Paper Information

Journal:   CELL JOURNAL (YAKHTEH)   WINTER 2011 , Volume 12 , Number SUPPLEMENT 1 (THE 1ST INTERNATIONAL STUDENT CONGRESS ON CELL AND MOLECULAR MEDICINE); Page(s) 104 To 105.
 
Paper: 

STEM CELL AND REGENERATIVE MEDICINE: P-144: EFFECT OF PPARγ AGONIST AND ANTAGONIST TREATMENT ON DURING NEURAL PRECURSOR CELLS AND MATURE NEURONS

 
 
Author(s):  PEYMANI M.*, GHOUCHANI A., HAEDI K., KARAMALI F., KARBALAEI KH., KIANI A., ESMAEILI A., HASHEMI M., NASR ESFAHANI M.H., BAHARVAND H.
 
* ROYAN INSITUE, ISFAHAN, IRAN
 
Abstract: 

Objective: Several evidences have suggested that PPARg activation might affect neural differentiation. To investigate the role of PPARg on neural precursor cells and mature neurons, embryoid bodies (EBs) were treated after retinoic acid and PPARg agonist (Rosiglitazone) and antagonist (GW9662). To evaluate the efficiency of embryoid formation of mouse embryonic stem cells, expression of nestin, MapII and GFAP were evaluated.
Data indicated that nestin expression on was not influenced by PPAR
g agonist, while, PPARg antagonist decreased expression of this neural precursor marker.
Assessment of mature neuron and glial markers was also not affected by agonist while a significant reduction in expression of MapII and GFAP upon treatment with the PPAR
g antagonist. This observation was further confirmed by staining of b-tubulin III and GFAP staining of EBs. In addition treatment with the PPARg antagonist resulted in significant reduction on the size of EBs.
Materials and Methods: For formation of neural precursor cells, embryoid bodies were derived from mouse embryonic stem cells by 2days culture in hanging drops followed by 4 days in suspensions in presence of retinoic acid. For differentiation and formation of mature neural cells, the embryo bodies were plated in neurobasal medium. To investigate the role of PPAR
g on neural precursor cells and mature neurons, EBs treated with RA and PPARg agonist (Rosiglitazone) and antagonist (GW9662). In this stage expression of Nestin as specific NPCs marker, MapII (mature neuron marker) and GFAP (mature glial marker) evaluated in 6th and 14th day, respectively.
Result: Data indicated Nestin expression did not be influenced by PPAR
g agonist (Rosiglitazone) while, PPARg antagonist (GW9662) decrease expression of this neural precursor marker. Also Mature neuron and glial cells were formed from these NPCs did not significant illustrate in expression of MapII and GFAP while, PPARg antagonist caused decrement in both expression of these markers.
Conclusion: Several evidences suggest that PPAR
g activation might affect neural differentiation and PPARg stimulated neurite extension in neuroblastoma cell line. Our results demonstrated increment of PPARg expression in neurogenesis is due to RA treatment and PPARg is maybe critical role in neural differentiation of mESCs during neural precursor cell formation.

 
Keyword(s): PPAR GAMMA, MOUSE EMBRYONIC STEM CELL, NEURAL DIFFERENTIATION
 
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