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[The effect or rosiglitazone on signal pathways of transforming growth factor-beta1 in human lung fibroblast]
Jun-Qing Shi1, Min Xie, You-Juan Wang
1Department of Respiratory, West China Hospital, Sichuan University, Chengdu 610041, China.
Objective:
To investigate the expression of CTGF, CTGF mRNA, NF-kappaB and AP-1 induced by TGF-beta1 in human lung fibroblast (HLF-02), and study the effect and possible mechanism of rosiglitazone on signal pathways of TGF-beta1 in HLF-02.
Methods:
The effects of TGF-beta1, curcumin, PDTC and rosiglitazone on the expression of CTGF, NF-kappaB and AP-1 were evaluated with Western blot. The expression of CTGF was also detected with immunohistochemistry assay. The level of CTGF mRNA was detected with RT-PCR.
Results:
(1) The CTGF protein levels of HLF-02 cells were significantly up-regulated after incubated with 1 ng/mL TGF-beta1 for 15 min (P<0.01 vs Control). The CTGF mRNA was also up-regulated. The levels of CTGF protein and CTGF mRNA expression was up-regulated by TGF-beta1 in a time-dependent manner. (2) The expression of NF-kappaB and AP-1 increased after HLF-02 cells were incubated with 1 ng/mL TGF-beta1 for 30 min (P<0.01 vs Control). The CTGF protein levels were inhibited obviously after HLF-02 cells were incubated with PDTC or curcumin. (3) The expression of CTGF, NF-kappaB and AP-1 decreased after pre-incubation with different doses of rosiglitazone (P<0.01 vs TGF-beta1 group). The CTGF mRNA were also markedly inhibited (P<0.01 vs TGF-beta1 group).
Conclusion:
It is supposed that rosiglitazone inhibits CTGF expression induced by TGF-beta1 in HLF-02 cells by activating PPARgamma through NF-kappaB and AP-1 signal transduction pathways.
Insights
Rosiglitazone inhibits connective tissue growth factor (CTGF) expression in human lung fibroblasts stimulated by TGF-beta1. This occurs via the NF-kappaB and AP-1 signaling pathways, suggesting a therapeutic mechanism.
Area of Science:
- Molecular Biology
- Cell Biology
- Pharmacology
Background:
- Transforming growth factor-beta1 (TGF-beta1) is implicated in fibrotic diseases.
- Connective tissue growth factor (CTGF) plays a key role in TGF-beta1-induced fibrosis.
- Understanding the signaling pathways involved is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate TGF-beta1-induced expression of CTGF, CTGF mRNA, NF-kappaB, and AP-1 in human lung fibroblasts (HLF-02).
- To determine the effect and mechanism of rosiglitazone on TGF-beta1 signaling pathways in HLF-02 cells.
Main Methods:
- Western blot analysis was used to assess protein expression of CTGF, NF-kappaB, and AP-1.
- Immunohistochemistry was employed to detect CTGF protein levels.
- Reverse transcription-polymerase chain reaction (RT-PCR) quantified CTGF mRNA expression.
Main Results:
- TGF-beta1 significantly up-regulated CTGF protein and mRNA expression in HLF-02 cells in a time-dependent manner.
- TGF-beta1 also increased the expression of NF-kappaB and AP-1.
- Rosiglitazone pre-treatment markedly inhibited TGF-beta1-induced CTGF, CTGF mRNA, NF-kappaB, and AP-1 expression.
Conclusions:
- Rosiglitazone inhibits TGF-beta1-induced CTGF expression in human lung fibroblasts.
- The mechanism involves the modulation of NF-kappaB and AP-1 signal transduction pathways.
- Activation of PPARgamma by rosiglitazone is suggested to mediate these inhibitory effects.
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