Relationship between peroxisome proliferator-activated receptor-γ and renal ischemia-reperfusion injury
The pathogenesis of ischemia-reperfusion (I/R) injury is known to involve cytokines and, in particular, surface adhesion molecules, the expression of which initiates inflammatory cell attachment. It has been suggested that peroxisome proliferator-activated receptor (PPAR)-γ is an important immunomodulatory factor as well as a regulator of fatty acid. In this study, we investigated the expression of PPAR-γ in a renal I/R injury rat model. The right kidney was harvested and the left renal artery and vein were clamped by means of a laparotomy. The kidney was reperfused following 90 min of ischemia. Rats were sacrificed at 0, 1.5, 3, 5, 12 and 24 h after reperfusion. PPAR-γ expression was analyzed by immunohistochemical staining using monoclonal antibody. PPAR-γ staining was weak in the endothelial cells, interstitial cells and collecting ducts in the normal kidney. From 1.5 to 5 h after reperfusion, PPAR-γ staining was strong. Twelve hours after reperfusion, necrosis had extended throughout the kidney, and nearly all the tubular epithelial cells were destroyed. However, 12 h after reperfusion, PPAR-γ staining was weak in the endothelial cells and its expression was moderate in the interstitial cells and collecting ducts. PPAR-γ was induced in the endothelial cells, including the mesangial cells, interstitial cells and collecting ducts in a rat model of renal I/R injury.
| Medienart: |
Artikel |
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| Erscheinungsjahr: |
2008 |
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| Erschienen: |
2008 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:1 |
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| Enthalten in: |
Molecular medicine reports - 1(2008), 4 vom: 05. Juli, Seite 499-503 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Matsuyama, Masahide [VerfasserIn] |
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| Themen: |
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| Anmerkungen: |
Date Completed 02.10.2012 Date Revised 22.02.2013 published: Print Citation Status PubMed-not-MEDLINE |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM207344868 |
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| 100 | 1 | |a Matsuyama, Masahide |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Relationship between peroxisome proliferator-activated receptor-γ and renal ischemia-reperfusion injury |
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| 500 | |a Date Revised 22.02.2013 | ||
| 500 | |a published: Print | ||
| 500 | |a Citation Status PubMed-not-MEDLINE | ||
| 520 | |a The pathogenesis of ischemia-reperfusion (I/R) injury is known to involve cytokines and, in particular, surface adhesion molecules, the expression of which initiates inflammatory cell attachment. It has been suggested that peroxisome proliferator-activated receptor (PPAR)-γ is an important immunomodulatory factor as well as a regulator of fatty acid. In this study, we investigated the expression of PPAR-γ in a renal I/R injury rat model. The right kidney was harvested and the left renal artery and vein were clamped by means of a laparotomy. The kidney was reperfused following 90 min of ischemia. Rats were sacrificed at 0, 1.5, 3, 5, 12 and 24 h after reperfusion. PPAR-γ expression was analyzed by immunohistochemical staining using monoclonal antibody. PPAR-γ staining was weak in the endothelial cells, interstitial cells and collecting ducts in the normal kidney. From 1.5 to 5 h after reperfusion, PPAR-γ staining was strong. Twelve hours after reperfusion, necrosis had extended throughout the kidney, and nearly all the tubular epithelial cells were destroyed. However, 12 h after reperfusion, PPAR-γ staining was weak in the endothelial cells and its expression was moderate in the interstitial cells and collecting ducts. PPAR-γ was induced in the endothelial cells, including the mesangial cells, interstitial cells and collecting ducts in a rat model of renal I/R injury | ||
| 650 | 4 | |a Journal Article | |
| 700 | 1 | |a Yoshimura, Rikio |e verfasserin |4 aut | |
| 700 | 1 | |a Kawahito, Yutaka |e verfasserin |4 aut | |
| 700 | 1 | |a Sano, Hajime |e verfasserin |4 aut | |
| 700 | 1 | |a Chargui, Jamel |e verfasserin |4 aut | |
| 700 | 1 | |a Touraine, Jean-Louis |e verfasserin |4 aut | |
| 700 | 1 | |a Nakatani, Tatsuya |e verfasserin |4 aut | |
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