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84 Publications visible to you, out of a total of 84
Hepatocyte-specific Smad7 deletion accelerates DEN-induced HCC via activation of STAT3 signaling in mice

Abstract

Not specified

Authors: T Feng, J Dzieran, X Yuan, A Dropmann, T Maass, A Teufel, S Marhenke, T Gaiser, F Rückert, I Kleiter, S Kanzler, M P Ebert, A Vogel, P ten Dijke, S Dooley, N M Meindl-Beinker

Date Published: 2017

Publication Type: Not specified

Caveolin-1 in the regulation of cell metabolism: a cancer perspective.

Abstract (Expand)

Caveolin-1 (CAV1) is an oncogenic membrane protein associated with endocytosis, extracellular matrix organisation, cholesterol distribution, cell migration and signaling. Recent studies reveal that … CAV1 is involved in metabolic alterations - a critical strategy adopted by cancer cells to their survival advantage. Consequently, research findings suggest that CAV1, which is altered in several cancer types, influences tumour development or progression by controlling metabolism. Understanding the molecular interplay between CAV1 and metabolism could help uncover druggable metabolic targets or pathways of clinical relevance in cancer therapy. Here we review from a cancer perspective, the findings that CAV1 modulates cell metabolism with a focus on glycolysis, mitochondrial bioenergetics, glutaminolysis, fatty acid metabolism, and autophagy.

Authors: Z. C. Nwosu, M. P. Ebert, S. Dooley, C. Meyer

Date Published: 18th Nov 2016

Publication Type: Not specified

Creation of Three-Dimensional Liver Tissue Models from Experimental Images for Systems Medicine.

Abstract (Expand)

In this chapter, we illustrate how three-dimensional liver tissue models can be created from experimental image modalities by utilizing a well-established processing chain of experiments, microscopic … imaging, image processing, image analysis and model construction. We describe how key features of liver tissue architecture are quantified and translated into model parameterizations, and show how a systematic iteration of experiments and model simulations often leads to a better understanding of biological phenomena in systems biology and systems medicine.

Authors: S. Hoehme, A. Friebel, S. Hammad, D. Drasdo, J. G. Hengstler

Date Published: 11th Nov 2016

Publication Type: Not specified

Orphan nuclear receptor SHP regulates iron metabolism through inhibition of BMP6-mediated hepcidin expression.

Abstract (Expand)

Small heterodimer partner (SHP) is a transcriptional corepressor regulating diverse metabolic processes. Here, we show that SHP acts as an intrinsic negative regulator of iron homeostasis. SHP-deficient … mice maintained on a high-iron diet showed increased serum hepcidin levels, decreased expression of the iron exporter ferroportin as well as iron accumulation compared to WT mice. Conversely, overexpression of either SHP or AMP-activated protein kinase (AMPK), a metabolic sensor inducing SHP expression, suppressed BMP6-induced hepcidin expression. In addition, an inhibitory effect of AMPK activators metformin and AICAR on BMP6-mediated hepcidin gene expression was significantly attenuated by ablation of SHP expression. Interestingly, SHP physically interacted with SMAD1 and suppressed BMP6-mediated recruitment of the SMAD complex to the hepcidin gene promoter by inhibiting the formation of SMAD1 and SMAD4 complex. Finally, overexpression of SHP and metformin treatment of BMP6 stimulated mice substantially restored hepcidin expression and serum iron to baseline levels. These results reveal a previously unrecognized role for SHP in the transcriptional control of iron homeostasis.

Authors: D. K. Kim, Y. H. Kim, Y. S. Jung, K. S. Kim, J. H. Jeong, Y. S. Lee, J. M. Yuk, B. C. Oh, H. E. Choy, S. Dooley, M. U. Muckenthaler, C. H. Lee, H. S. Choi

Date Published: 1st Oct 2016

Publication Type: Not specified

Delta-Like Ligand 4 Modulates Liver Damage by Down-Regulating Chemokine Expression

Abstract

Not specified

Authors: Zhe Shen, Yan Liu, Bedair Dewidar, Junhao Hu, Ogyi Park, Teng Feng, Chengfu Xu, Chaohui Yu, Qi Li, Christoph Meyer, Iryna Ilkavets, Alexandra Müller, Carolin Stump-Guthier, Stefan Munker, Roman Liebe, Vincent Zimmer, Frank Lammert, Peter R. Mertens, Hai Li, Peter ten Dijke, Hellmut G. Augustin, Jun Li, Bin Gao, Matthias P. Ebert, Steven Dooley, Youming Li, Hong-Lei Weng

Date Published: 1st Jul 2016

Publication Type: Not specified

Evolving Insights on Metabolism, Autophagy, and Epigenetics in Liver Myofibroblasts.

