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| 1 | Daily genetic profiling indicates JAK/STAT signaling promotes early hepatic stellate cell transdifferentiation显示文摘AIM: To identify signaling pathways and genes that initiate and commit hepatic stellate cells (HSCs) to transdifferentiation. METHODS: Primary HSCs were isolated from male Sprague-Dawley rats and cultured on plastic for 0-10 d. Gene expression was assessed daily (quiescent to day 10 culture-activation) by real time polymerase chain reaction and data clustered using AMADA software. The significance of JAK/STAT signaling to HSC transdifferentiation was determined by treating cells with a JAK2 inhibitor. RESULTS: Genetic cluster analyses, based on expression of these 21 genes, showed similar expression profiles on days 1-3, days 5 and 6, and days 7-10, while freshly isolated cells (day Q) and day 4 cells were genotypically distinct from any of the other days. Additionally, gene expression clustering revealed strong upregulation of interleukin-6, JAK2 and STAT3 mRNA in the early stages of activation. Inhibition of the JAK/STAT signaling pathway impeded the morphological transdifferentiation of HSCs which correlated with decreased mRNA expression of several profibrotic genes including collagens, α-SMA, PDGFR and TGFβR. CONCLUSION: These data demonstrate unique clustered genetic profiles during the daily progression of HSC transdifferentiation and that JAK/STAT signaling may be critical in the early stages of transdifferentiation. | Ashley M Lakner Cathy C Moore Alyssa A Gulledge Laura W Schrum | 2010 | World Journal of Gastroenterology2010，16，40： | 23 |
| 2 | microRNAs: Fad or future of liver disease显示文摘microRNAs (miRs) are small non-coding RNAs that regulate both mRNA and protein expression of target genes, which results in alterations in mRNA stability or translation inhibition. miRs influence at least one third of all human transcripts and are known regulators of various important cellular growth and differentiation factors. miRs have recently emerged as key regulatory molecules in chronic liver disease. This review details recent contributions to the field of miRs that influence liver development and the broad spectrum of disease, from non-alcoholic fatty liver disease to fibrosis/cirrhosis, with particular emphasis on hepatic stellate cells and potential use of miRs as therapeutic tools. | Ashley M Lakner Herbert L Bonkovsky Laura W Schrum | 2011 | World Journal of Gastroenterology2011，17，20： | 13 |
| 3 | Targeting collagen expression in alcoholic liver disease显示文摘Alcoholic liver disease(ALD)is a leading cause of liver disease and liver-related deaths globally,particularly in developed nations.Liver fibrosis is a consequence of ALD and other chronic liver insults,which can progress to cirrhosis and hepatocellular carcinoma if left un-treated.Liver fibrosis is characterized by accumulation of excess extracellular matrix components,including typeⅠcollagen,which disrupts liver microcirculation and leads to injury.To date,there is no therapy for the treatment of liver fibrosis;thus treatments that either prevent the accumulation of typeⅠcollagen or hasten its degradation are desirable.The focus of this review is to examine the regulation of typeⅠcollagen in fibrogenic cells of the liver and to discuss current advances in therapeutics to eliminate excessive collagen deposition. | Kyle J Thompson Iain H McKillop Laura W Schrum | 2011 | World Journal of Gastroenterology2011，17，20： | 7 |
