« Previous
Next »
Surgery
Volume 146, Issue 2
, Pages 198-205
, August 2009
MEK mediates the novel cross talk between TNFR2 and TGF-EGFR in enhancing vascular endothelial growth factor (VEGF) secretion from human mesenchymal stem cells
References
- . Bone marrow stem cell transplantation for cardiac repair. Am J Physiol. 2005;288:H2557–H2567
- . Implantation of bone marrow stem cells reduces the infarction and fibrosis in ischemic mouse heart. J Mol Cell Cardiol. 2003;35:1113–1119
- Regeneration of ischemic cardiac muscle and vascular endothelium by adult stem cells. J Clin Invest. 2001;107:1395–1402
- Paracrine action accounts for marked protection of ischemic heart by Akt-modified mesenchymal stem cells. Nat Med. 2005;11:367–368
- . Administered mesenchymal stem cells protect against ischemic acute renal failure through differentiation-independent mechanisms. Am J Physiol Renal Physiol. 2005;289:F31–F42
- Evidence supporting paracrine hypothesis for Akt-modified mesenchymal stem cell-mediated cardiac protection and functional improvement. FASEB J. 2006;20:661–669
- . TGF-{alpha} increases human mesenchymal stem cell-secreted VEGF by MEK- and PI3-K- but not JNK- or ERK-dependent mechanisms. Am J Physiol Regul Integr Comp Physiol. 2008;295:R1115–R1123
- . The role of vascular endothelial growth factor in wound healing. Int J Low Extrem Wounds. 2003;2:107–120
- Expression of vascular permeability factor (vascular endothelial growth factor) by epidermal keratinocytes during wound healing. J Exp Med. 1992;176:1375–1379
- . Vascular permeability factor/vascular endothelial growth factor, microvascular hyperpermeability, and angiogenesis. Am J Pathol. 1995;146:1029–1039
- . Vascular permeability factor/vascular endothelial growth factor and the significance of microvascular hyperpermeability in angiogenesis. Curr Top Microbiol Immunol. 1999;237:97–132
- Estradiol-treated mesenchymal stem cells improve myocardial recovery after ischemia. J Surg Res. 2009;152:319–324
- . Tumor necrosis factor in the heart. Am J Physiol. 1998;274:R577–R595
- . Regulation of TNFR1 and CD95 signaling by receptor compartmentalization. Nat Rev Mol Cell Biol. 2008;9:655–662
- . Tumor necrosis factor (TNF)-mediated neuroprotection against glutamate-induced excitotoxicity is enhanced by N-methyl-D-aspartate receptor activation. Essential role of a TNF receptor 2-mediated phosphatidylinositol 3-kinase-dependent NF-kappa B pathway. J Biol Chem. 2004;279:32869–32881
- . Human mesenchymal stem cells stimulated by TNF-{alpha}, LPS, or hypoxia produce growth factors by an NF{kappa}B- but not JNK-dependent mechanism. Am J Physiol Cell Physiol. 2008;294:C675–C682
- Tumor necrosis factor (TNF)-{alpha} persistently activates nuclear factor-{kappa}B signaling through the type 2 TNF receptor in chromaffin cells: implications for long-term regulation of neuropeptide gene expression in inflammation. Endocrinology. 2008;149:2840–2852
- . Adult bone marrow-derived cells do not acquire functional attributes of cardiomyocytes when transplanted into peri-infarct myocardium. Mol Ther. 2008;16:1129–1137
- . Tumor necrosis factor, other cytokines and disease. Annu Rev Cell Biol. 1993;9:317–343
- Tumor necrosis factor receptor 1 is a negative regulator of progenitor proliferation in adult hippocampal neurogenesis. J Neurosci. 2006;26:9703–9712
- . Activation of individual tumor necrosis factor receptors differentially affects stem cell growth factor and cytokine production. Am J Physiol Gastrointest Liver Physiol. 2007;293:G657–G662
- . TNF mediated neuroprotection against glutamate induced excitotoxicity is enhanced by NMDA receptor activation: Essential role of a TNF receptor 2 mediated, PI3 kinase dependent NF-kB pathway. J Biol Chem. 2004;279:32869–32881
- STAT3 mediates bone marrow mesenchymal stem cell VEGF production. J Mol Cell Cardiol. 2007;42:1009–1015
- Targeting Stat3 blocks both HIF-1 and VEGF expression induced by multiple oncogenic growth signaling pathways. Oncogene. 2005;24:5552–5560
Supported by Grants NIH R01GM070628, NIH R01HL085595, NIH K99/R00 HL0876077-01, NIH F32 HL092718-01, NIH F32 HL092719-01, and F32 HL093987-01A1.
PII: S0039-6060(09)00263-3
doi: 10.1016/j.surg.2009.04.013
© 2009 Mosby, Inc. All rights reserved.
« Previous
Next »
Surgery
Volume 146, Issue 2
, Pages 198-205
, August 2009
