Growth Differentiation Factor 15 Ameliorates Anti-Glomerular Basement Membrane Glomerulonephritis in Mice
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Growth Differentiation Factor 15 Ameliorates Anti-Glomerular Basement Membrane Glomerulonephritis in Mice. / Moschovaki-Filippidou, Foteini; Steiger, Stefanie; Lorenz, Georg; Schmaderer, Christoph; Ribeiro, Andrea; von Rauchhaupt, Ekaterina; Cohen, Clemens D; Anders, Hans-Joachim; Lindenmeyer, Maja; Lech, Maciej.
In: INT J MOL SCI, Vol. 21, No. 19, 23.09.2020.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Growth Differentiation Factor 15 Ameliorates Anti-Glomerular Basement Membrane Glomerulonephritis in Mice
AU - Moschovaki-Filippidou, Foteini
AU - Steiger, Stefanie
AU - Lorenz, Georg
AU - Schmaderer, Christoph
AU - Ribeiro, Andrea
AU - von Rauchhaupt, Ekaterina
AU - Cohen, Clemens D
AU - Anders, Hans-Joachim
AU - Lindenmeyer, Maja
AU - Lech, Maciej
PY - 2020/9/23
Y1 - 2020/9/23
N2 - Growth differentiation factor 15 (GDF15) is a member of the transforming growth factor-β (TGF-β) 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.
AB - Growth differentiation factor 15 (GDF15) is a member of the transforming growth factor-β (TGF-β) 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.
U2 - 10.3390/ijms21196978
DO - 10.3390/ijms21196978
M3 - SCORING: Journal article
C2 - 32977372
VL - 21
JO - INT J MOL SCI
JF - INT J MOL SCI
SN - 1661-6596
IS - 19
ER -