Dabeva M D, Hurston E, Shafritz D A
Marion Bessin Liver Research Center, Albert Einstein College of Medicine, Bronx, New York 10461, USA.
Am J Pathol. 1995 Dec;147(6):1633-48.
The pattern of mRNA expression for liver-specific proteins and liver-enriched transcription factors was studied in two models of facultative gut epithelial progenitor cells activation: D-galactosamine (GalN)-induced liver injury and dietary copper depletion leading to pancreatic acinar atrophy. After 5 weeks of copper deficiency (CuD), pancreatic acini of Fischer 344 rats underwent atrophy, associated with intense proliferation of small duct-like cells with oval-shaped nuclei. These cells resemble morphologically epithelial progenitor cells of the liver that proliferate after GalN administration. Activated pancreatic epithelial cells express mRNAs for liver-specific genes normally expressed in fetal liver, including alpha-fetoprotein, albumin, alpha-1 antitrypsin, glucose-6-phosphatase, and others, but not genes that are turned on after birth such as serine dehydratase, tyrosine aminotransferase, and multidrug resistance gene-1b. They express mRNAs for liver-enriched transcription factors including HNF-1 alpha, HNF-3 beta and gamma, HNF-4, and members of the CCAAT-enhancer binding protein (C/EBP) family. The only mRNA for a liver-enriched transcription factor not detected in the pancreas of CuD animals was HNF-3 alpha. Expression of HNF-3 alpha, beta, and gamma, and C/EBP-beta mRNA was highly activated in proliferating liver epithelial cells on days 2 and 3 after GalN injury. Increased expression of C/EBP-delta was observed first in the liver on day 1 after GalN administration and in the pancreas at 4 weeks after initiating CuD. We suggest that C/EBP-delta could be involved in the initial activation of epithelial progenitor cells and that HNF-3 alpha, beta, and gamma, and C/EBP-beta might participate in their maturation. We conclude further that pancreatic epithelial progenitor cells undertake differentiation through the hepatocyte lineage but cannot complete the differentiation program within the pancreatic milieu.
在两种兼性肠道上皮祖细胞激活模型中,研究了肝脏特异性蛋白和肝脏富集转录因子的mRNA表达模式:D - 半乳糖胺(GalN)诱导的肝损伤和饮食性铜缺乏导致胰腺腺泡萎缩。在铜缺乏(CuD)5周后,Fischer 344大鼠的胰腺腺泡发生萎缩,伴有核呈椭圆形的小导管样细胞强烈增殖。这些细胞在形态上类似于GalN给药后增殖的肝脏上皮祖细胞。活化的胰腺上皮细胞表达通常在胎儿肝脏中表达的肝脏特异性基因的mRNA,包括甲胎蛋白、白蛋白、α - 1抗胰蛋白酶、葡萄糖 - 6 - 磷酸酶等,但不表达出生后开启的基因,如丝氨酸脱水酶、酪氨酸转氨酶和多药耐药基因 - 1b。它们表达肝脏富集转录因子的mRNA,包括肝细胞核因子 - 1α(HNF - 1α)、肝细胞核因子 - 3β和γ(HNF - 3β和γ)、肝细胞核因子 - 4(HNF - 4)以及CCAAT增强子结合蛋白(C/EBP)家族成员。在CuD动物的胰腺中未检测到的肝脏富集转录因子的唯一mRNA是HNF - 3α。在GalN损伤后第2天和第3天,增殖的肝脏上皮细胞中HNF - 3α、β和γ以及C/EBP - β mRNA的表达高度活化。在GalN给药后第1天在肝脏中以及在开始CuD后4周在胰腺中首先观察到C/EBP - δ表达增加。我们认为C/EBP - δ可能参与上皮祖细胞的初始激活,而HNF - 3α、β和γ以及C/EBP - β可能参与它们的成熟。我们进一步得出结论,胰腺上皮祖细胞通过肝细胞谱系进行分化,但不能在胰腺环境中完成分化程序。