Research ExplorerPublicationsEndothelial-Specific Deletion of CD146 Protects Against Expe...

Endothelial-Specific Deletion of CD146 Protects Against Experimental Glomerulonephritis in Mice

Standard

Endothelial-Specific Deletion of CD146 Protects Against Experimental Glomerulonephritis in Mice. / Abed, Ahmed; Leroyer, Aurélie S; Kavvadas, Panagiotis; Authier, Florence; Bachelier, Richard; Foucault-Bertaud, Alexandrine; Bardin, Nathalie; Cohen, Clemens D; Lindenmeyer, Maja T; Genest, Magali; Joshkon, Ahmad; Jourde-Chiche, Noémie; Burtey, Stéphane; Blot-Chabaud, Marcel; Dignat-George, Françoise; Chadjichristos, Christos E.

In: HYPERTENSION, Vol. 77, No. 4, 04.2021, p. 1260-1272.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Abed, A, Leroyer, AS, Kavvadas, P, Authier, F, Bachelier, R, Foucault-Bertaud, A, Bardin, N, Cohen, CD, Lindenmeyer, MT, Genest, M, Joshkon, A, Jourde-Chiche, N, Burtey, S, Blot-Chabaud, M, Dignat-George, F & Chadjichristos, CE 2021, 'Endothelial-Specific Deletion of CD146 Protects Against Experimental Glomerulonephritis in Mice', HYPERTENSION, vol. 77, no. 4, pp. 1260-1272. https://doi.org/10.1161/HYPERTENSIONAHA.119.14176

APA

Abed, A., Leroyer, A. S., Kavvadas, P., Authier, F., Bachelier, R., Foucault-Bertaud, A., Bardin, N., Cohen, C. D., Lindenmeyer, M. T., Genest, M., Joshkon, A., Jourde-Chiche, N., Burtey, S., Blot-Chabaud, M., Dignat-George, F., & Chadjichristos, C. E. (2021). Endothelial-Specific Deletion of CD146 Protects Against Experimental Glomerulonephritis in Mice. HYPERTENSION, 77(4), 1260-1272. https://doi.org/10.1161/HYPERTENSIONAHA.119.14176

Vancouver

Abed A, Leroyer AS, Kavvadas P, Authier F, Bachelier R, Foucault-Bertaud A et al. Endothelial-Specific Deletion of CD146 Protects Against Experimental Glomerulonephritis in Mice. HYPERTENSION. 2021 Apr;77(4):1260-1272. https://doi.org/10.1161/HYPERTENSIONAHA.119.14176

Bibtex

@article{57ce55178ea1442e8c1a403c26d255e1,
title = "Endothelial-Specific Deletion of CD146 Protects Against Experimental Glomerulonephritis in Mice",
abstract = "CD146 is an endothelial junctional adhesion molecule, which expression is increased in human glomerular diseases. However, the pathological significance of this overexpression remains unknown. Induction of glomerulonephritis in mice, by using nephrotoxic serum, showed that CD146 expression was highly induced within damaged glomeruli and was associated with renal inflammation and fibrosis. Interestingly, 2 weeks after glomerulonephritis induction, CD146 knockout mice showed preserved renal function as proteinuria and blood urea nitrogen levels were significantly lower compared with wild-type littermates. Furthermore, renal structure was considerably conserved, since crescents formation, tubular dilation, monocyte and lymphocyte infiltration, and interstitial renal fibrosis were highly reduced. Colocalization with markers for different types of glomerular cells showed that CD146 expression was mainly increased within the injured endothelium of the glomerular tuft. Consequently, we generated a new transgenic strain in which CD146 was specifically deleted in the vascular endothelium. Similarly to CD146 knockout, these mice showed preservation of renal structure and function after the induction of glomerulonephritis compared with wild-type animals. These data show that endothelial CD146 plays a major role in glomerulonephritis and may represent a novel therapeutic target to reduce glomerular damage and the progression of renal disease.",
keywords = "Animals, CD146 Antigen/genetics, Disease Models, Animal, Drug Discovery, Endothelial Cells/metabolism, Fibrosis/metabolism, Gene Knockout Techniques/methods, Glomerulonephritis/immunology, Inflammation/metabolism, Intercellular Junctions/immunology, Kidney Glomerulus/immunology, Mice, Up-Regulation",
author = "Ahmed Abed and Leroyer, {Aur{\'e}lie S} and Panagiotis Kavvadas and Florence Authier and Richard Bachelier and Alexandrine Foucault-Bertaud and Nathalie Bardin and Cohen, {Clemens D} and Lindenmeyer, {Maja T} and Magali Genest and Ahmad Joshkon and No{\'e}mie Jourde-Chiche and St{\'e}phane Burtey and Marcel Blot-Chabaud and Fran{\c c}oise Dignat-George and Chadjichristos, {Christos E}",
year = "2021",
month = apr,
doi = "10.1161/HYPERTENSIONAHA.119.14176",
language = "English",
volume = "77",
pages = "1260--1272",
journal = "HYPERTENSION",
issn = "0194-911X",
publisher = "Lippincott Williams and Wilkins",
number = "4",

