FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2034182103> ?p ?o ?g. }

• W2034182103 endingPage "205" @default.
• W2034182103 startingPage "198" @default.
• W2034182103 abstract "Background Bone marrow mesenchymal stem cells (MSCs) may mediate their beneficial effects by paracrine mechanisms. Recently, we reported that tumor necrosis factor-alpha (TNF-α) increased the release of vascular endothelial growth factor (VEGF) from human MSCs and augmented transforming growth factor-alpha (TGF-α)-stimulated VEGF secretion. However, it is unknown whether TNF-α stimulates VEGF production via TNF receptor 1 (TNFR1) or 2 (TNFR2) and the mechanism by which TNF-α augments TGF-α (a ligand of epidermal growth factor receptor, EGFR) stimulated VEGF production. We hypothesized that the ablation of TNFR2 would decrease TNF-α–stimulated and/or TGF-α– stimulated VEGF production via MEK-dependent mechanisms. Methods MSCs transfected with TNFR1, TNFR2, or GAPDH siRNA were stimulated with TNF-α and/or TGF-α for 24 h. VEGF levels in the supernatant were determined by enzyme-linked immunosorbent assay (ELISA). A Western blot analysis was performed to measure the activation of MEK and ERK and the expression of TNFR1 and TNFR2. Results TNF-α or TGF-α increased VEGF secretion in cells transfected with GAPDH or TNFR1 siRNA. The combination of TNF-α and TGF-α increased VEGF production. TNF-α and/or TGF-α stimulation increased phospho-MEK and phospho-ERK in cells transfected with TNFR1 siRNA. Conversely, the effects of TNF-α and/or TGF-α on MSC VEGF production were significantly decreased, and MEK/ERK activation was negated in cells transfected TNFR2 siRNA. Conclusion TNFR2 plays a vital role in the effects of TNF-α and TGF-α on MSC VEGF production. The activation of MEK was implicated in this novel cross talk between TNFR2 and TGF-α–EGFR in regulating the production of VEGF in human MSCs. Bone marrow mesenchymal stem cells (MSCs) may mediate their beneficial effects by paracrine mechanisms. Recently, we reported that tumor necrosis factor-alpha (TNF-α) increased the release of vascular endothelial growth factor (VEGF) from human MSCs and augmented transforming growth factor-alpha (TGF-α)-stimulated VEGF secretion. However, it is unknown whether TNF-α stimulates VEGF production via TNF receptor 1 (TNFR1) or 2 (TNFR2) and the mechanism by which TNF-α augments TGF-α (a ligand of epidermal growth factor receptor, EGFR) stimulated VEGF production. We hypothesized that the ablation of TNFR2 would decrease TNF-α–stimulated and/or TGF-α– stimulated VEGF production via MEK-dependent mechanisms. MSCs transfected with TNFR1, TNFR2, or GAPDH siRNA were stimulated with TNF-α and/or TGF-α for 24 h. VEGF levels in the supernatant were determined by enzyme-linked immunosorbent assay (ELISA). A Western blot analysis was performed to measure the activation of MEK and ERK and the expression of TNFR1 and TNFR2. TNF-α or TGF-α increased VEGF secretion in cells transfected with GAPDH or TNFR1 siRNA. The combination of TNF-α and TGF-α increased VEGF production. TNF-α and/or TGF-α stimulation increased phospho-MEK and phospho-ERK in cells transfected with TNFR1 siRNA. Conversely, the effects of TNF-α and/or TGF-α on MSC VEGF production were significantly decreased, and MEK/ERK activation was negated in cells transfected TNFR2 siRNA. TNFR2 plays a vital role in the effects of TNF-α and TGF-α on MSC VEGF production. The activation of MEK was implicated in this novel cross talk between TNFR2 and TGF-α–EGFR in regulating the production of VEGF in human MSCs." @default.
• W2034182103 created "2016-06-24" @default.
• W2034182103 creator A5013438877 @default.
• W2034182103 creator A5018600971 @default.
• W2034182103 creator A5030838551 @default.
• W2034182103 creator A5030977453 @default.
• W2034182103 creator A5036860312 @default.
• W2034182103 creator A5039173798 @default.
• W2034182103 creator A5040323862 @default.
• W2034182103 creator A5041898942 @default.
• W2034182103 creator A5076314648 @default.
• W2034182103 date "2009-08-01" @default.
• W2034182103 modified "2023-10-16" @default.
• W2034182103 title "MEK mediates the novel cross talk between TNFR2 and TGF-EGFR in enhancing vascular endothelial growth factor (VEGF) secretion from human mesenchymal stem cells" @default.
• W2034182103 cites W1971248512 @default.
• W2034182103 cites W1977031737 @default.
• W2034182103 cites W2020509670 @default.
• W2034182103 cites W2028705859 @default.
