Matches in SemOpenAlex for { <https://semopenalex.org/work/W4291178289> ?p ?o ?g. }
- W4291178289 abstract "Abstract Background Numerous studies have shown that mesenchymal stromal cells (MSCs) promote cutaneous wound healing via paracrine signaling. Our previous study found that the secretome of MSCs was significantly amplified by treatment with IFN-γ and TNF-α (IT). It has been known that macrophages are involved in the initiation and termination of inflammation, secretion of growth factors, phagocytosis, cell proliferation, and collagen deposition in wound, which is the key factor during wound healing. In this study, we aim to test whether the supernatant of MSCs pretreated with IT (S-IT MSCs) possesses a more pronounced effect on improving wound healing and describe the interplay between S-IT MSCs and macrophages as well as the potential mechanism in skin wound healing. Methods In the present study, we used a unique supernatant of MSCs from human umbilical cord-derived MSCs (UC-MSCs) pretreated with IT, designated S-IT MSCs, subcutaneously injected into a mice total skin excision. We evaluated the effect of S-IT MSCs on the speed and quality of wound repair via IT MSCs-derived IL-6-dependent M2 polarization in vivo by hematoxylin–eosin staining (H&E), immunohistochemistry (IHC), immunofluorescence (IF), Masson’s trichrome staining, Sirius red staining, quantitative real-time PCR (qPCR). In addition, the effect of S-IT MSCs on the polarization of macrophages toward M2 phenotype and the potential mechanism of it were also investigated in vitro by flow cytometry (FCM), enzyme-linked immunosorbent assay (ELISA), tube formation assay, and western blot analysis. Results Compared with control supernatant (S-MSCs), our H&E and IF results showed that S-IT MSCs were more effectively in promoting macrophages convert to the M2 phenotype and enhancing phagocytosis of M2 macrophages. Meanwhile, the results of tube formation assay, IHC, Masson’s trichrome staining, Sirius red staining showed that the abilities of M2 phenotype to promote vascularization and collagen deposition were significantly enhanced by S-IT MSCs-treated, thereby accelerating higher quality wound healing. Further, our ELISA, FCM, qPCR and western blot results showed that IL-6 was highly enriched in S-IT MSCs and acted as a key regulator to induce macrophages convert to the M2 phenotype through IL-6-dependent signaling pathways, ultimately achieving the above function of promoting wound repair. Conclusions These findings provide the first evidence that the S-IT MSCs is more capable of eliciting M2 polarization of macrophages via IL-6-dependent signaling pathways and accelerating wound healing, which may represent a new strategy for optimizing the therapeutic effect of MSCs on wound healing." @default.
- W4291178289 created "2022-08-13" @default.
- W4291178289 creator A5015553206 @default.
- W4291178289 creator A5015928630 @default.
- W4291178289 creator A5016745818 @default.
- W4291178289 creator A5036322554 @default.
- W4291178289 creator A5040179741 @default.
- W4291178289 creator A5041265490 @default.
- W4291178289 creator A5062876262 @default.
- W4291178289 creator A5085581217 @default.
- W4291178289 creator A5088533080 @default.
- W4291178289 date "2022-08-13" @default.
- W4291178289 modified "2023-10-14" @default.
- W4291178289 title "Mesenchymal stromal cells pretreated with proinflammatory cytokines enhance skin wound healing via IL-6-dependent M2 polarization" @default.
- W4291178289 cites W1594905954 @default.
- W4291178289 cites W1797422316 @default.
- W4291178289 cites W1920534265 @default.
- W4291178289 cites W1925325876 @default.
- W4291178289 cites W1967106066 @default.
- W4291178289 cites W1969644104 @default.
- W4291178289 cites W1973636045 @default.
- W4291178289 cites W1979043688 @default.
- W4291178289 cites W1981575054 @default.
- W4291178289 cites W1985859986 @default.
- W4291178289 cites W1990386050 @default.
- W4291178289 cites W1990932830 @default.
