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PPARγ-mediated advanced glycation end products regulate neural stem cell proliferation but not neural differentiation
Shao-hua Wang1, Yi-jing Guo, Yang Yuan
1The Department of Endocrinology, Affiliated ZhongDa Hospital of Southeast University, No. 87 DingJiaQiao Road, Nanjing 210009, PR China. gyjwsh@yahoo.cn
Aims:
To investigate the roles of PPARγ in advanced glycation end product (AGE)-mediated characteristics of neural stem cells (NSCs) and the molecular mechanisms of action.
Methods:
We prepared pLentiLox3.7 lentiviral vectors expressing short hairpin RNA (shRNA) against PPARγ and transduced NSCs. MTT absorbance and cell counts were used to assay cell growth, and cell differentiation was analysed by confocal laser-scanning and western blots for the expression of MAP2/nestin. The protein and gene expression of the BDNF-CREB pathway components were examined by western blotting and real-time PCR.
Results:
Immunoblot analysis indicated that shRNA delivered by lentiviral vectors silenced PPARγ expression in NSCs. The proliferation of NSCs and expression of BDNF pathway components dropped in AGE-BSA culture medium (400 mg/L and 200 mg/L) on Day 3 and Day 7, respectively (all P<0.001). PPARγ-silenced NSCs exhibited a significant increase in cell growth and expression of BDNF pathway components compared with NSCs incubated with AGE-BSA (all P<0.001). Immunocytochemistry and western blotting analysis showed that AGE-BSA (400 mg/L) induced a significant decrease in the expression of MAP2 both in NSCs and PPARγ-silenced NSCs, as standardised by nestin. There was no significant difference between NSCs and PPARγ-silenced NSCs in the presence of AGE-BSA.
Conclusions:
PPARγ plays roles in the AGE-mediated regulation of NSC proliferation but not neural differentiation through the BDNF-CREB pathway.
Insights
Peroxisome proliferator-activated receptor gamma (PPARγ) influences neural stem cell (NSC) proliferation under advanced glycation end product (AGE) conditions. PPARγ silencing impacts NSC growth and the BDNF-CREB pathway but not neural differentiation.
Area of Science:
- Neuroscience
- Cell Biology
- Molecular Biology
Background:
- Advanced glycation end products (AGEs) are implicated in cellular dysfunction.
- Neural stem cells (NSCs) are crucial for brain development and repair.
- The role of PPARγ in AGE-mediated effects on NSCs requires elucidation.
Purpose of the Study:
- To investigate the function of PPARγ in AGE-induced alterations of NSC characteristics.
- To explore the underlying molecular mechanisms involving the BDNF-CREB pathway.
Main Methods:
- Lentiviral vectors expressing shRNA were used to silence PPARγ in NSCs.
- Cell proliferation was assessed using MTT assays and cell counts.
- Neural differentiation markers (MAP2, nestin) and BDNF-CREB pathway components were analyzed via western blotting and real-time PCR.
Main Results:
- PPARγ silencing was confirmed in NSCs.
- AGE-BSA treatment reduced NSC proliferation and BDNF pathway component expression.
- PPARγ-silenced NSCs showed increased proliferation and BDNF pathway component expression compared to controls under AGE-BSA.
- AGE-BSA decreased MAP2 expression in both NSCs and PPARγ-silenced NSCs, indicating no effect on differentiation.
Conclusions:
- PPARγ is involved in regulating NSC proliferation in response to AGEs.
- The BDNF-CREB pathway is implicated in AGE-mediated effects on NSC proliferation.
- PPARγ does not appear to influence AGE-mediated neural differentiation of NSCs.
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