Research Paper Volume 13, Issue 4 pp 5967—5985

Transfer of lncRNA UCA1 by hUCMSCs-derived exosomes protects against hypoxia/reoxygenation injury through impairing miR-143-targeted degradation of Bcl-2

LncRNA UCA1 in hUCMSC-ex protects CMECs against autophagy following H/R injury through impairing miR-143-targeted inhibition of Bcl-2. (A) Viability of CMECs detected by CCK-8. (B) Invasion of CMECs assessed by Transwell assay. (C) Migration of CMECs evaluated by scratch test. (E) Transmission electron microscopic observation of autophagosomes; (F) Fluorescence localization of LC3 in CMECs under exposure to H/R injury. LC3 was labeled as green fluorescence, nucleus were labeled by DAPI and CMEC marker CD31 was labeled as red fluorescence. (G) LC3-II/LC3-I and Beclin-1 protein levels in CMECs under exposure to H/R injury measured by Western blot assay. *p vs. the control group; # p vs. the H/R group. All experiments were repeated 3 times. Data in panels (A–G) were analyzed with independent t test.

Figure 8. LncRNA UCA1 in hUCMSC-ex protects CMECs against autophagy following H/R injury through impairing miR-143-targeted inhibition of Bcl-2. (A) Viability of CMECs detected by CCK-8. (B) Invasion of CMECs assessed by Transwell assay. (C) Migration of CMECs evaluated by scratch test. (E) Transmission electron microscopic observation of autophagosomes; (F) Fluorescence localization of LC3 in CMECs under exposure to H/R injury. LC3 was labeled as green fluorescence, nucleus were labeled by DAPI and CMEC marker CD31 was labeled as red fluorescence. (G) LC3-II/LC3-I and Beclin-1 protein levels in CMECs under exposure to H/R injury measured by Western blot assay. *p < 0.05, vs. the control group; # p < 0.05, vs. the H/R group. All experiments were repeated 3 times. Data in panels (AG) were analyzed with independent t test.