Matches in SemOpenAlex for { <https://semopenalex.org/work/W2886051086> ?p ?o ?g. }
- W2886051086 endingPage "151S.e2" @default.
- W2886051086 startingPage "137S" @default.
- W2886051086 abstract "ObjectiveRegenerative medicine seeks to stall or to reverse the pathologic consequences of chronic diseases. Many people with diabetes have peripheral arterial disease (PAD), which increases their already high risk of major amputation. Cellular therapies are a promising regenerative medicine approach to PAD that can be used to focally inject regenerative cells to endangered tissue beds. Mesenchymal stem cells (MSCs) are known to promote tissue regeneration through stromal support and paracrine stimulation of new blood vessels (angiogenesis). Whereas little is known about human diabetic MSCs (dMSCs), particularly those from patients with PAD, dMSCs have a limited expansion capacity but can be improved with human platelet lysate (PL) supplementation. PL is rich in many growth factors, including epidermal growth factor (EGF), which is known to be important to cell proliferation and survival signaling pathways. We hypothesize that dMSCs have a reversible defect in EGF receptor pathways. The objective of this work was to test this hypothesis using dMSCs from PAD patients.MethodsThe secretome expression of EGF and prominent angiogens was characterized from bone marrow (BM)-derived and adipose tissue-derived (ATD) dMSCs from five patients (six limbs) undergoing major amputation. Western blot was used to characterize the AKT and extracellular signal-regulated protein kinases 1 and 2 expression in dMSCs under standard culture (5% fetal bovine serum plus fibroblast growth factor 2 [FGF2]), 5% human PL, or 5% fetal bovine serum plus EGF. Healthy donor MSCs were control cells. The angiogenic activity of BM- and ATD-dMSCs was tested on human umbilical vein endothelial cells (ECs). Paired t-test, analysis of variance, and Kruskal-Wallis tests were used as appropriate.ResultsBoth BM- and ATD-dMSCs had typical MSC surface marker expression and similar expansion profiles, and they did not express EGF in their secretome. PL supplementation of dMSCs improved AKT signaling, but they were resistant to FGF2 activation of extracellular signal-regulated protein kinases 1 and 2. EGF supplementation led to similar AKT expression as with PL, but PL had greater phosphorylation of AKT at 30 and 60 minutes. The conditioned media from both BM- and ATD-dMSCs had robust levels of prominent angiogens (vascular endothelial growth factor, monocyte chemoattractant protein 1, hepatocyte growth factor), which stimulated EC proliferation and migration, and the co-culture of dMSCs with ECs led to significantly longer EC sprouts in three-dimensional gel than EC-alone pellets.ConclusionsPL and EGF supplementation improves AKT expression in dMSCs over that of FGF2, but PL improved pAKT over that of EGF. Thus, PL supplementation strategies may improve AKT signaling, which could be important to MSC survival in cellular therapies. Furthermore, BM- and ATD-dMSCs have similar secretomes and robust in vitro angiogenic activity, which supports pursuing dMSCs from both reservoirs in regenerative medicine strategies." @default.
- W2886051086 created "2018-08-22" @default.
- W2886051086 creator A5014686511 @default.
- W2886051086 creator A5020608576 @default.
- W2886051086 creator A5023204958 @default.
- W2886051086 creator A5024239839 @default.
- W2886051086 creator A5031410125 @default.
- W2886051086 creator A5068773395 @default.
- W2886051086 creator A5074997611 @default.
- W2886051086 creator A5089984864 @default.
- W2886051086 date "2018-12-01" @default.
- W2886051086 modified "2023-09-30" @default.
- W2886051086 title "Reversible secretome and signaling defects in diabetic mesenchymal stem cells from peripheral arterial disease patients" @default.
- W2886051086 cites W125204626 @default.
- W2886051086 cites W1969047355 @default.
- W2886051086 cites W1976604464 @default.
- W2886051086 cites W1995286643 @default.
- W2886051086 cites W2002702688 @default.
- W2886051086 cites W2009254740 @default.
- W2886051086 cites W2009891045 @default.
- W2886051086 cites W2025371271 @default.
- W2886051086 cites W2031280595 @default.