• W2034182103 cites W2030927418 @default.
• W2034182103 cites W2037814474 @default.
• W2034182103 cites W2053298425 @default.
• W2034182103 cites W2066027939 @default.
• W2034182103 cites W2067591094 @default.
• W2034182103 cites W2085926680 @default.
• W2034182103 cites W2087935545 @default.
• W2034182103 cites W2088053894 @default.
• W2034182103 cites W2088750322 @default.
• W2034182103 cites W2090068113 @default.
• W2034182103 cites W2104898886 @default.
• W2034182103 cites W2129889907 @default.
• W2034182103 cites W2147485426 @default.
• W2034182103 cites W2158682140 @default.
• W2034182103 cites W2171630160 @default.
• W2034182103 doi "https://doi.org/10.1016/j.surg.2009.04.013" @default.
• W2034182103 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19628074" @default.
• W2034182103 hasPublicationYear "2009" @default.
• W2034182103 type Work @default.
• W2034182103 sameAs 2034182103 @default.
• W2034182103 citedByCount "25" @default.
• W2034182103 countsByYear W20341821032012 @default.
• W2034182103 countsByYear W20341821032013 @default.
• W2034182103 countsByYear W20341821032014 @default.
• W2034182103 countsByYear W20341821032015 @default.
• W2034182103 countsByYear W20341821032018 @default.
• W2034182103 countsByYear W20341821032019 @default.
• W2034182103 countsByYear W20341821032020 @default.
• W2034182103 countsByYear W20341821032021 @default.
• W2034182103 countsByYear W20341821032023 @default.
• W2034182103 crossrefType "journal-article" @default.
• W2034182103 hasAuthorship W2034182103A5013438877 @default.
• W2034182103 hasAuthorship W2034182103A5018600971 @default.
• W2034182103 hasAuthorship W2034182103A5030838551 @default.
• W2034182103 hasAuthorship W2034182103A5030977453 @default.
• W2034182103 hasAuthorship W2034182103A5036860312 @default.
• W2034182103 hasAuthorship W2034182103A5039173798 @default.
• W2034182103 hasAuthorship W2034182103A5040323862 @default.
• W2034182103 hasAuthorship W2034182103A5041898942 @default.
• W2034182103 hasAuthorship W2034182103A5076314648 @default.
• W2034182103 hasConcept C118131993 @default.
• W2034182103 hasConcept C126322002 @default.
• W2034182103 hasConcept C128240485 @default.
• W2034182103 hasConcept C134018914 @default.
• W2034182103 hasConcept C167734588 @default.
• W2034182103 hasConcept C170493617 @default.
• W2034182103 hasConcept C17991360 @default.
• W2034182103 hasConcept C198826908 @default.
• W2034182103 hasConcept C2777025900 @default.
• W2034182103 hasConcept C2780394083 @default.
• W2034182103 hasConcept C502942594 @default.
• W2034182103 hasConcept C54009773 @default.
• W2034182103 hasConcept C54355233 @default.
• W2034182103 hasConcept C57074206 @default.
• W2034182103 hasConcept C62478195 @default.
• W2034182103 hasConcept C71924100 @default.
• W2034182103 hasConcept C7876069 @default.
• W2034182103 hasConcept C81885089 @default.
• W2034182103 hasConcept C86803240 @default.
• W2034182103 hasConcept C95444343 @default.
• W2034182103 hasConceptScore W2034182103C118131993 @default.
• W2034182103 hasConceptScore W2034182103C126322002 @default.
• W2034182103 hasConceptScore W2034182103C128240485 @default.
• W2034182103 hasConceptScore W2034182103C134018914 @default.
• W2034182103 hasConceptScore W2034182103C167734588 @default.
• W2034182103 hasConceptScore W2034182103C170493617 @default.
• W2034182103 hasConceptScore W2034182103C17991360 @default.
• W2034182103 hasConceptScore W2034182103C198826908 @default.
• W2034182103 hasConceptScore W2034182103C2777025900 @default.
• W2034182103 hasConceptScore W2034182103C2780394083 @default.
• W2034182103 hasConceptScore W2034182103C502942594 @default.
• W2034182103 hasConceptScore W2034182103C54009773 @default.
• W2034182103 hasConceptScore W2034182103C54355233 @default.
• W2034182103 hasConceptScore W2034182103C57074206 @default.
• W2034182103 hasConceptScore W2034182103C62478195 @default.
• W2034182103 hasConceptScore W2034182103C71924100 @default.
• W2034182103 hasConceptScore W2034182103C7876069 @default.
• W2034182103 hasConceptScore W2034182103C81885089 @default.
• W2034182103 hasConceptScore W2034182103C86803240 @default.
• W2034182103 hasConceptScore W2034182103C95444343 @default.

• next