Stem cells under the influence of alcohol: effects of ethanol consumption on stem/progenitor cells

Abstract

Stem cells drive embryonic and fetal development. In several adult tissues, they retain the ability to self-renew and differentiate into a variety of specialized cells, thus contributing to tissue homeostasis and repair throughout life span. Alcohol consumption is associated with an increased risk for several diseases and conditions. Growing and developing tissues are particularly vulnerable to alcohol’s influence, suggesting that stem- and progenitor-cell function could be affected. Accordingly, recent studies have revealed the possible relevance of alcohol exposure in impairing stem-cell properties, consequently affecting organ development and injury response in different tissues. Here, we review the main studies describing the effects of alcohol on different types of progenitor/stem cells including neuronal, hepatic, intestinal and adventitial progenitor cells, bone-marrow-derived stromal cell, dental pulp, embryonic and hematopoietic stem cells, and tumor-initiating cells. A better understanding of the nature of the cellular damage induced by chronic and episodic heavy (binge) drinking is critical for the improvement of current therapeutic strategies designed to treat patients suffering from alcohol-related disorders.

Ethanol exposure drives colon location specific cell composition changes in a normal colon crypt 3D organoid model

“…The identification of an enrichment for downregulated genes involved in DNA repair and in chromosome organization in colon stem cells exposed to ethanol may be a potential mechanism by which alcohol increases CRC risk. Alcohol may contribute to DNA damage in stem cells by increasing reactive oxygen species (ROS) 41 . Increased ROS has been consistently associated with alcohol in multiple cell-types and experimental designs 41 .…”

miR‐136‐3p targets PTEN to regulate vascularization and bone formation and ameliorates alcohol‐induced osteopenia

“…For skeletal system, low dosage of ethanol might be beneficial but high levels of ethanol consumption resulted in turnover imbalance where bone resorption exceeded formation. 2,[58][59][60] A very recent study indicated that a high dose of ethanol mainly decreased the function of osteoblast, without a significant impact on osteoclast activity. 61 Our pilot study, as well as some others', revealed that both trabecular and cortical bone were sensitive to long-term and high-dose ethanol.…”

Pooling of Patient-Derived Mesenchymal Stromal Cells Reduces Inter-Individual Confounder-Associated Variation without Negative Impact on Cell Viability, Proliferation and Osteogenic Differentiation

“…Furthermore, studies have to be conducted using several patient-derived cell lines in order to compensate for donor-caused variations [9]. Various donor specific factors such as age [14,21], sex [12,15], alcohol and/or tobacco consumption [19,22,31], and morbidities such as obesity or diabetes [17,20] have been identified in the past to cause this inter-individual variability via complex mechanisms [16,18]. Inter alia, Hong et al have shown that osteogenic differentiation and cell proliferation are influenced by intrinsic steroid regulation causing considerable sex-linked variability [15].…”