice, fibrogenesis, access, cell, hepatocyte, caspases, injury, expression, activation, privacy, cookies, content, mcd, diet, steatosis, gores, information, publish, research, search, death, model, thapaliya, wree, berk, dixon, casp, inflammation, showed, ccr, open, dis, gastroenterology,

Topics {✒️}

month download article/chapter high fat diet-induced diet-induced nash model wt mcd-fed mice pan-caspase inhibitor emricasan article digestive diseases inflammatory gr1 + monocyte subset population-based cohort study mcd diet showed hepatic stellate cells stimulating tnf-alpha expression maria eugenia inzaugarat & ariel full article pdf related subjects nash-related apoptosis decreases liver injury privacy choices/manage cookies lerner research institute hepatic cell death innate immune cells maria eugenia inzaugarat liver cell apoptosis control cell death semin liver dis elevated liver enzymes central regulator article thapaliya fatty liver clin liver dis mcd showed human nonalcoholic steatohepatitis 2016 cxcl10-mediates macrophage intrahepatic monocyte subsets pan-caspase inhibition liver injury liver disease european economic area curr opin pediatr invasive versus noninvasive long-term follow histological scoring system shape caspase activity check access instant access annu rev biochem hepatic steatosis sensitizes conditions privacy policy ccr2-dependent infiltration feldstein ae article log

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         description:Hepatocyte cell death is a key feature of nonalcoholic steatohepatitis (NASH). As the contribution of specific caspases remains unclear, our aim was to ascertain the effect of caspase 3 suppression on liver injury and fibrogenesis. C57BL/6 wild-type (WT) and caspase 3 knock out (Casp3 −/−) mice were placed on a methionine- and choline-deficient (MCD) diet for 6 weeks to induce steatohepatitis and liver fibrosis. Thereafter, liver injury, liver fibrosis and hepatocellular apoptosis were quantified in liver sections. Additionally, expression of proteins associated with liver inflammation and fibrogenesis was analyzed. WT mice fed MCD diet showed marked activation of caspase 3 in hepatocytes, in conjunction with steatohepatitis and increased hepatic triglyceride levels, hepatocyte ballooning, inflammation and fibrosis. Casp3 −/− mice fed the MCD diet showed similar serum aminotransferase levels and NAFLD activity scores (NAS) compared with WT MCD-fed mice. However, Casp3 −/− mice on the MCD diet showed a marked reduction in expression of transcripts for profibrogenic genes, which translated into reduced hepatic collagen deposition. These changes were associated with decreased levels of apoptosis, and a significant reduction in the expression of cytokines involved in inflammatory signaling. Casp3 −/− mice on the MCD showed a reduction in expression of chemokine receptor 2 (CCR2) leading to ameliorated infiltration of inflammatory lymphocyte antigen 6 complex, locus C1 (Ly6c) positive monocytes. These findings support a prominent role for hepatocyte caspase 3 activation in NASH-related apoptosis, fibrogenesis and fibrosis which in part is mediated via CCR2-dependent infiltration of Ly6c positive monocytes.
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      description:Hepatocyte cell death is a key feature of nonalcoholic steatohepatitis (NASH). As the contribution of specific caspases remains unclear, our aim was to ascertain the effect of caspase 3 suppression on liver injury and fibrogenesis. C57BL/6 wild-type (WT) and caspase 3 knock out (Casp3 −/−) mice were placed on a methionine- and choline-deficient (MCD) diet for 6 weeks to induce steatohepatitis and liver fibrosis. Thereafter, liver injury, liver fibrosis and hepatocellular apoptosis were quantified in liver sections. Additionally, expression of proteins associated with liver inflammation and fibrogenesis was analyzed. WT mice fed MCD diet showed marked activation of caspase 3 in hepatocytes, in conjunction with steatohepatitis and increased hepatic triglyceride levels, hepatocyte ballooning, inflammation and fibrosis. Casp3 −/− mice fed the MCD diet showed similar serum aminotransferase levels and NAFLD activity scores (NAS) compared with WT MCD-fed mice. However, Casp3 −/− mice on the MCD diet showed a marked reduction in expression of transcripts for profibrogenic genes, which translated into reduced hepatic collagen deposition. These changes were associated with decreased levels of apoptosis, and a significant reduction in the expression of cytokines involved in inflammatory signaling. Casp3 −/− mice on the MCD showed a reduction in expression of chemokine receptor 2 (CCR2) leading to ameliorated infiltration of inflammatory lymphocyte antigen 6 complex, locus C1 (Ly6c) positive monocytes. These findings support a prominent role for hepatocyte caspase 3 activation in NASH-related apoptosis, fibrogenesis and fibrosis which in part is mediated via CCR2-dependent infiltration of Ly6c positive monocytes.
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         Liver fibrosis
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         Oncology
         Transplant Surgery
         Biochemistry
         general
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