AIM: To study the effect of retinoid X receptor-α (RXR-α) expression on rat hepatic fibrosis. METHODS: Rat hepatic fibrosis was induced by CCl(4) , and the rats were randomly divided into an early-phase hepatic fibrosis group (2 weeks) and a sustained hepatic fibrosis group (8 weeks). They were then divided into four groups (normal control, hepatic fibrosis, negative control and RXR-α groups). A recombinant lentiviral expression vector carrying the rat RXR-α gene was injected into the rats to induce RXR-α expression by intraportal infusion, hepatic tissue pathological examination was performed, and hydroxyproline content was detected. Hepatic stellate cells (HSC) were cultured in vitro, an RXR-α lentivirus vector was used to activate HSC, and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) activation was assayed to detect HSC proliferation. RESULTS: In vivo experiments indicated that in the sustained hepatic fibrosis group, there were significant differences in the hydroxyproline content, and expression of RXR-α, α-smooth muscle actin (α-SMA) and type I collagen (P < 0.01). However, in the early-phase hepatic fibrosis group, hydroxyproline content and the protein level of RXR-α showed no significant difference compared with the normal control group (P > 0.05). In vitro studies revealed that expression of RXR-α significantly inhibited expression of α-SMA and type I collagen in activated HSC (P < 0.01), as well as HSC proliferation (P < 0.01). CONCLUSION: The increased RXR-α gene expression inhibited HSC activation and proliferation and the degree of hepatic fibrosis.
AIM: To study the effect of retinoid X receptor-α (RXR-α) expression on rathepatic fibrosis. METHODS:Rathepatic fibrosis was induced by CCl(4) , and the rats were randomly divided into an early-phase hepatic fibrosis group (2 weeks) and a sustained hepatic fibrosis group (8 weeks). They were then divided into four groups (normal control, hepatic fibrosis, negative control and RXR-α groups). A recombinant lentiviral expression vector carrying the rat RXR-α gene was injected into the rats to induce RXR-α expression by intraportal infusion, hepatic tissue pathological examination was performed, and hydroxyproline content was detected. Hepatic stellate cells (HSC) were cultured in vitro, an RXR-α lentivirus vector was used to activate HSC, and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) activation was assayed to detect HSC proliferation. RESULTS: In vivo experiments indicated that in the sustained hepatic fibrosis group, there were significant differences in the hydroxyproline content, and expression of RXR-α, α-smooth muscle actin (α-SMA) and type I collagen (P < 0.01). However, in the early-phase hepatic fibrosis group, hydroxyproline content and the protein level of RXR-α showed no significant difference compared with the normal control group (P > 0.05). In vitro studies revealed that expression of RXR-α significantly inhibited expression of α-SMA and type I collagen in activated HSC (P < 0.01), as well as HSC proliferation (P < 0.01). CONCLUSION: The increased RXR-α gene expression inhibited HSC activation and proliferation and the degree of hepatic fibrosis.
Authors: Karen R Jonscher; Alba Alfonso-Garcia; Jeffrey L Suhalim; David J Orlicky; Eric O Potma; Virginia L Ferguson; Mary L Bouxsein; Ted A Bateman; Louis S Stodieck; Moshe Levi; Jacob E Friedman; Daila S Gridley; Michael J Pecaut Journal: PLoS One Date: 2016-04-20 Impact factor: 3.240
Authors: Eugene Makarev; Evgeny Izumchenko; Fumiaki Aihara; Piotr T Wysocki; Qingsong Zhu; Anton Buzdin; David Sidransky; Alex Zhavoronkov; Anthony Atala Journal: Cell Cycle Date: 2016-06-07 Impact factor: 4.534