Effects of C-reactive protein on the expression of transforming growth factor β1 and receptors on human renal tubular epithelial cells
OBJECTIVE: To explore the effect of C-reactive protein (CRP) on the expression of Fcγ receptors in human renal tubular epithelial cells and determine the role of Fcγ receptors in CRP-induced expression of transforming growth factor β1 (TGFβ1).
METHODS: Human renal tubular epithelial cells (HK-2) were cultured and stimulated with recombinant human CRP. The mRNA expression of Fcγ receptors, including FcγRI (CD64), FcγRIIa (CD32a) and FcγRIII (CD16), was detected by real-time polymerase chain reaction (PCR). On the basis of real-time PCR results, CD32a was selected for further analysis: the CD32a expression in HK-2 cells incubated with 10 mg/L CRP for 24 h was determined by flow cytometry and Western blotting. HK-2 cells were preincubated with or without anti-CD32a IgG, followed by the addition of recombinant human CRP. Subsequently the biological effects of CRP were tested. TGFβ1, type I collagen (ColI) and type IV collagen (ColIV) released into media were detected by enzyme-linked immunosorbent assay. And TGFβ1 mRNA expression was measured by real-time PCR.
RESULTS: On real-time PCR, CRP was found to significantly up-regulate the CD32a mRNA expression in HK-2 cells in a dose-dependent manner (P < 0.01). The peak up-regulation was observed at a dose of 10 mg/L. In contrast, mRNAs of CD16 and CD64 were not detected in HK-2 cells. Flow cytometry showed that CD32a expressed on HK-2 cells incubated with 10 mg/L recombinant human CRP for 24 h accounted for 23.35% ± 7.43%, significantly higher than that on non-CRP-treated cells (1.66% ± 0.28%, P < 0.01). Western blotting showed that CRP up-regulated CD32a expression in a dose-dependent manner. And 10 mg/L CRP induced the peak effect. Antibodies to CD32a inhibited the stimulatory effect of CRP on the generation of TGFβ1, ColI and ColIV (all P < 0.05) and down-regulated the expression of TGFβ1 mRNA (P < 0.01).
CONCLUSION: The stimulation of CRP can significantly increase CD32a expression in renal tubular epithelial cells and up-regulate the expression of transforming growth factor TGFβ1 through CD32a receptor.
| Medienart: |
Artikel |
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| Erscheinungsjahr: |
2012 |
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| Erschienen: |
2012 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:92 |
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| Enthalten in: |
Zhonghua yi xue za zhi - 92(2012), 18 vom: 15. Mai, Seite 1281-4 |
| Sprache: |
Chinesisch |
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| Beteiligte Personen: |
Xie, Kai-Qing [VerfasserIn] |
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| Themen: |
9007-41-4 |
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| Anmerkungen: |
Date Completed 20.03.2013 Date Revised 13.08.2012 published: Print Citation Status MEDLINE |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM220138524 |
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| LEADER | 01000naa a22002652 4500 | ||
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| 041 | |a chi | ||
| 100 | 1 | |a Xie, Kai-Qing |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Effects of C-reactive protein on the expression of transforming growth factor β1 and receptors on human renal tubular epithelial cells |
| 264 | 1 | |c 2012 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a ohne Hilfsmittel zu benutzen |b n |2 rdamedia | ||
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| 500 | |a Date Completed 20.03.2013 | ||
| 500 | |a Date Revised 13.08.2012 | ||
| 500 | |a published: Print | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a OBJECTIVE: To explore the effect of C-reactive protein (CRP) on the expression of Fcγ receptors in human renal tubular epithelial cells and determine the role of Fcγ receptors in CRP-induced expression of transforming growth factor β1 (TGFβ1) | ||
| 520 | |a METHODS: Human renal tubular epithelial cells (HK-2) were cultured and stimulated with recombinant human CRP. The mRNA expression of Fcγ receptors, including FcγRI (CD64), FcγRIIa (CD32a) and FcγRIII (CD16), was detected by real-time polymerase chain reaction (PCR). On the basis of real-time PCR results, CD32a was selected for further analysis: the CD32a expression in HK-2 cells incubated with 10 mg/L CRP for 24 h was determined by flow cytometry and Western blotting. HK-2 cells were preincubated with or without anti-CD32a IgG, followed by the addition of recombinant human CRP. Subsequently the biological effects of CRP were tested. TGFβ1, type I collagen (ColI) and type IV collagen (ColIV) released into media were detected by enzyme-linked immunosorbent assay. And TGFβ1 mRNA expression was measured by real-time PCR | ||
| 520 | |a RESULTS: On real-time PCR, CRP was found to significantly up-regulate the CD32a mRNA expression in HK-2 cells in a dose-dependent manner (P < 0.01). The peak up-regulation was observed at a dose of 10 mg/L. In contrast, mRNAs of CD16 and CD64 were not detected in HK-2 cells. Flow cytometry showed that CD32a expressed on HK-2 cells incubated with 10 mg/L recombinant human CRP for 24 h accounted for 23.35% ± 7.43%, significantly higher than that on non-CRP-treated cells (1.66% ± 0.28%, P < 0.01). Western blotting showed that CRP up-regulated CD32a expression in a dose-dependent manner. And 10 mg/L CRP induced the peak effect. Antibodies to CD32a inhibited the stimulatory effect of CRP on the generation of TGFβ1, ColI and ColIV (all P < 0.05) and down-regulated the expression of TGFβ1 mRNA (P < 0.01) | ||
| 520 | |a CONCLUSION: The stimulation of CRP can significantly increase CD32a expression in renal tubular epithelial cells and up-regulate the expression of transforming growth factor TGFβ1 through CD32a receptor | ||
| 650 | 4 | |a English Abstract | |
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Research Support, U.S. Gov't, Non-P.H.S. | |
| 650 | 7 | |a Fc gamma receptor IIA |2 NLM | |
| 650 | 7 | |a Receptors, IgG |2 NLM | |
| 650 | 7 | |a Transforming Growth Factor beta1 |2 NLM | |
| 650 | 7 | |a C-Reactive Protein |2 NLM | |
| 650 | 7 | |a 9007-41-4 |2 NLM | |
| 700 | 1 | |a Shi, Wei |e verfasserin |4 aut | |
| 700 | 1 | |a Li, Dong-Feng |e verfasserin |4 aut | |
| 700 | 1 | |a Zhang, Bin |e verfasserin |4 aut | |
| 700 | 1 | |a Liu, Shuang-Xin |e verfasserin |4 aut | |
| 700 | 1 | |a Zhou, Hong-Wei |e verfasserin |4 aut | |
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