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ENGLISH ABSTRACT
JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
[Vitamin C promotes in vitro proliferation of bone marrow mesenchymal stem cells derived from aging mice].
OBJECTIVE: To investigate whether vitamin C can promote the proliferation ability of bone marrow mesenchymal stem cells (BMMSCs) derived from aging mice.
METHODS: The senescence-accelerated mouse prone 6 (SAMP6) mice and senescence-accelerated mouse resistant 1 (SAMR1) mice were used as the test group and the control group, respectively, and the SAMP6 mice were examined by micro-CT to verify the senescent phenotype. BMMSCs were harvested from the two mouse lines and cultured in vitro, and the cells from SAMP6 mice were subjected to treatment with different concentrations of vitamin C. The proliferation ability of the cells from the two mouse lines was tested using MTT assay and growth curves, and TeloTAGGG Telomerase PCR ELISA was used to measure the telomerase activity; PCR and Western blotting were performed to detect the expression level of telomerase reverse transcriptase (TERT) in the cells.
RESULTS: The SAMP6 mice displayed a bone senescent phenotype. The proliferation ability of BMMSCs derived from SAMP6 mice and their telomerase activity were significantly lower than those derived from SAMR1 mice (P<0.05). Vitamin C treatment significantly enhanced the proliferation ability of BMMSCs derived from SAMP6 mice in a dose-dependent manner (P<0.05) and increased telomerase activity and TERT expression in the cells (P<0.05). At the concentration of 100 µg/mL, vitamin C produced the strongest effect in promoting the proliferation of BMMSCs from SAMP6 mice, while at the concentration of 1000 µg/ml, growth suppression occurred in the cells.
CONCLUSION: Vitamin C can promote the proliferation of BMMSCs from aging mice possibly by increasing the cellular telomerase activity.
METHODS: The senescence-accelerated mouse prone 6 (SAMP6) mice and senescence-accelerated mouse resistant 1 (SAMR1) mice were used as the test group and the control group, respectively, and the SAMP6 mice were examined by micro-CT to verify the senescent phenotype. BMMSCs were harvested from the two mouse lines and cultured in vitro, and the cells from SAMP6 mice were subjected to treatment with different concentrations of vitamin C. The proliferation ability of the cells from the two mouse lines was tested using MTT assay and growth curves, and TeloTAGGG Telomerase PCR ELISA was used to measure the telomerase activity; PCR and Western blotting were performed to detect the expression level of telomerase reverse transcriptase (TERT) in the cells.
RESULTS: The SAMP6 mice displayed a bone senescent phenotype. The proliferation ability of BMMSCs derived from SAMP6 mice and their telomerase activity were significantly lower than those derived from SAMR1 mice (P<0.05). Vitamin C treatment significantly enhanced the proliferation ability of BMMSCs derived from SAMP6 mice in a dose-dependent manner (P<0.05) and increased telomerase activity and TERT expression in the cells (P<0.05). At the concentration of 100 µg/mL, vitamin C produced the strongest effect in promoting the proliferation of BMMSCs from SAMP6 mice, while at the concentration of 1000 µg/ml, growth suppression occurred in the cells.
CONCLUSION: Vitamin C can promote the proliferation of BMMSCs from aging mice possibly by increasing the cellular telomerase activity.
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