| 4 | Legalon-SIL downregulates HCV core and NS5A in human hepatocytes expressing full-length HCV显示文摘AIM: To determine the effect of Legalon-SIL (LS) on hepatitis C virus (HCV) core and NS5A expression and on heme oxygenase-1 (HMOX-1) and its transcriptional regulators in human hepatoma cells expressing full length HCV genotype 1b. METHODS: CON1 cells were treated with 50 μmol/L or 200 μmol/L LS. Cells were harvested after 2, 6 and 24 h. HCV RNA and protein levels were determined by quantitative real-time polymerase chain reaction and Western blotting, respectively. RESULTS: HCV RNA (core and NS5A regions) wasdecreased after 6 h with LS 200 μmol/L (P < 0.05). Both 50 and 200 μmol/L LS decreased HCV RNA levels [core region (by 55% and 88%, respectively) and NS5A region (by 62% and 87%, respectively) after 24 h compared with vehicle (dimethyl sulphoxide) control (P < 0.01). Similarly HCV core and NS5A protein were decreased (by 85%, P < 0.01 and by 65%, P < 0.05, respectively) by LS 200 μmol/L. Bach1 and HMOX-1 RNA were also downregulated by LS treatment (P < 0.01), while Nrf2 protein was increased (P < 0.05).CONCLUSION: Our results demonstrate that treatment with LS downregulates HCV core and NS5A expression in CON1 cells which express full length HCV genotype 1b, and suggests that LS may prove to be a valuable alternative or adjunctive therapy for the treatment of HCV infection. | Marjan Mehrab-Mohseni Hossein Sendi Nury Steuerwald Sriparna Ghosh Laura W Schrum Herbert L Bonkovsky | 2011 | World Journal of Gastroenterology2011，17，13： | 3 |
| 5 | Mechanism of T cell toler-ance induced by myeloid-derived suppressor cells显示文摘 | Nagaraj S Schrum A G Cho H I | 2010 | J Immunol2010，184，6： | 1 |
| 6 | c-Jun does not me diate hepatocyte apoptosis following NF-kappaB inhibi tion and partial hcpatectomy显示文摘 | Schrum I W Black D Iimuro Y | 2000 | J Surg Res2000，88，2： | 1 |
| 7 | Sulfate-reducing ammonium oxidation: A thermodynamically feasible metabolic pathway in subseafloor sediment 显示文摘 | Schrum H N Spivack A J Kastner M | 2009 | Geology2009，37，10： | 1 |
| 8 | Mechanism of T cell tolerance induced by myeloid-derived suppressor ceiis 显示文摘 | Nagaraj S Schrum AG Cho HI | 2010 | J Immunol2010，184，6： | 1 |
| 9 | Long-term follow-up of allogeneic stem cell transplantation in patients with severe aplastic anemia after conditioning with cyclophosphamide plus antithymocyte globulin显示文摘 | N. Kr?ger T. Zabelina H. Renges W. Krüger U. Kordes J. Rischewski J. Schrum M. Horstmann F. Ayuk R. Erttmann H. Kabisch A. Zander | 2002 | Annals of Hematology2002，，11： | 1 |
| 10 | Bacterium-induced CXCL10 secretion by osteoblasts can be mediated in part through Toll-like receptor 4显示文摘 | Petty CC Schrum LW | 2002 | Infect Immun2002，70，8： | 1 |
| 11 | Peroxisone proliferator activated receptors and hepatic stellate cell activation显示文摘 | SCHRUM L RIPPE R | 2000 | J Biol Chem2000，275，35： | 1 |
| 12 | Apoptosis: cell death by proteolytic scalpel显示文摘 | Behrns KE Schrum LW Que FG | 1999 | Surgery1999，126，3： | 1 |
| 13 | Autocrine expression of activated transforming growth factor - beta(1) induces apoptosis in normal rat liver显示文摘 | Schrum LW Bird MA Salcher O | 2001 | Am J Physiol2001，280，1： | 1 |
| 14 | Expression of interleukin-10by in vitro and in vivo activated hepatic stellate cells显示文摘 | Wang SC Dhata M Schrum L | 1998 | J Biol Chem1998，273，： | 1 |
| 15 | Microchip flow cytometry using electrokinetic focusing显示文摘 | Schrum D Culbertson C T Jacobson S C | 1999 | Anal Chem1999，71，19： | 1 |
| 16 | Severe phototoxicityassociated w ith long-term voriconazole treatm ent显示文摘 | V ohringer S Schrum J O tt H | 2011 | J D tsch D erm atol G es2011，9，4： | 1 |
| 17 | Peroxisome proliferator-activated receptors and hepatic stellate cell activation 显示文摘 | Miyahara T Schrum L Rippe R | 2000 | J Biol Chem2000，275，35： | 1 |
| 18 | Autocrine expression of activated transforming growth factor-beta1 induces apoptosis in normal rat liver显示文摘 | Schrum L Bird MA Salcher O | 2001 | Am J Physiol Gastrointest Liver Physiol2001，280，1： | 1 |
| 19 | NF-kappaB inhibits expression of the alphal( I ) collagen gene显示文摘 | RIPPER A SCHRUM L W STEFANOVIC B | 1999 | DNA Cell Biol1999，18，10： | 1 |
| 20 | Mechanism of T cell tolerance induced by myeloid-derived suppressor cells显示文摘 | Nagaraj S Schrum AG Cho HI | 2010 | J Immunol2010，184，： | 1 |
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