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10.1172/JCI90086 http://scihub22266oqcxt.onion/10.1172/JCI90086 C5330741!5330741 !28218627     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28218627 &cmd=llinks): Failed to open stream: HTTP request failed! 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GATA4-dependent organ-specific endothelial differentiation controls liver development and embryonic hematopoiesis |pdf=|usr=}}{{28218627 }} gab.com Text GATA4-dependent organ-specific endothelial differentiation controls liver development and embryonic hematopoiesis JO: J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=28218627 #FOAvip Microvascular endothelial cells (ECs) are increasingly recognized as organ-specific gatekeepers of their microenvironment. Microvascular ECs instruct neighboring cells in their organ-specific vascular niches through angiocrine factors, which include secreted growth factors (angiokines), extracellular matrix molecules, and transmembrane proteins. However, the molecular regulators that drive organ-specific microvascular transcriptional programs and thereby regulate angiodiversity are largely elusive. In contrast to other ECs, which form a continuous cell layer, liver sinusoidal ECs (LSECs) constitute discontinuous, permeable microvessels. Here, we have shown that the transcription factor GATA4 controls murine LSEC specification and function. LSEC-restricted deletion of Gata4 caused transformation of discontinuous liver sinusoids into continuous capillaries. Capillarization was characterized by ectopic basement membrane deposition, formation of a continuous EC layer, and increased expression of VE-cadherin. Correspondingly, ectopic expression of GATA4 in cultured continuous ECs mediated the downregulation of continuous EC-associated transcripts and upregulation of LSEC-associated genes. The switch from discontinuous LSECs to continuous ECs during embryogenesis caused liver hypoplasia, fibrosis, and impaired colonization by hematopoietic progenitor cells, resulting in anemia and embryonic lethality. Thus, GATA4 acts as master regulator of hepatic microvascular specification and acquisition of organ-specific vascular competence, which are indispensable for liver development. The data also establish an essential role of the hepatic microvasculature in embryonic hematopoiesis. Twit Text FOAVip GATA4-dependent organ-specific endothelial differentiation controls liver development and embryonic hematopoiesis ????J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=28218627 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28218627 #FOAvip English Wikipedia <ref>{{Cite pmid|28218627 }}</ref> GATA4-dependent organ-specific endothelial differentiation controls liver development and embryonic hematopoiesis #MMPMID28218627 Géraud C ; Koch PS ; Zierow J ; Klapproth K ; Busch K ; Olsavszky V ; Leibing T ; Demory A ; Ulbrich F ; Diett M ; Singh S ; Sticht C ; Breitkopf-Heinlein K ; Richter K ; Karppinen SM ; Pihlajaniemi T ; Arnold B ; Rodewald HR ; Augustin HG ; Schledzewski K ; Goerdt S J Clin Invest 2017[Mar]; 127 (3 ): 1099-1114 PMID28218627 show ga Microvascular endothelial cells (ECs) are increasingly recognized as organ-specific gatekeepers of their microenvironment. Microvascular ECs instruct neighboring cells in their organ-specific vascular niches through angiocrine factors, which include secreted growth factors (angiokines), extracellular matrix molecules, and transmembrane proteins. However, the molecular regulators that drive organ-specific microvascular transcriptional programs and thereby regulate angiodiversity are largely elusive. In contrast to other ECs, which form a continuous cell layer, liver sinusoidal ECs (LSECs) constitute discontinuous, permeable microvessels. Here, we have shown that the transcription factor GATA4 controls murine LSEC specification and function. LSEC-restricted deletion of Gata4 caused transformation of discontinuous liver sinusoids into continuous capillaries. Capillarization was characterized by ectopic basement membrane deposition, formation of a continuous EC layer, and increased expression of VE-cadherin. Correspondingly, ectopic expression of GATA4 in cultured continuous ECs mediated the downregulation of continuous EC-associated transcripts and upregulation of LSEC-associated genes. The switch from discontinuous LSECs to continuous ECs during embryogenesis caused liver hypoplasia, fibrosis, and impaired colonization by hematopoietic progenitor cells, resulting in anemia and embryonic lethality. Thus, GATA4 acts as master regulator of hepatic microvascular specification and acquisition of organ-specific vascular competence, which are indispensable for liver development. The data also establish an essential role of the hepatic microvasculature in embryonic hematopoiesis. |Animals [MESH] |Capillaries/embryology [MESH] |Cell Differentiation/*physiology [MESH] |Embryo, Mammalian/*enzymology [MESH] |Endothelial Cells/*metabolism [MESH] |Endothelium/*embryology [MESH] |GATA4 Transcription Factor/genetics/*metabolism [MESH] |Hematopoiesis/*physiology [MESH] |Liver/blood supply/*embryology [MESH] |Mice [MESH] |Mice, Transgenic [MESH]GATA4-dependent organ-specific endothelial differentiation controls li(epmc).pdf DeepDyve Pubget Overpricing