- W2886051086 cites W2047709770 @default.
- W2886051086 cites W2050841999 @default.
- W2886051086 cites W2051254937 @default.
- W2886051086 cites W2054095354 @default.
- W2886051086 cites W2057926047 @default.
- W2886051086 cites W2058197610 @default.
- W2886051086 cites W2066545720 @default.
- W2886051086 cites W2066954473 @default.
- W2886051086 cites W2071746224 @default.
- W2886051086 cites W2071904806 @default.
- W2886051086 cites W2076282370 @default.
- W2886051086 cites W2076491580 @default.
- W2886051086 cites W2079623878 @default.
- W2886051086 cites W2080948969 @default.
- W2886051086 cites W2091128115 @default.
- W2886051086 cites W2111576152 @default.
- W2886051086 cites W2112267683 @default.
- W2886051086 cites W2113747401 @default.
- W2886051086 cites W2117463276 @default.
- W2886051086 cites W2118212786 @default.
- W2886051086 cites W2131092033 @default.
- W2886051086 cites W2140136269 @default.
- W2886051086 cites W2166193005 @default.
- W2886051086 cites W2279728460 @default.
- W2886051086 cites W2284278240 @default.
- W2886051086 cites W2333224671 @default.
- W2886051086 cites W2493480331 @default.
- W2886051086 cites W2550312821 @default.
- W2886051086 cites W2565152769 @default.
- W2886051086 cites W2573812177 @default.
- W2886051086 cites W2609827029 @default.
- W2886051086 cites W2772528916 @default.
- W2886051086 cites W2793891651 @default.
- W2886051086 cites W2884926531 @default.
- W2886051086 doi "https://doi.org/10.1016/j.jvs.2018.05.223" @default.
- W2886051086 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6252140" @default.
- W2886051086 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30104096" @default.
- W2886051086 hasPublicationYear "2018" @default.
- W2886051086 type Work @default.
- W2886051086 sameAs 2886051086 @default.
- W2886051086 citedByCount "6" @default.
- W2886051086 countsByYear W28860510862018 @default.
- W2886051086 countsByYear W28860510862019 @default.
- W2886051086 countsByYear W28860510862020 @default.
- W2886051086 countsByYear W28860510862021 @default.
- W2886051086 crossrefType "journal-article" @default.
- W2886051086 hasAuthorship W2886051086A5014686511 @default.
- W2886051086 hasAuthorship W2886051086A5020608576 @default.
- W2886051086 hasAuthorship W2886051086A5023204958 @default.
- W2886051086 hasAuthorship W2886051086A5024239839 @default.
- W2886051086 hasAuthorship W2886051086A5031410125 @default.
- W2886051086 hasAuthorship W2886051086A5068773395 @default.
- W2886051086 hasAuthorship W2886051086A5074997611 @default.
- W2886051086 hasAuthorship W2886051086A5089984864 @default.
- W2886051086 hasBestOaLocation W28860510861 @default.
- W2886051086 hasConcept C10854531 @default.
- W2886051086 hasConcept C126322002 @default.
- W2886051086 hasConcept C142724271 @default.
- W2886051086 hasConcept C170493617 @default.
- W2886051086 hasConcept C198826908 @default.
- W2886051086 hasConcept C203014093 @default.
- W2886051086 hasConcept C2780394083 @default.
- W2886051086 hasConcept C28328180 @default.
- W2886051086 hasConcept C502942594 @default.
- W2886051086 hasConcept C71924100 @default.
- W2886051086 hasConcept C7876069 @default.
- W2886051086 hasConcept C86803240 @default.
- W2886051086 hasConcept C95444343 @default.
- W2886051086 hasConceptScore W2886051086C10854531 @default.
- W2886051086 hasConceptScore W2886051086C126322002 @default.
- W2886051086 hasConceptScore W2886051086C142724271 @default.
- W2886051086 hasConceptScore W2886051086C170493617 @default.
- W2886051086 hasConceptScore W2886051086C198826908 @default.
- W2886051086 hasConceptScore W2886051086C203014093 @default.
- W2886051086 hasConceptScore W2886051086C2780394083 @default.
- W2886051086 hasConceptScore W2886051086C28328180 @default.