Growth Differentiation Factor 15 Ameliorates Anti-Glomerular Basement Membrane Glomerulonephritis in Mice

Autor: Maciej Lech, Clemens D. Cohen, Andrea Ribeiro, Stefanie Steiger, Ekaterina von Rauchhaupt, Georg Lorenz, Christoph Schmaderer, Hans-Joachim Anders, Maja T. Lindenmeyer, Foteini Moschovaki-Filippidou
Rok vydání: 2020
Předmět:
0301 basic medicine
inflammation
T cells
glomerulonephritis
innate immunity
chemokines
T-Lymphocytes
medicine.medical_treatment
030232 urology & nephrology
CXCR3
Glomerulonephritis
Membranous
lcsh:Chemistry
Mice
0302 clinical medicine
Cell Movement
Glomerular Basement Membrane
lcsh:QH301-705.5
Spectroscopy
Mice
Knockout
Chemistry
Glomerular basement membrane
Glomerulonephritis
General Medicine
ddc
Computer Science Applications
Proteinuria
medicine.anatomical_structure
Cytokine
Nephritis
Growth Differentiation Factor 15
Receptors
CXCR3
Article
Catalysis
Inorganic Chemistry
03 medical and health sciences
medicine
Animals
Physical and Theoretical Chemistry
Molecular Biology
Basement membrane
Organic Chemistry
medicine.disease
Chemokine CXCL10
030104 developmental biology
lcsh:Biology (General)
lcsh:QD1-999
Cancer research
GDF15
Transforming growth factor
Zdroj: International Journal of Molecular Sciences
Volume 21
Issue 19
International Journal of Molecular Sciences, Vol 21, Iss 6978, p 6978 (2020)
ISSN: 1422-0067
DOI: 10.3390/ijms21196978
Popis: Growth differentiation factor 15 (GDF15) is a member of the transforming growth factor-&beta
(TGF-&beta
) cytokine family and an inflammation-associated protein. Here, we investigated the role of GDF15 in murine anti-glomerular basement membrane (GBM) glomerulonephritis. Glomerulonephritis induction in mice induced systemic expression of GDF15. Moreover, we demonstrate the protective effects for GDF15, as GDF15-deficient mice exhibited increased proteinuria with an aggravated crescent formation and mesangial expansion in anti-GBM nephritis. Herein, GDF15 was required for the regulation of T-cell chemotactic chemokines in the kidney. In addition, we found the upregulation of the CXCR3 receptor in activated T-cells in GDF15-deficient mice. These data indicate that CXCL10/CXCR3-dependent-signaling promotes the infiltration of T cells into the organ during acute inflammation controlled by GDF15. Together, these results reveal a novel mechanism limiting the migration of lymphocytes to the site of inflammation during glomerulonephritis.
Databáze: OpenAIRE
Externí odkaz:
Nepřihlášeným uživatelům se plný text nezobrazuje