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000127165 0247_ $$2doi$$a10.15252/emmm.201404246
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000127165 0247_ $$2ISSN$$a1757-4684
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000127165 037__ $$aDKFZ-2017-03191
000127165 041__ $$aeng
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000127165 1001_ $$0P:(DE-He78)18e5b355e4a312d2065b1ae2a9d47654$$aMogler, Carolin$$b0$$eFirst author$$udkfz
000127165 245__ $$aHepatic stellate cell-expressed endosialin balances fibrogenesis and hepatocyte proliferation during liver damage.
000127165 260__ $$aWeinheim$$bWiley-VCH$$c2015
000127165 3367_ $$2DRIVER$$aarticle
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000127165 520__ $$aLiver fibrosis is a reversible wound-healing response to injury reflecting the critical balance between liver repair and scar formation. Chronic damage leads to progressive substitution of liver parenchyma by scar tissue and ultimately results in liver cirrhosis. Stromal cells (hepatic stellate cells [HSC] and endothelial cells) have been proposed to control the balance between liver fibrosis and regeneration. Here, we show that endosialin, a C-type lectin, expressed in the liver exclusively by HSC and portal fibroblasts, is upregulated in liver fibrosis in mouse and man. Chronic chemically induced liver damage resulted in reduced fibrosis and enhanced hepatocyte proliferation in endosialin-deficient (EN(KO)) mice. Correspondingly, acute-liver-damage-induced hepatocyte proliferation (partial hepatectomy) was increased in EN(KO) mice. A candidate-based screen of known regulators of hepatocyte proliferation identified insulin-like growth factor 2 (IGF2) as selectively endosialin-dependent hepatocyte mitogen. Collectively, the study establishes a critical role of HSC in the reciprocal regulation of fibrogenesis vs. hepatocyte proliferation and identifies endosialin as a therapeutic target in non-neoplastic settings.
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000127165 650_7 $$2NLM Chemicals$$aAntigens, CD
000127165 650_7 $$2NLM Chemicals$$aAntigens, Neoplasm
000127165 650_7 $$2NLM Chemicals$$aCD248 protein, human
000127165 650_7 $$2NLM Chemicals$$aNeoplasm Proteins
000127165 650_7 $$2NLM Chemicals$$atumor endothelial marker 1, mouse
000127165 7001_ $$0P:(DE-He78)0792aae05ea250d2937cdfa6c9ca05fc$$aWieland, Matthias$$b1$$udkfz
000127165 7001_ $$0P:(DE-He78)5ef958977fa3c0658679b496419ce762$$aKönig, Courtney$$b2$$udkfz
000127165 7001_ $$aHu, Junhao$$b3
000127165 7001_ $$0P:(DE-He78)cc84101e4a6f5a7a41c9012f423dbd0f$$aRunge, Anja$$b4$$udkfz
000127165 7001_ $$0P:(DE-He78)9f5445b47d46f5f026560c307119a7da$$aKorn, Claudia$$b5$$udkfz
000127165 7001_ $$0P:(DE-He78)9be9200416a88a73cc9c25339b19b58f$$aBesemfelder, Eva$$b6$$udkfz
000127165 7001_ $$aBreitkopf-Heinlein, Katja$$b7
000127165 7001_ $$0P:(DE-He78)30816ab8532422ad8d4a8af55bc0d24b$$aKomljenovic, Dorde$$b8$$udkfz
000127165 7001_ $$aDooley, Steven$$b9
000127165 7001_ $$aSchirmacher, Peter$$b10
000127165 7001_ $$aLongerich, Thomas$$b11
000127165 7001_ $$0P:(DE-He78)2e92d0ae281932fc7347d819fec36b0b$$aAugustin, Hellmut$$b12$$eLast author$$udkfz
000127165 773__ $$0PERI:(DE-600)2485479-7$$a10.15252/emmm.201404246$$gVol. 7, no. 3, p. 332 - 338$$n3$$p332 - 338$$tEMBO molecular medicine$$v7$$x1757-4684$$y2015
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