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Full-Text Articles in Molecular Biology

Hepatitis C Virus-Induced Monocyte Differentiation Into Polarized M2 Macrophages Promotes Stellate Cell Activation Via Tgf-Beta, Banishree Saha, Karen Kodys, Gyongyi Szabo May 2017

Hepatitis C Virus-Induced Monocyte Differentiation Into Polarized M2 Macrophages Promotes Stellate Cell Activation Via Tgf-Beta, Banishree Saha, Karen Kodys, Gyongyi Szabo

Gyongyi Szabo

BACKGROUND and AIMS: Monocyte and macrophage (MPhi) activation contributes to the pathogenesis of chronic hepatitis C virus (HCV) infection. Disease pathogenesis is regulated by both liver-resident MPhis and monocytes recruited as precursors of MPhis into the damaged liver. Monocytes differentiate into M1 (classic/proinflammatory) or M2 (alternative/anti-inflammatory) polarized MPhis in response to tissue microenvironment. We hypothesized that HCV-infected hepatoma cells (infected with Japanese fulminant hepatitis-1 [Huh7.5/JFH-1]) induce monocyte differentiation into polarized MPhis. METHODS: Healthy human monocytes were co-cultured with Huh7.5/JFH-1 cells or cell-free virus for 7 days and analyzed for MPhi markers and cytokine levels ...


Hepatitis C Virus-Induced Monocyte Differentiation Into Polarized M2 Macrophages Promotes Stellate Cell Activation Via Tgf-Beta, Banishree Saha, Karen Kodys, Gyongyi Szabo Jan 2016

Hepatitis C Virus-Induced Monocyte Differentiation Into Polarized M2 Macrophages Promotes Stellate Cell Activation Via Tgf-Beta, Banishree Saha, Karen Kodys, Gyongyi Szabo

UMass Metabolic Network Publications

BACKGROUND and AIMS: Monocyte and macrophage (MPhi) activation contributes to the pathogenesis of chronic hepatitis C virus (HCV) infection. Disease pathogenesis is regulated by both liver-resident MPhis and monocytes recruited as precursors of MPhis into the damaged liver. Monocytes differentiate into M1 (classic/proinflammatory) or M2 (alternative/anti-inflammatory) polarized MPhis in response to tissue microenvironment. We hypothesized that HCV-infected hepatoma cells (infected with Japanese fulminant hepatitis-1 [Huh7.5/JFH-1]) induce monocyte differentiation into polarized MPhis.

METHODS: Healthy human monocytes were co-cultured with Huh7.5/JFH-1 cells or cell-free virus for 7 days and analyzed for MPhi markers and cytokine levels ...


Novel Roles For The Tumor Suppressor Apc Through Regulation Of Gsk-3, Alexander James Valvezan Jan 2013

Novel Roles For The Tumor Suppressor Apc Through Regulation Of Gsk-3, Alexander James Valvezan

Publicly Accessible Penn Dissertations

Adenomatous Polyposis Coli (APC) is a tumor suppressor and essential negative regulator of the Wnt signaling pathway. Wnt signaling is crucial for proper patterning and cell fate specification during development and regulates stem cell homeostasis throughout adulthood. Mutations in Apc are strongly linked to human colorectal cancers and these mutations aberrantly activate Wnt signaling. How APC regulates the Wnt pathway and how oncogenic Apc mutations activate Wnt signaling and promote tumorigenesis are not fully understood. To address these questions, we utilized in vitro reconstitution assays, as well as Apc knockdown or mutation in human cells, zebrafish, and mice. We find ...


A Green Tea Component Suppresses Posttranslational Expression Of Basic Fibroblast Growth Factor In Colorectal Cancer, M Sukthanka, K Yamaguchi, Sh Lee, Michael Mcentee, T Eling, Y Hara, Seung Baek May 2008

A Green Tea Component Suppresses Posttranslational Expression Of Basic Fibroblast Growth Factor In Colorectal Cancer, M Sukthanka, K Yamaguchi, Sh Lee, Michael Mcentee, T Eling, Y Hara, Seung Baek

Seung J Baek

BACKGROUND & AIMS: Green tea catechins are known to have anticarcinogenic effects. Epigallocatechin-3-gallate (EGCG) accounts for almost 50% of the total catechin content in green tea extract and has very potent antioxidant effects. EGCG also inhibits angiogenesis, possibly through the inhibition of proangiogenic factors including vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF), which in turn, inhibits tumor growth and metastasis. However, the exact molecular mechanism by which EGCG suppresses bFGF expression is not known. Our objective was to elucidate the molecular mechanisms by which EGCG inhibits bFGF expression in colorectal cancer. METHODS: We examined posttranslational regulation of ...