Macrophage phenotype switching in diabetic wounds

NewsBot · Mar 9, 2018

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Pseudomonas aeruginosa infection alters the macrophage phenotype switching process during wound healing in diabetic mice.
Chen S et al
Cell Biol Int. 2018 Mar 7. doi: 10.1002/cbin.10955.

Macrophages play critical roles in wound healing process. They switch from "classically activated" (M1) phenotype in the early inflammatory phase to "alternatively activated" (M2) phenotype in the later healing phase. However, the dynamic process of macrophage phenotype switching in diabetic wounds burdened with bacteria is unclear. In this report, Pseudomonas aeruginosa, frequently detected in diabetic foot ulcers, was inoculated into cutaneous wounds of db/db diabetic mice to mimic bacterium-infected diabetic wound healing. We observed that P. aeruginosa infection impaired diabetic wound healing and quickly promoted the expression of pro-inflammatory genes (M1 macrophage markers) tumor necrosis factor-α (tnf-α), interleukin-1β (il-1β) and il-6 in wounds. The expression of markers of M2 macrophages, including il-10, arginase-1 and ym1 were also upregulated. In addition, similar gene expression patterns were observed in macrophages isolated directly from wounds. Immunostaining showed that P. aeruginosa infection increased both the ratios of M1 and M2 macrophages in wounds compared with that in control groups, which was further confirmed by in vitro culturing macrophages with P. aeruginosa and skin fibroblast conditioned medium. However, the ratios of the expression level of pro-inflammatory genes to anti-inflammatory gene il-10 was increased markedly in P. aeruginosa infected wounds and macrophages compared with that in control groups, and P. aeruginosa prolonged the presence of M1 macrophages in the wounds. These data demonstrated that P. aeruginosa in diabetic wounds activates a mixed M1/M2 macrophage phenotype with an excessive activation of M1 phenotype or relatively inadequate activation of M2 phenotype.
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NewsBot · Aug 9, 2024

Global trends in publications regarding macrophages-related diabetic foot ulcers in the last two decades
Jian-Ping Wen, Shuan-Ji Ou, Jia-Bao Liu, Wei Zhang, Yu-Dun Qu, Jia-Xuan Li, Chang-Liang Xia, Yang Yang, Yong Qi, and Chang-Peng Xu
World J Diabetes. 2024 Jul 15; 15(7): 1627–1644.

BACKGROUND
Diabetic foot ulcers (DFUs) are one of the most severe and popular complications of diabetes. The persistent non-healing of DFUs is the leading cause of ampu-tation, which causes significant mental and financial stress to patients and their families. Macrophages are critical cells in wound healing and perform essential roles in all phases of wound healing. However, no studies have been carried out to systematically illustrate this area from a scientometric point of view. Although there have been some bibliometric studies on diabetes, reports focusing on the investigation of macrophages in DFUs are lacking.

AIM
To perform a bibliometric analysis to systematically assess the current state of research on macrophage-related DFUs.

METHODS
The publications of macrophage-related DFUs from January 1, 2004, to December 31, 2023, were retrieved from the Web of Science Core Collection on January 9, 2024. Four different analytical tools: VOSviewer (v1.6.19), CiteSpace (v6.2.R4), HistCite (v12.03.07), and Excel 2021 were used for the scientometric research.

RESULTS
A total of 330 articles on macrophage-related DFUs were retrieved. The most published countries, institutions, journals, and authors in this field were China, Shanghai Jiao Tong University of China, Wound Repair and Regeneration, and Aristidis Veves. Through the analysis of keyword co-occurrence networks, historical direct citation networks, thematic maps, and trend topics maps, we synthesized the prevailing research hotspots and emerging trends in this field.

CONCLUSION
Our bibliometric analysis provides a comprehensive overview of macrophage-related DFUs research and insights into promising upcoming research.
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NewsBot · Oct 21, 2024

ETS1 Expression in Diabetic Foot Ulcers: Implications for Fibroblast Phenotype and Wound Healing Through the PP2A/YAP Pathway
Wenjuan Yi et al
J Inflamm Res. 2024 Oct 16:17:7373-7388.

Objective: Diabetic foot ulcers (DFUs) are a serious complication of diabetes, characterized by impaired wound healing and high morbidity and mortality risks. While ETS1 is known to influence fibroblast pathological remodeling, its specific role in DFU and fibroblast wound healing remains unclear.

