These findings also demonstrated a potent antifibrotic effect of FGF2lmw administration, which may provide a novel approach to treat chronic liver diseases. This article is protected by copyright. All rights reserved. “
“Chronic liver disease is characterized by the liver enrichment of myeloid DCs. To assess the role of disease on myelopoiesis, we utilized a systems biology approach to study development in liver-resident cells expressing stem cell marker CD34. In patients with end-stage liver disease, liver CD34+ cells were comprised by two subsets, designated CD34+CD146+ and CD34+CD146-, and hematopoietic function was restricted

to CD34+CD146- cells. Liver CD34 frequencies RG7204 cell line were reduced during nonalcoholic steatohepatitis (NASH) and chronic hepatitis C virus (HCV) compared to alcohol liver disease (ALD), and this reduction correlated with viral load in the HCV cohort. To better understand the relationship between liver CD34+CD146+ and CD34+CD146- subsets and any effects of disease on CD34 Acalabrutinib order development, we used gene expression profiling and computational modeling to

compare each subset during ALD and HCV. For CD34+CD146+ cells, increased expression of endothelial cell genes including von Willebrand factor, VE-cadherin and eNOS were observed when compared to CD34+CD146- cells, and minimal effects of ALD and HCV diseases on gene expression were observed. Importantly for CD34+CD146- cells, chronic HCV was associated with a distinct ‘imprint’ of programs related 上海皓元 to cell cycle, DNA repair, chemotaxis, development, and activation, with an emphasis on myeloid and B lymphocyte lineages. This HCV signature was further translated in side-by-side analyses, where HCV CD34+CD146-

cells demonstrated superior hematopoietic growth, colony formation, and diversification compared to ALD and NASH when cultured identically. Disease-associated effects on hematopoiesis were also evident by phenotypic alterations in the expression of CD14, HLA-DR and CD16 by myeloid progeny cells. Conclusion: Etiology drives progenitor fate within diseased tissues. The liver may be a useful source of hematopoietic cells for therapy, or as therapeutic targets. (Hepatology 2014;) “
“Petersen KF, Dufour S, Hariri A, Nelson-Williams C, Foo JN, Zhand XM, et al. Apolipoprotein C3 gene variants in nonalcoholic fatty liver disease. N Engl J Med 2010;362:1082-1089. (Reprinted with permission.) Background: Nonalcoholic fatty liver disease is associated with hepatic insulin resistance and type 2 diabetes mellitus. Whether this association has a genetic basis is unknown.