Retinoic acid signalling induces the differentiation of mouse fetal liver‐derived hepatic progenitor cells

• DOI: 10.1111/j.1478-3231.2009.02111.x
• Publication Date: 2009-09-08T08:53:48Z
• Authors: Jiayi Huang; Yang Bi; Gao‐Hui Zhu; Yun He; Yuxi Su; Bai‐Cheng He; Yi Wang; Quan Kang; Liang Chen; Guo‐Wei Zuo; Qing Luo; Qiong Shi; Bing‐Qiang Zhang; Ailong Huang; Lan Zhou; Tao Feng; Hue H. Luu; Rex C. Haydon; Tong‐Chuan He; Ni Tang
• Keywords: Retinoid X receptor; Hepatic stellate cell

Hepatic progenitor cells (HPCs) can be isolated from fetal liver and extrahepatic tissues. Retinoic acid (RA) signalling plays an important role in development, although the of RA liver-specific progenitors is poorly understood.We sought to determine regulating hepatic differentiation.RNA was tissues various developmental stages. Liver marker expression assessed by reverse transcriptase-polymerase chain reaction immunofluorescence staining. Reversibly immortalized HPCs derived mouse embryonic day 14.5 (E14.5) (aka, HP14.5) were established. Albumin promoter-driven reporter (Alb-GLuc) used monitor differentiation. Glycogen synthesis assayed as a for terminal differentiation.Retinoic receptor (RAR)-alpha, retinoid X (RXR)-alpha RXR-gamma expressed E12.5 postnatal 28 samples. Expression RAR-beta RXR-beta low perinatally, whereas RAR-gamma undetectable prenatal increased postnatally. Retinal dehydrogenase 1 2 (Raldh1 Raldh2) all tissues, while Raldh3 weakly samples but readily detected Nuclear corepressors highly nuclear co-activators decreased perinatal after birth. HP14.5 high levels early stem cell markers. components coregulators HP14.5. shown induce Alb-GLuc activity late hepatocyte further glycogen cells, function mature hepatocytes.Our results strongly suggest that may play