Figure 2.

CPT1C overexpression increases survival of hMSCs against cellular damage induced by glucose depletion or 2-deoxyglucose treatment. (A) Dental pulp MSCs were transduced with lentivirus containing the empty vector (EV) or the vector codifying for mCPT1C and subsequently separated by FACS. Endogenous human CPT1C and overexpressed mouse isoform were detected by western blot using antibodies specific to mouse CPT1c (mCPT1C) or commercial antibodies (SIGMA SAB2501194) that recognize both human and mouse CPT1C (hCPT1C). β-actin was used as a loading control. (B) Growth curve during 8 days of EV (squares) or CPT1C (triangles) –hMSCs cultured with 10% FBS or 1% FBS. (C–H) Cell survival analysis were performed in media with 1% FBS. EV or CPT1C-hMSCs were cultured in glucose-deprived media for 72 h (C), treated with 50 mM 2-DG for 72 h (D), OGD for 24 h (E). In (F), cells were glucose starved for 72 h and then returned to a medium with glucose for additional 24 h. Random or CPT1C-silenced cells were cultured in glucose depleted media (G) or treated with 2-DG (H) for 72 h. All results are shown as mean ± SEM of 3 independent experiments performed in sextuplet. *p < 0.05.