Potential role of fractalkine receptor expression in human renal fibrogenesis
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Potential role of fractalkine receptor expression in human renal fibrogenesis. / Koziolek, M J; Schmid, H; Cohen, C D; Blaschke, S; Hemmerlein, B; Zapf, A; Müller, G A; Strutz, F.
in: KIDNEY INT, Jahrgang 72, Nr. 5, 09.2007, S. 599-607.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Potential role of fractalkine receptor expression in human renal fibrogenesis
AU - Koziolek, M J
AU - Schmid, H
AU - Cohen, C D
AU - Blaschke, S
AU - Hemmerlein, B
AU - Zapf, A
AU - Müller, G A
AU - Strutz, F
PY - 2007/9
Y1 - 2007/9
N2 - The inhibition of several chemokine/chemokine receptors has been shown to reduce progressive renal interstitial fibrosis. In this study, we examined the expression of the CX(3)C receptor in human renal biopsies with interstitial fibrosis and from normal kidneys by real-time polymerase chain reaction (PCR) and immunohistochemistry. The CX(3)C receptor was not only detected in mononuclear, tubular epithelial, and dendritic cells but also in alpha-smooth muscle actin and vimentin-positive interstitial myofibroblasts in fibrotic kidneys. Real-time PCR indicated a significant upregulation of CX(3)C receptor mRNA in fibrotic kidneys compared with non-fibrotic nephropathies or donor biopsies. In renal fibroblasts in vitro, hydrogen peroxide increased the expression of the CX(3)C receptor, an increase that was inhibited by N-acetylcysteine and catalase. However, neither proinflammatory nor profibrotic cytokines resulted in this upregulation. Stimulation of fibroblasts by CX(3)C ligand led to a significant enhancement of migration, which was abrogated by pre-incubation with a blocking anti-CX(3)C receptor antibody. Our studies indicate that renal fibrosis is associated with the expression of CX(3)C receptors on human renal fibroblasts. The expression is induced by reactive oxygen species suggesting a role of oxidative stress.
AB - The inhibition of several chemokine/chemokine receptors has been shown to reduce progressive renal interstitial fibrosis. In this study, we examined the expression of the CX(3)C receptor in human renal biopsies with interstitial fibrosis and from normal kidneys by real-time polymerase chain reaction (PCR) and immunohistochemistry. The CX(3)C receptor was not only detected in mononuclear, tubular epithelial, and dendritic cells but also in alpha-smooth muscle actin and vimentin-positive interstitial myofibroblasts in fibrotic kidneys. Real-time PCR indicated a significant upregulation of CX(3)C receptor mRNA in fibrotic kidneys compared with non-fibrotic nephropathies or donor biopsies. In renal fibroblasts in vitro, hydrogen peroxide increased the expression of the CX(3)C receptor, an increase that was inhibited by N-acetylcysteine and catalase. However, neither proinflammatory nor profibrotic cytokines resulted in this upregulation. Stimulation of fibroblasts by CX(3)C ligand led to a significant enhancement of migration, which was abrogated by pre-incubation with a blocking anti-CX(3)C receptor antibody. Our studies indicate that renal fibrosis is associated with the expression of CX(3)C receptors on human renal fibroblasts. The expression is induced by reactive oxygen species suggesting a role of oxidative stress.
KW - CX3C Chemokine Receptor 1
KW - Fibroblasts
KW - Fibrosis
KW - Gene Expression
KW - Humans
KW - Immunohistochemistry
KW - Kidney Diseases
KW - Polymerase Chain Reaction
KW - Reactive Oxygen Species
KW - Receptors, Cytokine
KW - Receptors, HIV
KW - Tissue Distribution
KW - Up-Regulation
KW - Journal Article
KW - Research Support, Non-U.S. Gov't
U2 - 10.1038/sj.ki.5002368
DO - 10.1038/sj.ki.5002368
M3 - SCORING: Journal article
C2 - 17579663
VL - 72
SP - 599
EP - 607
JO - KIDNEY INT
JF - KIDNEY INT
SN - 0085-2538
IS - 5
ER -
