Expression of the anti‐inflammatory protein Annexin A1 in the renal interstitium during the time course of acute Thy1 nephritis
Aim of the present study was to identify Annexin A1 (ANXA1) expressing renal interstitial cells under control conditions and during the course of acute Thy1 nephritis. ANXA1 immunoreactive interstitial cells were characterized by double labelling immunofluorescence using antibodies against ANXA1 and...
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Published in: | The FASEB journal Vol. 25; no. S1; p. 1030.3 |
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Main Authors: | , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Federation of American Societies for Experimental Biology
01-04-2011
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Online Access: | Get full text |
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Summary: | Aim of the present study was to identify Annexin A1 (ANXA1) expressing renal interstitial cells under control conditions and during the course of acute Thy1 nephritis. ANXA1 immunoreactive interstitial cells were characterized by double labelling immunofluorescence using antibodies against ANXA1 and rat endothelial cell antigen for endothelial cells, 5′ecto‐nucleotidase for interstitial fibroblasts, Major Histocompatibility Complex II for dendritic cells and CD68 for macrophages. In addition, ANXA1 expression of CD68 positive macrophages was studied during the time course of acute Thy1 nephritis (control, 24h, 5d, 15d). In control rats ANXA1 was detected in all interstitial fibroblasts, and in a subset of macrophages and endothelial cells. Dendritic cells were negative. Thy1 nephritis caused a transient glomerular infiltration of CD68 positive/ANXA1 negative macrophages with peak levels at 24h (610 +/− 126% of controls) and lower levels at the later time points (5d: 395 +/− 26% and 15d: 282 +/− 29% of control; p < .05 for each time point). The number of ANXA1 immunoreactive interstitial macrophages increased to 140 +/− 6% and to 175 +/− 21% of controls on d5 and d15 (p < .05). We have thus shown that ANXA1 is produced by numerous renal interstitial cell types of healthy rats and that infiltrating macrophages may be an important source of renal ANXA1 during the resolution phase of renal inflammatory disease.
Work was supported by the German Research Foundation (FOR 667). |
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ISSN: | 0892-6638 1530-6860 |
DOI: | 10.1096/fasebj.25.1_supplement.1030.3 |