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Sphingosylphosphorylcholine stimulates expression of fibronectin through TGF-beta1-Smad-dependent mechanism in human mesenchymal stem cells.
Int J Biochem Cell Biol. 2007; 39(6):1224-34.IJ

Abstract

Sphingosylphosphorylcholine (SPC) has been reported to stimulate the expression of fibronectin (FN), which plays a key role in cell recruitment and adhesion during wound healing. In a previous study, we reported that SPC induces differentiation of human adipose tissue-derived mesenchymal stem cells (hATSCs) to smooth muscle-like cell types through ERK-dependent autocrine secretion of TGF-beta1 and delayed activation of the TGF-beta1-Smad pathway. In the present study, we demonstrated that SPC dose- and time-dependently increased the expression of FN in hATSCs. Pretreatment of the cells with U0126, an MEK inhibitor, markedly attenuated the SPC-induced expression of FN and delayed phosphorylation of Smad2, suggesting that ERK is involved in the SPC induction of FN expression through activation of Smad2. In addition, the SPC-induced expression of FN and delayed activation of Smad2 were abrogated by SB-431542, a TGF-beta type I receptor kinase inhibitor, or anti-TGF-beta1 neutralizing antibody. Furthermore, the SPC-induced expression of FN was abrogated by adenoviral expression of Smad7, an inhibitory Smad, or short interference RNA (siRNA)-mediated depletion of endogenous Smad2 expression, suggesting that SPC induces the expression of FN through ERK-dependent activation of the TGF-beta1-Smad2 crosstalk pathway. Adhesion of U937 monocytic cells to hATSCs was enhanced by pretreatment of hATSCs with SPC or TGF-beta1 for 4 days, and the peptide GRGDSP (an antagonist of fibronectin receptors) blocked the adhesion of U937 cells to the hATSCs. These results led us to suggest that SPC-induced FN expression plays a pivotal role in the wound healing by stimulating adhesion and recruitment of leukocytes.

Authors+Show Affiliations

Medical Research Center for Ischemic Tissue Regeneration of Pusan National University, Medical Research Institute, Busan 602-739, Republic of Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17481939

Citation

Moon, Hyun Jung, et al. "Sphingosylphosphorylcholine Stimulates Expression of Fibronectin Through TGF-beta1-Smad-dependent Mechanism in Human Mesenchymal Stem Cells." The International Journal of Biochemistry & Cell Biology, vol. 39, no. 6, 2007, pp. 1224-34.
Moon HJ, Jeon ES, Kim YM, et al. Sphingosylphosphorylcholine stimulates expression of fibronectin through TGF-beta1-Smad-dependent mechanism in human mesenchymal stem cells. Int J Biochem Cell Biol. 2007;39(6):1224-34.
Moon, H. J., Jeon, E. S., Kim, Y. M., Lee, M. J., Oh, C. K., & Kim, J. H. (2007). Sphingosylphosphorylcholine stimulates expression of fibronectin through TGF-beta1-Smad-dependent mechanism in human mesenchymal stem cells. The International Journal of Biochemistry & Cell Biology, 39(6), 1224-34.
Moon HJ, et al. Sphingosylphosphorylcholine Stimulates Expression of Fibronectin Through TGF-beta1-Smad-dependent Mechanism in Human Mesenchymal Stem Cells. Int J Biochem Cell Biol. 2007;39(6):1224-34. PubMed PMID: 17481939.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Sphingosylphosphorylcholine stimulates expression of fibronectin through TGF-beta1-Smad-dependent mechanism in human mesenchymal stem cells. AU - Moon,Hyun Jung, AU - Jeon,Eun Su, AU - Kim,Young Mi, AU - Lee,Mi Jeong, AU - Oh,Chang-Keun, AU - Kim,Jae Ho, Y1 - 2007/03/30/ PY - 2007/01/02/received PY - 2007/03/18/revised PY - 2007/03/23/accepted PY - 2007/5/8/pubmed PY - 2007/9/26/medline PY - 2007/5/8/entrez SP - 1224 EP - 34 JF - The international journal of biochemistry & cell biology JO - Int J Biochem Cell Biol VL - 39 IS - 6 N2 - Sphingosylphosphorylcholine (SPC) has been reported to stimulate the expression of fibronectin (FN), which plays a key role in cell recruitment and adhesion during wound healing. In a previous study, we reported that SPC induces differentiation of human adipose tissue-derived mesenchymal stem cells (hATSCs) to smooth muscle-like cell types through ERK-dependent autocrine secretion of TGF-beta1 and delayed activation of the TGF-beta1-Smad pathway. In the present study, we demonstrated that SPC dose- and time-dependently increased the expression of FN in hATSCs. Pretreatment of the cells with U0126, an MEK inhibitor, markedly attenuated the SPC-induced expression of FN and delayed phosphorylation of Smad2, suggesting that ERK is involved in the SPC induction of FN expression through activation of Smad2. In addition, the SPC-induced expression of FN and delayed activation of Smad2 were abrogated by SB-431542, a TGF-beta type I receptor kinase inhibitor, or anti-TGF-beta1 neutralizing antibody. Furthermore, the SPC-induced expression of FN was abrogated by adenoviral expression of Smad7, an inhibitory Smad, or short interference RNA (siRNA)-mediated depletion of endogenous Smad2 expression, suggesting that SPC induces the expression of FN through ERK-dependent activation of the TGF-beta1-Smad2 crosstalk pathway. Adhesion of U937 monocytic cells to hATSCs was enhanced by pretreatment of hATSCs with SPC or TGF-beta1 for 4 days, and the peptide GRGDSP (an antagonist of fibronectin receptors) blocked the adhesion of U937 cells to the hATSCs. These results led us to suggest that SPC-induced FN expression plays a pivotal role in the wound healing by stimulating adhesion and recruitment of leukocytes. SN - 1357-2725 UR - https://www.unboundmedicine.com/medline/citation/17481939/Sphingosylphosphorylcholine_stimulates_expression_of_fibronectin_through_TGF_beta1_Smad_dependent_mechanism_in_human_mesenchymal_stem_cells_ DB - PRIME DP - Unbound Medicine ER -