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2018 ; 7
(2
): ä Nephropedia Template TP
gab.com Text
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CERA Attenuates Kidney Fibrogenesis in the db/db Mouse by Influencing the Renal
Myofibroblast Generation
#MMPMID29385703
Fischer C
; Deininger N
; Wolf G
; Loeffler I
J Clin Med
2018[Jan]; 7
(2
): ä PMID29385703
show ga
Tubulointerstitial fibrosis (TIF) is a pivotal pathophysiological process in
patients with diabetic nephropathy (DN). Multiple profibrotic factors and cell
types, including transforming growth factor beta 1 (TGF-?1) and interstitial
myofibroblasts, respectively, are responsible for the accumulation of
extracellular matrix in the kidney. Matrix-producing myofibroblasts can originate
from different sources and different mechanisms are involved in the activation
process of the myofibroblasts in the fibrotic kidney. In this study, 16-week-old
db/db mice, a model for type 2 DN, were treated for two weeks with continuous
erythropoietin receptor activator (CERA), a synthetic erythropoietin variant with
possible non-hematopoietic, tissue-protective effects. Non-diabetic and diabetic
mice treated with placebo were used as controls. The effects of CERA on
tubulointerstitial fibrosis (TIF) as well as on the generation of the
matrix-producing myofibroblasts were evaluated by morphological,
immunohistochemical, and molecular biological methods. The placebo-treated
diabetic mice showed significant signs of beginning renal TIF (shown by
picrosirius red staining; increased connective tissue growth factor (CTGF),
fibronectin and collagen I deposition; upregulated KIM1 expression) together with
an increased number of interstitial myofibroblasts (shown by different
mesenchymal markers), while kidneys from diabetic mice treated with CERA revealed
less TIF and fewer myofibroblasts. The mechanisms, in which CERA acts as an
anti-fibrotic agent/drug, seem to be multifaceted: first, CERA inhibits the
generation of matrix-producing myofibroblasts and second, CERA increases the
ability for tissue repair. Many of these CERA effects can be explained by the
finding that CERA inhibits the renal expression of the cytokine TGF-?1.
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