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Human amniotic epithelial cells possess hepatocyte-like characteristics and functions
Seiji Takashima1, Hirohiko Ise, Peng Zhao
1Department of Organ Regeneration, Institutes of Organ Transplants, Reconstructive Medicine and Tissue Engineering, Shinshu University Graduate School of Medicine, Asahi, Matsumoto, Japan.
Cell Structure and Function
|November 6, 2004
Summary
Human amniotic epithelial cells show potential as a source for hepatocyte transplantation. These cells and the amnion can produce liver-specific proteins and may treat liver diseases.
Area of Science:
- Regenerative Medicine
- Hepatology
- Stem Cell Biology
Background:
- Hepatocyte transplantation offers a novel therapeutic approach for liver diseases.
- Donor cell availability and function are critical challenges in hepatocyte transplantation.
Purpose of the Study:
- To investigate the potential of human amniotic epithelial cells (HAECs) as a cell source for hepatocyte transplantation.
- To analyze the hepatic gene expression and functions of HAECs.
Main Methods:
- Reverse transcription-polymerase chain reaction (RT-PCR) to detect hepatocyte-related gene expression.
- In vitro cell culture to assess albumin production, glycogen storage, and secretion.
- Organ culture of amnion to evaluate albumin and alpha(1)-antitrypsin secretion.
- In vivo transplantation of amnion into mice to assess survival and function.
Main Results:
- HAECs express key hepatocyte genes, including albumin and alpha(1)-antitrypsin.
- Cultivated HAECs exhibit albumin production, glycogen storage, and secretion.
- Amnion in organ culture showed significantly higher albumin secretion (30-fold) and alpha(1)-antitrypsin secretion compared to monolayer HAECs.
- Transplanted amnion survived in mice and continued to secrete albumin.
Conclusions:
- Human amniotic epithelial cells and amnion possess characteristics suitable for hepatocyte transplantation.
- These cells represent a promising novel therapeutic strategy for hepatic diseases.
- Potential applications include the treatment of alpha(1)-antitrypsin deficiency.