Published online Sep 26, 2018. doi: 10.4252/wjsc.v10.i9.119
Peer-review started: April 27, 2018
First decision: June 6, 2018
Revised: July 27, 2018
Accepted: August 5, 2018
Article in press: August 5, 2018
Published online: September 26, 2018
Processing time: 152 Days and 1 Hours
Balanced sphingolipid signaling is important for the maintenance of homeostasis. Sphingolipids were demonstrated to function as structural components, second messengers, and regulators of cell growth and survival in normal and disease-affected tissues. Particularly, sphingosine kinase 1 (SphK1) and its product sphingosine-1-phosphate (S1P) operate as mediators and facilitators of proliferation-linked signaling. Unlimited proliferation (self-renewal) within the regulated environment is a hallmark of progenitor/stem cells that was recently associated with the S1P signaling network in vasculature, nervous, muscular, and immune systems. S1P was shown to regulate progenitor-related characteristics in normal and cancer stem cells (CSCs) via G-protein coupled receptors S1Pn (n = 1 to 5). The SphK/S1P axis is crucially involved in the regulation of embryonic development of vasculature and the nervous system, hematopoietic stem cell migration, regeneration of skeletal muscle, and development of multiple sclerosis. The ratio of the S1P receptor expression, localization, and specific S1P receptor-activated downstream effectors influenced the rate of self-renewal and should be further explored as regeneration-related targets. Considering malignant transformation, it is essential to control the level of self-renewal capacity. Proliferation of the progenitor cell should be synchronized with differentiation to provide healthy lifelong function of blood, immune systems, and replacement of damaged or dead cells. The differentiation-related role of SphK/S1P remains poorly assessed. A few pioneering investigations explored pharmacological tools that target sphingolipid signaling and can potentially confine and direct self-renewal towards normal differentiation. Further investigation is required to test the role of the SphK/S1P axis in regulation of self-renewal and differentiation.
Core tip: The aim of this study is to review the role of sphingosine kinase, sphingosine-1-phosphate (S1P), and its receptors in the regulation of stem/progenitor cell function. Our analysis indicates that S1P receptor expression, localization, and specific downstream effectors influence the rate of self-renewal and differentiation of myogenic, hematopoietic, endothelial, neural, and cancer progenitor cells.