Abstract
BackgroundRestoration of damaged tissues through the activation of endogenous progenitors is an attractive therapeutic option. A deep evaluation of the intrinsic stem/progenitor cell properties as well as the reciprocal interactions with injured environments is of critical importance.MethodsHere, we show that bone marrow stromal cell antigen 2 (BST2) allows the isolation of a population of circulating progenitors, the circulating healing (CH) cells, characterized by a distinctive core signature. The bone marrow (BM) origin of BST2pos CH cells has been strengthened by the co-expression of leptin receptor, the hallmark of a subpopulation of BM-skeletal stem cells.ResultsBST2pos CH cells retained the capacity to (i) respond to injury signals generated by a bone fracture, (ii) modify the expression of cell motility genes following damage, and (iii) react to hepatocyte growth factor-activator (HGFA), an injury-related stimulus sufficient to induce their transition into GALERT, a state in which cells are functionally activated and participate in tissue repair.ConclusionsTaken together, these results could pave the way for the identification of new strategies to enhance and potentiate endogenous regenerative mechanisms for future therapies.
Highlights
Restoration of damaged tissues through the activation of endogenous progenitors is an attractive therapeutic option
bone marrow stromal cell antigen 2 (BST2)-expressing circulating healing (CH) cells maintained the capacity to (i) respond to injury environmental cues, actively proliferating and migrating toward the damaged site; (ii) modify the expression profile of specific cell motility-associated genes following the injury occurrence; and (iii) respond to the systemic factor hepatocyte growth factor activator (HGFA), a stimulus sufficient to induce the transition of multiple pools of quiescent progenitor cells into a GALERT state [13]
We provide an integrative data analysis by comparing the already published transcriptome dataset of highly purified CH cells isolated from peripheral blood (PB) of naive mice (Fig. 1a) with publicly available profiles of other stem/progenitor cells characterized by different stemness degree and capabilities to enter the blood flow, including embryonic stem cells (ESC), very small embryonic-like stem cells (VSEL), hematopoietic stem cells (HSC), hemangioblasts (HEM), multipotent adult stem cells (MAPC), and bone marrow stromal cells (BMSC) [11]
Summary
Restoration of damaged tissues through the activation of endogenous progenitors is an attractive therapeutic option. The activation of quiescent stem cells into the cell cycle is a key step in initiating the process of tissue repair [9, 10] In this context, it has been recently shown that a population of circulating progenitors, defined as circulating healing (CH) cells, characterized by a lineage-negative/CD45-negative (LinnegCD45neg) profile, possess a strong chemotactic potential, being responsive to the signals released by an injured environment as the one generated by a bone fracture [11]. It has been recently shown that a population of circulating progenitors, defined as circulating healing (CH) cells, characterized by a lineage-negative/CD45-negative (LinnegCD45neg) profile, possess a strong chemotactic potential, being responsive to the signals released by an injured environment as the one generated by a bone fracture [11] These stimuli direct their migration, with subsequent engraftment and differentiation into specific cells belonging to the affected tissue [11]. BST2-expressing CH cells maintained the capacity to (i) respond to injury environmental cues, actively proliferating and migrating toward the damaged site; (ii) modify the expression profile of specific cell motility-associated genes following the injury occurrence; and (iii) respond to the systemic factor hepatocyte growth factor activator (HGFA), a stimulus sufficient to induce the transition of multiple pools of quiescent progenitor cells into a GALERT state [13]
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