Abstract (Expand)

Liver myofibroblasts (MFB) are crucial mediators of extracellular matrix (ECM) deposition in liver fibrosis. They arise mainly from hepatic stellate cells (HSCs) upon a process termed "activation." … To a lesser extent, and depending on the cause of liver damage, portal fibroblasts, mesothelial cells, and fibrocytes may also contribute to the MFB population. Targeting MFB to reduce liver fibrosis is currently an area of intense research. Unfortunately, a clog in the wheel of antifibrotic therapies is the fact that although MFB are known to mediate scar formation, and participate in liver inflammatory response, many of their molecular portraits are currently unknown. In this review, we discuss recent understanding of MFB in health and diseases, focusing specifically on three evolving research fields: metabolism, autophagy, and epigenetics. We have emphasized on therapeutic prospects where applicable and mentioned techniques for use in MFB studies. Subsequently, we highlighted uncharted territories in MFB research to help direct future efforts aimed at bridging gaps in current knowledge.

Authors: Z. C. Nwosu, H. Alborzinia, S. Wolfl, S. Dooley, Y. Liu

Date Published: 18th Jun 2016

Publication Type: Not specified

Transforming Growth Factor β1 (TGF-β1) Activates Hepcidin mRNA Expression in Hepatocytes

Abstract

Not specified

Authors: Simeng Chen, Teng Feng, Maja Vujić Spasić, Sandro Altamura, Katja Breitkopf-Heinlein, Jutta Altenöder, Thomas S. Weiss, Steven Dooley, Martina U. Muckenthaler

Date Published: 17th Jun 2016

Publication Type: Not specified

TGF-β1 and TGF-β2 abundance in liver diseases of mice and men

Abstract

Not specified

Authors: Anne Dropmann, Tatjana Dediulia, Katja Breitkopf-Heinlein, Hanna Korhonen, Michel Janicot, Susanne N. Weber, Maria Thomas, Albrecht Piiper, Esther Bertran, Isabel Fabregat, Kerstin Abshagen, Jochen Hess, Peter Angel, Cédric Coulouarn, Steven Dooley, Nadja M. Meindl-Beinker

Date Published: 12th Apr 2016

Publication Type: Not specified

Cholestasis-induced adaptive remodeling of interlobular bile ducts.

Abstract (Expand)

UNLABELLED: Cholestasis is a common complication in liver diseases that triggers a proliferative response of the biliary tree. Bile duct ligation (BDL) is a frequently used model of cholestasis in … rodents. To determine which changes occur in the three-dimensional (3D) architecture of the interlobular bile duct during cholestasis, we used 3D confocal imaging, surface reconstructions, and automated image quantification covering a period up to 28 days after BDL. We show a highly reproducible sequence of interlobular duct remodeling, where cholangiocyte proliferation initially causes corrugation of the luminal duct surface, leading to an approximately five-fold increase in surface area. This is analogous to the function of villi in the intestine or sulci in the brain, where an expansion of area is achieved within a restricted volume. The increase in surface area is further enhanced by duct branching, branch elongation, and loop formation through self-joining, whereby an initially relatively sparse mesh surrounding the portal vein becomes five-fold denser through elongation, corrugation, and ramification. The number of connections between the bile duct and the lobular bile canalicular network by the canals of Hering decreases proportionally to the increase in bile duct length, suggesting that no novel connections are established. The diameter of the interlobular bile duct remains constant after BDL, a response that is qualitatively distinct from that of large bile ducts, which tend to enlarge their diameters. Therefore, volume enhancement is only due to net elongation of the ducts. Because curvature and tortuosity of the bile duct are unaltered, this enlargement of the biliary tree is caused by branching and not by convolution. CONCLUSION: BDL causes adaptive remodeling that aims at optimizing the intraluminal surface area by way of corrugation and branching.

Authors: N. Vartak, A. Damle-Vartak, B. Richter, O. Dirsch, U. Dahmen, S. Hammad, J. G. Hengstler

Date Published: 27th Nov 2015

Publication Type: Not specified

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