Influence of ERK1/2 signal-transduction pathway on differentiation of mesenephalic neural stem cells induced by bone marrow stromal cell-conditioned medium
- Author:
Ping GU
1
Author Information
1. Brain Aging and Cognitive Neuroscience Laboratory of Hebei Province
- Publication Type:Journal Article
- Keywords:
Bone marrow stromal cells;
Conditioned medium;
ERK1/2 signal-transduction pathway;
Neural stem cells
- From:
Academic Journal of Second Military Medical University
2010;28(6):589-592
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the effect of the ERK1/2 signal-transduction pathway on differentiation of rat mesencephalic neural stem cells (NSCs) in presence of bone marrow stromal cell-conditioned medium (BMSCs-CM) in vitro. Methods: NSCs were cultured on poly-L-lysine (PLL) coated 35 nun dishes. The neurospheres adhered to the bottom 30 min later; then the culture medium of natural differentiation group was replaced by neurobasal medium containing 2% B27; the control group was replaced with BMSCS-CM; and the inhibition group was replaced with BMSCs-CM containing PD98059 (5 μmol/L). The proportions of neurons and astrocytes and their morphological difference were observed by immunocytochemistry technique 7 d later. Results: We successfully cultured NSCs from adult rat BMSCs-CM. The proportion of neurons in the natural differentiation group (15.70±10.3)% was lower than that in the control group ([51.17±10.30]%, P<0.05); the proportion of astrocytes in the natural differentiation group (66.9± 14.8)% was higher than that in the control group ([23.26 ± 5.60]%, P<0.05). The proportion of neurons in the inhibition group (39.48 ± 7.29)% was lower than that in the control group ([51.17 ± 10.30]%, P< 0.05); the proportion of astrocytes in the inhibition group (31.01 ± 8.96)% was higher than that in the control group ([23.26 ± 5.60]%, P<0.01). Conclusion: BMSCs-CM can up-regulate the proportion of neurons in cultured NSCs and down-regulate the proportion of astrocytes, which might be mediated by the ERK1/2 signal-transduction pathway.
