Department of Medicine, Division of Gastrointestinal and Liver Diseases, University of Southern California, Keck School of Medicine, Los Angeles, California, USA.
Research and Development Department, PhoenixBio, Co., Ltd, Hiroshima, Japan.
FASEB J. 2023 Feb;37(2):e22750. doi: 10.1096/fj.202201292RR.
Human hepatocyte culture system represents by far the most physiologically relevant model for our understanding of liver biology and diseases; however, its versatility has been limited due to the rapid and progressive loss of genuine characteristics, indicating the inadequacy of in vitro milieu for fate maintenance. This study, therefore, is designed to define environmental requirements necessary to sustain the homeostasis of terminally differentiated hepatocytes. Our study reveals that the supplementation of dimethyl sulfoxide (DMSO) is indispensable in mitigating fate deterioration and promoting adaptation to the in vitro environment, resulting in the restoration of tight cell-cell contact, cellular architecture, and polarity. The morphological recovery was overall accompanied by the restoration of hepatocyte marker gene expression, highlighting the interdependence between the cellular architecture and the maintenance of cell fate. However, beyond the recovery phase culture, DMSO supplementation is deemed detrimental due to the potent inhibitory effect on a multitude of hepatocyte functionalities while its withdrawal results in the loss of cell fate. In search of DMSO substitute, our screening of organic substances led to the identification of dimethyl sulfone (DMSO2), which supports the long-term maintenance of proper morphology, marker gene expression, and hepatocytic functions. Moreover, hepatocytes maintained DMSO2 exhibited clinically relevant toxicity in response to prolonged exposure to xenobiotics as well as alcohol. These observations suggest that the stepwise culture configuration consisting of the consecutive supplementation of DMSO and DMSO2 confers the microenvironment essential for the fate and functional maintenance of terminally differentiated human hepatocytes.
人肝细胞培养系统是目前为止理解肝脏生物学和疾病最具生理相关性的模型;然而,由于其真正特征的迅速和逐渐丧失,其多功能性受到限制,表明体外环境不足以维持其命运。因此,本研究旨在确定维持终末分化肝细胞内稳态所需的环境要求。我们的研究表明,二甲基亚砜(DMSO)的补充对于减轻命运恶化和促进适应体外环境是必不可少的,从而恢复紧密的细胞-细胞接触、细胞结构和极性。形态恢复总体上伴随着肝细胞标记基因表达的恢复,突出了细胞结构与细胞命运维持之间的相互依存关系。然而,在恢复阶段培养之外,由于 DMSO 对多种肝细胞功能具有强烈的抑制作用,其补充被认为是有害的,而其去除则导致细胞命运的丧失。在寻找 DMSO 的替代品时,我们对有机物质的筛选导致鉴定出二甲基砜(DMSO2),它支持适当形态、标记基因表达和肝细胞功能的长期维持。此外,用 DMSO2 维持的肝细胞在长期暴露于外源化合物和酒精后表现出与临床相关的毒性。这些观察结果表明,由连续补充 DMSO 和 DMSO2 组成的逐步培养结构赋予了终末分化人肝细胞命运和功能维持所必需的微环境。