ArticleJournal of immunology (Baltimore, Md. : 1950)2016
Enforced Expression of Hoxa3 Inhibits Classical and Promotes Alternative Activation of Macrophages In Vitro and In Vivo.
Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
25 citing papers in PubMed, 30 citations in OpenAlex.
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- Pharmacological restriction of genomic binding sites redirects PU.1 pioneer transcription factor activity.Nature genetics · 2024Article
- HOXA3 accelerates wound healing in diabetic and aged non-diabetic mammals.Scientific reports · 2023Article
- Genome-wide association study for the free amino acid and nucleotide components of breast meat in an FJournal of animal science and technology · 2023Article
- Macrophage Phenotypes in Normal and Diabetic Wound Healing and Therapeutic Interventions.Cells · 2022Review
- Signaling Pathways Associated with Chronic Wound Progression: A Systems Biology Approach.Antioxidants (Basel, Switzerland) · 2022Article
- Identification of macrophages in normal and injured mouse tissues using reporter lines and antibodies.Scientific reports · 2022Article
- Induction of HOXA3 by Porcine Reproductive and Respiratory Syndrome Virus Inhibits Type I Interferon Response through Negative Regulation of HO-1 Transcription.Journal of virology · 2022Article
- Age-Related Alterations in Macrophage Distribution and Function Are Associated With Delayed Cutaneous Wound Healing.Frontiers in immunology · 2022Article
- Molecular subtypes, clinical significance, and tumor immune landscape of angiogenesis-related genes in ovarian cancer.Frontiers in oncology · 2022Article
- MiRNA-494 enhances M1 macrophage polarization via Nrdp1 in ICH mice model.Journal of inflammation (London, England) · 2020Article
- The Immunosuppressant Fingolimod (FTY720) for the Treatment of Mechanical Force-Induced Abnormal Scars.Journal of immunology research · 2020Article
- DNA methylation analysis of negative pressure therapy effect in diabetic foot ulcers.Endocrine connections · 2019Article
- LncRNA HOXA-AS3 confers cisplatin resistance by interacting with HOXA3 in non-small-cell lung carcinoma cells.Oncogenesis · 2019Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The regulated differentiation of macrophages (mφs) and their subsequent activation into proinflammatory or prohealing subtypes is critical for efficient wound healing. Chronic wounds such as diabetic (db) ulcers are associated with dysregulation of macrophage function. Whereas non-db mφs polarize to an M2-like, prohealing phenotype during the late stages of healing, db-derived mφs continue to display an M1-like, proinflammatory, or a mixed M1-like/M2-like phenotype. We have previously shown that sustained expression of Hoxa3 reduces the excessive number of leukocytes within the db wound; however, the effect of Hoxa3 on mφ polarization was unknown. In this study, we show that Hoxa3 protein transduction of mφs in vitro enhances macrophage maturation, inhibits M1 polarization, and promotes M2 polarization, in part via regulation of Pu.1/Spi1 and Stat6. Sustained expression of Hoxa3 in vivo in db wounds reduces the number of Nos2(+) (M1-like) mφs, increases the number of Arg1(+) and VEGF(+) (M2-like) mφs, and accelerates healing in a DNA-binding independent manner. Our findings suggest a role for Hox protein activity in promoting M1-to-M2-like phenotypic switching via interactions with myeloid transcription factors and provide insight into mechanisms regulating this process in db wound healing.
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Registered trials
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