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胰腺肝细胞。成年大鼠胰腺细胞谱系的体内模型。

Pancreatic hepatocytes. An in vivo model for cell lineage in pancreas of adult rat.

作者信息

Reddy J K, Rao M S, Yeldandi A V, Tan X D, Dwivedi R S

机构信息

Department of Pathology, Northwestern University Medical School, Chicago, Illinois 60611.

出版信息

Dig Dis Sci. 1991 Apr;36(4):502-9. doi: 10.1007/BF01298883.

DOI:10.1007/BF01298883
PMID:2007367
Abstract

Multiple foci of hepatocytes differentiate in the pancreas of adult rats subjected to a copper depletion-repletion regimen. Copper deficiency for seven to nine weeks causes an irreversible depletion of over 80% of the acinar cells in the pancreas. When transferred to a normal diet, these rats exhibit only a minimal and spotty acinar cell recovery. This disruption of tissue organization appears to trigger a profound change in cellular commitment, which leads to hepatocyte differentiation in the "oval cells" in the periductal interstitium and the epithelial cells lining the small pancreatic ductules. Pancreatic hepatocytes express several liver-specific genes including albumin, a2u-globulin, carbamoylphosphate synthetase-I, and urate oxidase. Both carbamoylphosphate synthetase-I and glutamine synthetase, the ammonia-metabolizing enzymes, are expressed by all pancreatic hepatocytes; in liver, these are expressed by different populations of hepatocytes. The magnitude of hepatocyte differentiation in this model should facilitate studies on the molecular events regulating changes in cell lineage or differentiation commitment within the pancreas.

摘要

在接受铜缺乏-补充方案的成年大鼠胰腺中,多个肝细胞灶发生分化。七至九周的铜缺乏会导致胰腺中超过80%的腺泡细胞发生不可逆的耗竭。当这些大鼠转至正常饮食时,它们仅表现出极少且散在的腺泡细胞恢复。这种组织结构的破坏似乎引发了细胞定向的深刻变化,进而导致导管周围间质中的“卵圆细胞”和小胰管内衬上皮细胞向肝细胞分化。胰腺肝细胞表达几种肝脏特异性基因,包括白蛋白、α2u球蛋白、氨甲酰磷酸合成酶-I和尿酸氧化酶。氨代谢酶氨甲酰磷酸合成酶-I和谷氨酰胺合成酶在所有胰腺肝细胞中均有表达;而在肝脏中,这些酶由不同群体的肝细胞表达。该模型中肝细胞分化的程度应有助于研究调节胰腺内细胞谱系变化或分化定向的分子事件。

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