}

RIS

TY - JOUR

T1 - Endothelial-Specific Deletion of CD146 Protects Against Experimental Glomerulonephritis in Mice

AU - Abed, Ahmed

AU - Leroyer, Aurélie S

AU - Kavvadas, Panagiotis

AU - Authier, Florence

AU - Bachelier, Richard

AU - Foucault-Bertaud, Alexandrine

AU - Bardin, Nathalie

AU - Cohen, Clemens D

AU - Lindenmeyer, Maja T

AU - Genest, Magali

AU - Joshkon, Ahmad

AU - Jourde-Chiche, Noémie

AU - Burtey, Stéphane

AU - Blot-Chabaud, Marcel

AU - Dignat-George, Françoise

AU - Chadjichristos, Christos E

PY - 2021/4

Y1 - 2021/4

N2 - CD146 is an endothelial junctional adhesion molecule, which expression is increased in human glomerular diseases. However, the pathological significance of this overexpression remains unknown. Induction of glomerulonephritis in mice, by using nephrotoxic serum, showed that CD146 expression was highly induced within damaged glomeruli and was associated with renal inflammation and fibrosis. Interestingly, 2 weeks after glomerulonephritis induction, CD146 knockout mice showed preserved renal function as proteinuria and blood urea nitrogen levels were significantly lower compared with wild-type littermates. Furthermore, renal structure was considerably conserved, since crescents formation, tubular dilation, monocyte and lymphocyte infiltration, and interstitial renal fibrosis were highly reduced. Colocalization with markers for different types of glomerular cells showed that CD146 expression was mainly increased within the injured endothelium of the glomerular tuft. Consequently, we generated a new transgenic strain in which CD146 was specifically deleted in the vascular endothelium. Similarly to CD146 knockout, these mice showed preservation of renal structure and function after the induction of glomerulonephritis compared with wild-type animals. These data show that endothelial CD146 plays a major role in glomerulonephritis and may represent a novel therapeutic target to reduce glomerular damage and the progression of renal disease.

AB - CD146 is an endothelial junctional adhesion molecule, which expression is increased in human glomerular diseases. However, the pathological significance of this overexpression remains unknown. Induction of glomerulonephritis in mice, by using nephrotoxic serum, showed that CD146 expression was highly induced within damaged glomeruli and was associated with renal inflammation and fibrosis. Interestingly, 2 weeks after glomerulonephritis induction, CD146 knockout mice showed preserved renal function as proteinuria and blood urea nitrogen levels were significantly lower compared with wild-type littermates. Furthermore, renal structure was considerably conserved, since crescents formation, tubular dilation, monocyte and lymphocyte infiltration, and interstitial renal fibrosis were highly reduced. Colocalization with markers for different types of glomerular cells showed that CD146 expression was mainly increased within the injured endothelium of the glomerular tuft. Consequently, we generated a new transgenic strain in which CD146 was specifically deleted in the vascular endothelium. Similarly to CD146 knockout, these mice showed preservation of renal structure and function after the induction of glomerulonephritis compared with wild-type animals. These data show that endothelial CD146 plays a major role in glomerulonephritis and may represent a novel therapeutic target to reduce glomerular damage and the progression of renal disease.

KW - Animals

KW - CD146 Antigen/genetics

KW - Disease Models, Animal

KW - Drug Discovery

KW - Endothelial Cells/metabolism

KW - Fibrosis/metabolism

KW - Gene Knockout Techniques/methods

KW - Glomerulonephritis/immunology

KW - Inflammation/metabolism

KW - Intercellular Junctions/immunology

KW - Kidney Glomerulus/immunology

KW - Mice

KW - Up-Regulation

U2 - 10.1161/HYPERTENSIONAHA.119.14176

DO - 10.1161/HYPERTENSIONAHA.119.14176

M3 - SCORING: Journal article

C2 - 33689459

VL - 77

SP - 1260

EP - 1272

JO - HYPERTENSION

JF - HYPERTENSION

SN - 0194-911X

IS - 4

ER -