Macrophages Regulate Smooth Muscle Differentiation of Mesenchymal Stem Cells via a Prostaglandin F _2α −Mediated Paracrine Mechanism

Thromboxane Governs the Differentiation of Adipose-Derived Stromal Cells Toward Endothelial Cells In Vitro and In Vivo

“…7 Analogous to previous reports, 9,10,12,49-51 we observed that the transplanted ASCs were incorporated in the vessels (RFP + /PCNA + / CD31 + ) in ischemic hindlimbs of mice, implying that some ASCs can differentiate into ECs in vivo. Moreover, the transplanted ASCs may also differentiate into vascular smooth muscle cells 52,53 and even pericyte-like cells in vivo 14 to stabilize the neovasculature and exert proangiogenic paracrine effects as well. [54][55][56] Indeed, both TP-KO ASC (RFP + /PCNA + / CD31 + ) and recipient-cell-derived (RFP -/PCNA + /CD31 + ) neovascularization were more than doubled than that in hindlimbs transplanted with WT ASCs, indicating enhanced differentiation toward ECs and paracine activity in TP-KO ASCs.…”

Functional expression of smooth muscle-specific ion channels in TGF-β1-treated human adipose-derived mesenchymal stem cells

“…28,64), sphingosylphosphotylcholine (SPC; Refs. 22,23), thromboxane A 2 (26), mechanical stress (32), coculture with vascular endothelial cells (4), and PGF 2␣ (35) can cause MSCs to differentiate into SMCs.…”

Stem/Progenitor Cells in Vascular Regeneration

“…A recently published article demonstrated that macrophages induce differentiation of human adipose tissue-derived mesenchymal stem cells to α-actin+ smooth muscle cells, displaying a contractility in response to KCl and carbachol treatment. 50 Transplantation of the differentiated smooth muscle cells attenuated severe hindlimb ischemia and promoted vascular regeneration through a prostaglandin F 2α -mediated paracrine mechanism. 50 However, monocyte chemoattractant protein-1 mediated migration of mesenchymal stem cells that serve as a source of intimal hyperplasia.…”

“…50 Transplantation of the differentiated smooth muscle cells attenuated severe hindlimb ischemia and promoted vascular regeneration through a prostaglandin F 2α -mediated paracrine mechanism. 50 However, monocyte chemoattractant protein-1 mediated migration of mesenchymal stem cells that serve as a source of intimal hyperplasia. 51 Transplantation experiments with labeled cells demonstrated that the adventitia served as a major source of cells migrating to the intima, in which monocyte chemotactic protein-1 is a potent chemokine for the recruitment of stem/progenitor cells to the lesions.…”