VAP-PLGA microspheres (VAP-PLGA) promote adipose-derived stem cells (ADSCs)-induced wound healing in chronic skin ulcers in mice via PI3K/Akt/HIF-1α pathway

Jiang, Wen; Zhang, Jun; Zhang, Xudong; Fan, Chenghong; Huang, Jianguo

doi:10.1080/21655979.2021.1990193

Cited by 21 publications

(12 citation statements)

References 54 publications

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“…3 e) and histogram (Supplementary Fig. 1 d) showed the top 12 signalling pathways, many of which were closely associated with a variety of chronic wounds, such as apoptosis 70 , HIF-1 signalling pathways 71 and ROS 72 . Additionally, the AGE-RAGE signalling pathway in diabetic complications 73 was involved in diabetic wound healing; hepatitis B 74 , human cytomegalovirus infection and hepatitis C 75 signalling pathways might participate in chronic infectious wounds 76 .…”

Section: Resultsmentioning

confidence: 99%

Integrated network pharmacology and experimental validation to explore the mechanisms underlying naringenin treatment of chronic wounds

Sun

Liu

et al. 2023

Sci Rep

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Naringenin is a citrus flavonoid with various biological functions and a potential therapeutic agent for skin diseases, such as UV radiation and atopic dermatitis. The present study investigates the therapeutic effect and pharmacological mechanism of naringenin on chronic wounds. Using network pharmacology, we identified 163 potential targets and 12 key targets of naringenin. Oxidative stress was confirmed to be the main biological process modulated by naringenin. The transcription factor p65 (RELA), alpha serine/threonine-protein kinase (AKT1), mitogen-activated protein kinase 1 (MAPK1) and mitogen-activated protein kinase 3 (MAPK3) were identified as common targets of multiple pathways involved in treating chronic wounds. Molecular docking verified that these four targets stably bound naringenin. Naringenin promoted wound healing in mice in vivo by inhibiting wound inflammation. Furthermore, in vitro experiments showed that a low naringenin concentration did not significantly affect normal skin cell viability and cell apoptosis; a high naringenin concentration was cytotoxic and reduced cell survival by promoting apoptosis. Meanwhile, comprehensive network pharmacology, molecular docking and in vivo and in vitro experiments revealed that naringenin could treat chronic wounds by alleviating oxidative stress and reducing the inflammatory response. The underlying mechanism of naringenin in chronic wound therapy involved modulating the RELA, AKT1 and MAPK1/3 signalling pathways to inhibit ROS production and inflammatory cytokine expression.

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Section: Resultsmentioning

confidence: 99%

Integrated network pharmacology and experimental validation to explore the mechanisms underlying naringenin treatment of chronic wounds

Sun

Liu

et al. 2023

Sci Rep

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“…53 Similarly, VAP-PLGA microspheres have been found to promote the healing of chronic skin ulcer wounds by encouraging the growth, migration, and tube formation of adipose-derived stem cells through the PI3K/AKT/HIF-1α pathway. 54 In this study, we have shown that the Nrf2/HIF-1α pathway also plays a regulatory role in angiogenesis during wound healing. Hydrogen sulfide donors have been found to upregulate vascular endothelial growth factor via the Nrf2/HIF-1α pathway and stimulate EC migration and tube formation.…”

Section: Discussionmentioning

confidence: 82%

Fucoidan promotes angiogenesis and accelerates wound healing through AKT/Nrf2/HIF‐1α signalling pathway

Wen,

Yang,

Wang

et al. 2023

International Wound Journal

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After skin injury, wound repair involves a complex process in which angiogenesis plays a crucial role. Previous research has indicated that fucoidan may aid in wound healing; we therefore hypothesised that fucoidan may speed up the process by promoting angiogenesis. In this study, we investigated the potential molecular mechanism underlying fucoidan's ability to accelerate wound healing by promoting angiogenesis. Using a full‐cut wound model, we observed that fucoidan significantly intensified wound closure and promoted granulation formation and collagen deposition. Immunofluorescence staining revealed that fucoidan also promoted wound angiogenesis, specifically by accelerating the migration of new blood vessels to the middle area of the wound. Furthermore, fucoidan demonstrated the ability to enhance the proliferation of human umbilical vein endothelial cells (HUVECs) damaged by hydrogen peroxide (H2O2) and to improve the formation of endothelial tubes. Mechanistic studies revealed that fucoidan upregulated the protein levels of the AKT/Nrf2/HIF‐1α signalling pathway, which plays a crucial role in angiogenesis. This was further confirmed using the inhibitor LY294002, which reversed the promotion of endothelial tube formation by fucoidan. Overall, our findings suggest that fucoidan can promote angiogenesis via the AKT/Nrf2/HIF‐1α signalling pathway and accelerate wound healing.

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“…Those mice treated with ASCs, VAP-PLGA, VAP-PLGA + ASCs had notably higher rates of wound healing than the control, with the highest rate in the VAP-PLGA + ASCs. VEGFR, CXCL12, CXCR4, TGF-B were all upregulated in treated groups, highest in VAP-PLGA + ASCs, and IL-1B, IL-18 and IL-6 were all downregulated, lowest in VAP-PLGA + ASCs group (Jiang et al, 2021). Activation of the CXCL12-CXCR4 axis may be the mechanism by which the synergy of the peptide and autologous stem cells in this biomaterial are promoting wound healing.…”

Section: Poly(lactic-co-glycolic Acid) or Plgamentioning

confidence: 88%

Immunomodulatory biomaterials on chemokine signaling in wound healing

2023

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Normal wound healing occurs through a careful orchestration of cytokine and chemokine signaling in response to injury. Chemokines are a small family of chemotactic cytokines that are secreted by immune cells in response to injury and are primarily responsible for recruiting appropriate immune cell types to injured tissue at the appropriate time. Dysregulation of chemokine signaling is suspected to contribute to delayed wound healing and chronic wounds in diseased states. Various biomaterials are being used in the development of new therapeutics for wound healing and our understanding of their effects on chemokine signaling is limited. It has been shown that modifications to the physiochemical properties of biomaterials can affect the body’s immune reaction. Studying these effects on chemokine expression by various tissues and cell type can help us develop novel biomaterial therapies. In this review, we summarize the current research available on both natural and synthetic biomaterials and their effects on chemokine signaling in wound healing. In our investigation, we conclude that our knowledge of chemokines is still limited and that many in fact share both pro-inflammatory and anti-inflammatory properties. The predominance of either a pro-inflammatory or anti-inflammatory profile is mostly likely dependent on timing after injury and exposure to the biomaterial. More research is needed to better understand the interaction and contribution of biomaterials to chemokine activity in wound healing and their immunomodulatory effects.

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VAP-PLGA microspheres (VAP-PLGA) promote adipose-derived stem cells (ADSCs)-induced wound healing in chronic skin ulcers in mice via PI3K/Akt/HIF-1α pathway

Cited by 21 publications

References 54 publications

Integrated network pharmacology and experimental validation to explore the mechanisms underlying naringenin treatment of chronic wounds

Integrated network pharmacology and experimental validation to explore the mechanisms underlying naringenin treatment of chronic wounds

Fucoidan promotes angiogenesis and accelerates wound healing through AKT/Nrf2/HIF‐1α signalling pathway

Immunomodulatory biomaterials on chemokine signaling in wound healing

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