- W4291178289 cites W2016868307 @default.
- W4291178289 cites W2019221616 @default.
- W4291178289 cites W2021916724 @default.
- W4291178289 cites W2022915249 @default.
- W4291178289 cites W2024326908 @default.
- W4291178289 cites W2025294489 @default.
- W4291178289 cites W2029725511 @default.
- W4291178289 cites W2036348189 @default.
- W4291178289 cites W2036396816 @default.
- W4291178289 cites W2041591721 @default.
- W4291178289 cites W2052268146 @default.
- W4291178289 cites W2060766291 @default.
- W4291178289 cites W2061172918 @default.
- W4291178289 cites W2061591828 @default.
- W4291178289 cites W2061954405 @default.
- W4291178289 cites W2065210647 @default.
- W4291178289 cites W2065769697 @default.
- W4291178289 cites W2071904806 @default.
- W4291178289 cites W2077636159 @default.
- W4291178289 cites W2081810806 @default.
- W4291178289 cites W2085216114 @default.
- W4291178289 cites W2095132685 @default.
- W4291178289 cites W2112270957 @default.
- W4291178289 cites W2112310312 @default.
- W4291178289 cites W2118654016 @default.
- W4291178289 cites W2126134953 @default.
- W4291178289 cites W2127903487 @default.
- W4291178289 cites W2139167732 @default.
- W4291178289 cites W2160130477 @default.
- W4291178289 cites W2168203604 @default.
- W4291178289 cites W2171630160 @default.
- W4291178289 cites W2325727928 @default.
- W4291178289 cites W2417667791 @default.
- W4291178289 cites W2469689396 @default.
- W4291178289 cites W2534854440 @default.
- W4291178289 cites W2734365706 @default.
- W4291178289 cites W2808158796 @default.
- W4291178289 cites W2884747526 @default.
- W4291178289 cites W2898482203 @default.
- W4291178289 cites W2904564895 @default.
- W4291178289 cites W2970718184 @default.
- W4291178289 cites W2972642636 @default.
- W4291178289 cites W3006291133 @default.
- W4291178289 cites W3119829476 @default.
- W4291178289 cites W4239894970 @default.
- W4291178289 doi "https://doi.org/10.1186/s13287-022-02934-9" @default.
- W4291178289 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/35964139" @default.
- W4291178289 hasPublicationYear "2022" @default.
- W4291178289 type Work @default.
- W4291178289 citedByCount "12" @default.
- W4291178289 countsByYear W42911782892022 @default.
- W4291178289 countsByYear W42911782892023 @default.
- W4291178289 crossrefType "journal-article" @default.
- W4291178289 hasAuthorship W4291178289A5015553206 @default.
- W4291178289 hasAuthorship W4291178289A5015928630 @default.
- W4291178289 hasAuthorship W4291178289A5016745818 @default.
- W4291178289 hasAuthorship W4291178289A5036322554 @default.
- W4291178289 hasAuthorship W4291178289A5040179741 @default.
- W4291178289 hasAuthorship W4291178289A5041265490 @default.
- W4291178289 hasAuthorship W4291178289A5062876262 @default.
- W4291178289 hasAuthorship W4291178289A5085581217 @default.
- W4291178289 hasAuthorship W4291178289A5088533080 @default.
- W4291178289 hasBestOaLocation W42911782891 @default.
- W4291178289 hasConcept C142724271 @default.
- W4291178289 hasConcept C164027704 @default.
- W4291178289 hasConcept C170493617 @default.
- W4291178289 hasConcept C185592680 @default.
- W4291178289 hasConcept C198826908 @default.
- W4291178289 hasConcept C202751555 @default.
- W4291178289 hasConcept C203014093 @default.
- W4291178289 hasConcept C2776682551 @default.
- W4291178289 hasConcept C2776914184 @default.
- W4291178289 hasConcept C2779244956 @default.
- W4291178289 hasConcept C2780269544 @default.