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Fig. 6 | BMC Medicine

Fig. 6

From: LncRNA Airn maintains LSEC differentiation to alleviate liver fibrosis via the KLF2-eNOS-sGC pathway

Fig. 6

Airn promoted HC proliferation directly and indirectly by paracrine secretion of Wnt2a and HGF from LSEC. A Primary HCs were transfected with siAirn-1, siAirn-2, or siRNA-Control for 48 h. The RNA level of Airn, Ki67, and Pcna was detected by qRT-PCR. B The protein level of PCNA was determined by western blot and quantitatively compared with GAPDH as a reference control. C The expression of Ki67 was determined by confocal microscopy and quantitatively compared. DAPI-stained nuclei blue; scale bar, 20μm. D Primary HC were infected with LV-Airn and LV-Control for 72 h. The RNA level of Airn, Ki67, and Pcna was detected by qRT-PCR. E The protein level of PCNA was determined by western blot and quantitatively compared with GAPDH as a reference control. F Primary LSEC were transfected with siAirn-1, siAirn-2, or siRNA-Control for 48 h. The RNA level of Wnt2a and HGF was detected by qRT-PCR. G Airn was silenced by siRNA in primary LSEC and cultured in vitro for 48 h, the expression of HGF was detected in culture supernatants by ELISA. H Schematic diagram illustrating the design of the co-culture experiments. The primary HC derived from health mice were co-cultured with the Airn-silenced or -over-expressed of primary LSEC by transwell, or co-cultured with untreated LSEC. I The expression of Ki67 was detected by qRT-PCR in co-cultured condition. J The expression of Ki67 was determined by confocal microscopy in co-cultured condition and quantitatively compared. DAPI-stained nuclei blue; scale bar, 20μm. The data are expressed as the mean ± SD for at least triplicate experiments, *p<0.05 stands for vs siRNA-Control or LV-Control

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