Gene interactions and pathways from curated databases and text-mining
Chin Med J (Engl) 2012, PMID: 23158146

Rapamycin and 3-methyladenine regulate apoptosis and autophagy in bone-derived endothelial progenitor cells.

Lei, Feng-rui; Li, Xiao-qiang; Liu, Hui; Zhu, Ren-da; Meng, Qing-you; Rong, Jian-jie

BACKGROUND

Mammalian target of rapamycin (mTOR) is involved in a caspase independent form of programmed cell death called autophagy. The aim of this research was to investigate the effects of rapamycin and 3-methyladenine (3-MA) on autophagy, proliferation, apoptosis, and cell-cycle parameters of rat bone marrow-derived endothelial progenitor cells (EPCs).

METHODS

Mononuclear cells isolated from rat bone marrow were treated with rapamycin (0.01, 0.1, 1, or 10 µg/L) or 3-MA (1.25, 2.5, 5, or 10 mmol/L) for 24 hours. Expression of the autophagy marker protein LC3-II was analyzed by Western blotting. Apoptosis and cell-cycle progression were analyzed by flow cytometry. Cell proliferation was measured using the MTT assay.

RESULTS

Rapamycin treatment of EPCs induced apoptosis and autophagy and inhibited proliferation and cell-cycle progression in a dose-dependent manner. Treatment with 5 mmol/L 3-MA promoted cell proliferation; in contrast, treatment with 10 mmol/L 3-MA promoted apoptosis and induced S-phase arrest.

CONCLUSIONS

Rapamycin treatment of EPCs induced apoptosis and autophagy. Low concentrations of 3-MA had no significant effect on the proliferation and apoptosis of EPCs; The 5 mmol/L group promoted cell proliferation, but had no effect on the apoptosis; the 10 mmol/L group inhibited the proliferation and promoted apoptosis through the cell cycle.

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Text Mining Data

programmed cell death → Mammalian target of rapamycin (mTOR): " Mammalian target of rapamycin (mTOR) is involved in a caspase independent form of programmed cell death called autophagy "

Manually curated Databases

No curated data.