Methods: Skin tissue samples from DFU patients were categorized by Wagner grades to analyze ETS1 expression. Primary fibroblasts derived from diabetes mellitus wound (DMFBs) were collected from wound margins to test migration ability and analyze cell phenotype by immunofluorescence; they were further treated with siETS1 and the ETS1 inhibitor YK-4-279. Techniques including Western blotting, quantitative Real-Time PCR (qRT-PCR), and immunofluorescence were used to assess the expressionof ETS1, Collagen I, and phenotype in DMFBs. Additionally, the binding sites between human ETS1 and the PP2A promoter were predicted by the UCSC and JASPAR databases. It intended to explore the negative transcriptional regulation of PP2A by ETS1 and its implications in fibroblast function and wound healing.

Results: Fibroblasts derived from Wagner Grades II-IV exhibit differences in cell morphology, migratory ability, and phenotype. Our findings indicate a significant upregulation of ETS1 in Wagner III and IV. The downregulation of ETS1 was observed to enhance DMFB migration and increase the expression of Collagen I and α-SMA. These changes suggest a potential mechanism by which PP2A regulates the YAP/Hippo pathway in diabetic wound healing.

Conclusion: ETS1 appears to impede the repair processes in DFUs, likely through the negative regulation of PP2A, affecting fibroblast function and wound healing.
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NewsBot · Oct 29, 2024

SFRP2 modulates functional phenotype transition and energy metabolism of macrophages during diabetic wound healing
Jiaqi Yang et al
Front Immunol. 2024 Oct 11:15:1432402

Diabetic foot ulcer (DFU) is a serious complication of diabetes mellitus, which causes great health damage and economic burden to patients. The pathogenesis of DFU is not fully understood. We screened wound healing-related genes using bioinformatics analysis, and full-thickness skin injury mice model and cellular assays were used to explore the role of target genes in diabetic wound healing. SFRP2 was identified as a wound healing-related gene, and the expression of SFRP2 is associated with immune cell infiltration in DFU. In vivo study showed that suppression of SFRP2 delayed the wound healing process of diabetic mice, impeded angiogenesis and matrix remodeling, but did not affect wound healing process of control mice. In addition, suppression of SFRP2 increased macrophage infiltration and impeded the transition of macrophages functional phenotypes during diabetic wound healing, and affected the transcriptome signatures-related to inflammatory response and energy metabolism at the early stage of wound healing. Extracellular flux analysis (EFA) showed that suppression of SFRP2 decreased mitochondrial energy metabolism and increased glycolysis in injury-related macrophages, but impeded both glycolysis and mitochondrial energy metabolism in inflammatory macrophages. In addition, suppression of SFRP2 inhibited wnt signaling-related genes in macrophages. Treatment of AAV-SFRP2 augmented wound healing in diabetic mice and demonstrated the therapeutic potential of SFRP2. In conclusions, SFRP2 may function as a wound healing-related gene in DFU by modulating functional phenotype transition of macrophages and the balance between mitochondrial energy metabolism and glycolysis.
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NewsBot · Nov 26, 2024

Macrophages: Key players in diabetic wound healing
Xin Zhou et al
World J Diabetes. 2024 Nov 15;15(11):2177-2181

In this editorial, we discuss the article by Wen et al published. Diabetic foot ulcers are prevalent and serious complications of diabetes, significantly impacting patients' quality of life and often leading to disability or death, thereby placing a heavy burden on society. Effective diabetic wound healing is hindered by an imbalance in macrophage polarization; many macrophages fail to transition from the pro-inflammatory M1 phenotype to the anti-inflammatory M2 phenotype, which is crucial for tissue remodelling and repair. The wound healing process is both dynamic and complex. Healthy M1 macrophages, which have strong phagocytic abilities, are vital during the inflammatory phase of diabetic wound healing. However, the failure to transition to M2 macrophages during the proliferative phase hinders wound healing. We anticipate the development of new therapies that can repair damaged M1 macrophages during the inflammatory phase and promote M2 macrophage polarization during the proliferative phase, thereby enhancing the overall healing process.
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Macrophage phenotype switching in diabetic wounds

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Macrophage phenotype switching in diabetic wounds

NewsBot The Admin that posts the news.

NewsBot The Admin that posts the news.

NewsBot The Admin that posts the news.

NewsBot The Admin that posts the news.

NewsBot The Admin that posts the news.

Macrophage stimulating agent for diabetic foot ulcers

Monocyte Phenotype as a Predictive Marker for Wound Healing in Diabetic Foot Ulcers

Feeling of cold feet is a heritable phenotype

Share This Page

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