{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T18:11:11Z","timestamp":1790791871269,"version":"4.1.0"},"reference-count":49,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"4","license":[{"start":{"date-parts":[[2019,5,31]],"date-time":"2019-05-31T00:00:00Z","timestamp":1559260800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2019,5,31]],"date-time":"2019-05-31T00:00:00Z","timestamp":1559260800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["Hepatology"],"published-print":{"date-parts":[[2019,10]]},"abstract":"<jats:p>\n                    Bone morphogenetic protein 9 (BMP9) is a circulating factor produced by hepatic stellate cells that plays a critical role in vascular quiescence through its endothelial receptor activin receptor\u2010like kinase 1 (ALK1). Mutations in the gene encoding ALK1 cause hereditary hemorrhagic telangiectasia type 2, a rare genetic disease presenting hepatic vessel malformations. Variations of both the circulating levels and the hepatic mRNA levels of BMP9 have been recently associated with various forms of hepatic fibrosis. However, the molecular mechanism that links BMP9 with liver diseases is still unknown. Here, we report that\n                    <jats:italic toggle=\"yes\">Bmp9<\/jats:italic>\n                    gene deletion in 129\/Ola mice triggers hepatic perisinusoidal fibrosis that was detectable from 15\u00a0weeks of age. An inflammatory response appeared within the same time frame as fibrosis, whereas sinusoidal vessel dilation developed later on. Proteomic and mRNA analyses of primary liver sinusoidal endothelial cells (LSECs) both revealed that the expression of the LSEC\u2010specifying transcription factor GATA\u2010binding protein 4 was strongly reduced in\n                    <jats:italic toggle=\"yes\">Bmp9<\/jats:italic>\n                    gene knockout (\n                    <jats:italic toggle=\"yes\">Bmp9<\/jats:italic>\n                    \u2010KO) mice as compared with wild\u2010type mice. LSECs from\n                    <jats:italic toggle=\"yes\">Bmp9<\/jats:italic>\n                    \u2010KO mice also lost the expression of several terminal differentiation markers (\n                    <jats:italic toggle=\"yes\">Lyve1<\/jats:italic>\n                    , S\n                    <jats:italic toggle=\"yes\">tab1<\/jats:italic>\n                    ,\n                    <jats:italic toggle=\"yes\">Stab2<\/jats:italic>\n                    ,\n                    <jats:italic toggle=\"yes\">Ehd3<\/jats:italic>\n                    ,\n                    <jats:italic toggle=\"yes\">Cd209b<\/jats:italic>\n                    ,\n                    <jats:italic toggle=\"yes\">eNos, Maf<\/jats:italic>\n                    ,\n                    <jats:italic toggle=\"yes\">Plvap<\/jats:italic>\n                    ). They gained CD34 expression and deposited a basal lamina, indicating that they were capillarized. Another main characteristic of differentiated LSECs is the presence of permeable fenestrae. LSECs from\n                    <jats:italic toggle=\"yes\">Bmp9<\/jats:italic>\n                    \u2010KO mice had a significantly reduced number of fenestrae. This was already observable in 2\u2010week\u2010old pups. Moreover, we could show that addition of BMP9 to primary cultures of LSECs prevented the loss of their fenestrae and maintained the expression levels of\n                    <jats:italic toggle=\"yes\">Gata4<\/jats:italic>\n                    and\n                    <jats:italic toggle=\"yes\">Plvap<\/jats:italic>\n                    .\n                    <jats:italic toggle=\"yes\">Conclusion:<\/jats:italic>\n                    Taken together, our observations show that BMP9 is a key paracrine regulator of liver homeostasis, controlling LSEC fenestration and protecting against perivascular hepatic fibrosis.\n                  <\/jats:p>","DOI":"10.1002\/hep.30655","type":"journal-article","created":{"date-parts":[[2019,4,9]],"date-time":"2019-04-09T08:22:56Z","timestamp":1554798176000},"page":"1392-1408","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":130,"title":["Bone Morphogenetic Protein 9 Is a Paracrine Factor Controlling Liver Sinusoidal Endothelial Cell Fenestration and Protecting Against Hepatic Fibrosis"],"prefix":"10.1097","volume":"70","author":[{"given":"Agn\u00e8s","family":"Desroches\u2010Castan","sequence":"first","affiliation":[{"name":"BCI Laboratory,Universit\u00e9 Grenoble Alpes, Inserm, CEA,Grenoble,France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Emmanuelle","family":"Tillet","sequence":"additional","affiliation":[{"name":"BCI Laboratory,Universit\u00e9 Grenoble Alpes, Inserm, CEA,Grenoble,France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicolas","family":"Ricard","sequence":"additional","affiliation":[{"name":"BCI Laboratory,Universit\u00e9 Grenoble Alpes, Inserm, CEA,Grenoble,France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marie","family":"Ouarn\u00e9","sequence":"additional","affiliation":[{"name":"BCI Laboratory,Universit\u00e9 Grenoble Alpes, Inserm, CEA,Grenoble,France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christine","family":"Mallet","sequence":"additional","affiliation":[{"name":"BCI Laboratory,Universit\u00e9 Grenoble Alpes, Inserm, CEA,Grenoble,France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lucid","family":"Belmudes","sequence":"additional","affiliation":[{"name":"BGE Laboratory,Universit\u00e9 Grenoble Alpes, CEA, Inserm,Grenoble,France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yohann","family":"Cout\u00e9","sequence":"additional","affiliation":[{"name":"BGE Laboratory,Universit\u00e9 Grenoble Alpes, CEA, Inserm,Grenoble,France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Olivier","family":"Boillot","sequence":"additional","affiliation":[{"name":"Liver Transplant Unit,Edouard Herriot Hospital, Hospices Civils de Lyon,Lyon,France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jean\u2010Yves","family":"Scoazec","sequence":"additional","affiliation":[{"name":"Department of Pathology,Gustave Roussy Cancer Campus,Villejuif,France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sabine","family":"Bailly","sequence":"additional","affiliation":[{"name":"BCI Laboratory,Universit\u00e9 Grenoble Alpes, Inserm, CEA,Grenoble,France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1354-7692","authenticated-orcid":false,"given":"Jean\u2010Jacques","family":"Feige","sequence":"additional","affiliation":[{"name":"BCI Laboratory,Universit\u00e9 Grenoble Alpes, Inserm, CEA,Grenoble,France"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","published-online":{"date-parts":[[2019,5,31]]},"reference":[{"key":"hep30655-bib-0001-20241017","doi-asserted-by":"crossref","first-page":"a021899","DOI":"10.1101\/cshperspect.a021899","article-title":"Bone morphogenetic proteins","volume":"8","year":"2016","journal-title":"Cold Spring Harb Perspect Biol"},{"key":"hep30655-bib-0002-20241017","doi-asserted-by":"crossref","first-page":"203","DOI":"10.1016\/j.cytogfr.2009.05.001","article-title":"Emerging role of bone morphogenetic proteins in angiogenesis","volume":"20","year":"2009","journal-title":"Cytokine Growth Factor Rev"},{"key":"hep30655-bib-0003-20241017","doi-asserted-by":"crossref","first-page":"65","DOI":"10.1016\/j.cytogfr.2015.12.005","article-title":"BMP signaling in vascular biology and dysfunction","volume":"27","year":"2016","journal-title":"Cytokine Growth Factor 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