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Article

Differential Consequences of Bmp9 Deletion on Sinusoidal Endothelial Cell Differentiation and Liver Fibrosis in 129/Ola and C57BL/6 Mice

Biology of Cancer and Infection Laboratory, University Grenoble Alpes, Inserm, CEA, F-38000 Grenoble, France
*
Author to whom correspondence should be addressed.
Present address: Yale Cardiovascular Research Center, Yale University School of Medicine, New Haven, CT 06511, USA.
Present address: Instituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa,1649-028 Lisbon, Portugal.
Cells 2019, 8(9), 1079; https://doi.org/10.3390/cells8091079
Received: 29 July 2019 / Revised: 6 September 2019 / Accepted: 10 September 2019 / Published: 13 September 2019
(This article belongs to the Special Issue TGF-beta/BMP Signaling Pathway)
The aim of the present work was to address the role of BMP9 in different genetic backgrounds (C57BL/6, BALB/c, and 129/Ola) of mice deleted for Bmp9. We found that Bmp9 deletion led to premature mortality only in the 129/Ola strain. We have previously shown that Bmp9 deletion led to liver sinusoidal endothelial cells (LSEC) capillarization and liver fibrosis in the 129/Ola background. Here, we showed that this is not the case in the C57BL/6 background. Analysis of LSEC from Wild-type (WT) versus Bmp9-KO mice in the C57BL/6 background showed no difference in LSEC fenestration and in the expression of differentiation markers. Comparison of the mRNA expression of LSEC differentiation markers between WT C57BL/6 and 129/Ola mice showed a significant decrease in Stabilin2, Plvap, and CD209b, suggesting a more capillary-like phenotype in WT C57BL/6 LSECs. C57BL/6 mice also had lower BMP9 circulating concentrations and hepatic Vegfr2 mRNA levels, compared to the 129/Ola mice. Taken together, our observations support a role for BMP9 in liver endothelial cell fenestration and prevention of fibrosis that is dependent on genetic background. It also suggests that 129/Ola mice are a more suitable model than C57BL/6 for the study of liver fibrosis subsequent to LSEC capillarization. View Full-Text
Keywords: BMP9; genetic background; liver; fibrosis; capillarization; liver sinusoidal endothelial cells; HHT; mouse; fenestrae; plvap BMP9; genetic background; liver; fibrosis; capillarization; liver sinusoidal endothelial cells; HHT; mouse; fenestrae; plvap
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MDPI and ACS Style

Desroches-Castan, A.; Tillet, E.; Ricard, N.; Ouarné, M.; Mallet, C.; Feige, J.-J.; Bailly, S. Differential Consequences of Bmp9 Deletion on Sinusoidal Endothelial Cell Differentiation and Liver Fibrosis in 129/Ola and C57BL/6 Mice. Cells 2019, 8, 1079. https://doi.org/10.3390/cells8091079

AMA Style

Desroches-Castan A, Tillet E, Ricard N, Ouarné M, Mallet C, Feige J-J, Bailly S. Differential Consequences of Bmp9 Deletion on Sinusoidal Endothelial Cell Differentiation and Liver Fibrosis in 129/Ola and C57BL/6 Mice. Cells. 2019; 8(9):1079. https://doi.org/10.3390/cells8091079

Chicago/Turabian Style

Desroches-Castan, Agnès, Emmanuelle Tillet, Nicolas Ricard, Marie Ouarné, Christine Mallet, Jean-Jacques Feige, and Sabine Bailly. 2019. "Differential Consequences of Bmp9 Deletion on Sinusoidal Endothelial Cell Differentiation and Liver Fibrosis in 129/Ola and C57BL/6 Mice" Cells 8, no. 9: 1079. https://doi.org/10.3390/cells8091079

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