ArticleMolecular medicine (Cambridge, Mass.)2014
Activation of poly(ADP-ribose) polymerase-1 delays wound healing by regulating keratinocyte migration and production of inflammatory mediators.
Article in Molecular medicine (Cambridge, Mass.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- Assessment of the Wound-Healing Properties of Almond Oil in a Murine Excisional Wound Model: Biochemical Mechanisms and Translational Perspectives.ACS pharmacology & translational science · 2026Article
- Protein Post-Translational Modifications in UV-Induced Skin Damage.Experimental dermatology · 2026Review
- Expression of Tissue Remodeling- and Inflammation-Related Factors During the Wound-Healing Process in Humans.Journal of personalized medicine · 2025Article
- Investigating Inflammatory Markers in Wound Healing: Understanding Implications and Identifying Artifacts.ACS pharmacology & translational science · 2024Review
- Rosmarinus officinalis L. hexane extract: phytochemical analysis, nanoencapsulation, and in silico, in vitro, and in vivo anti-photoaging potential evaluation.Scientific reports · 2022Article
- Emerging Roles of Post-Translational Modifications in Skin Diseases: Current Knowledge, Challenges and Future Perspectives.Journal of inflammation research · 2022Review
- Review
- The PARP Enzyme Family and the Hallmarks of Cancer Part 2: Hallmarks Related to Cancer Host Interactions.Cancers · 2021Review
- The role of ADP-ribose metabolism in metabolic regulation, adipose tissue differentiation, and metabolism.Genes & development · 2020Review
- The Role of Poly(ADP-Ribose) Polymerase-1 in Cutaneous Wound Healing.Advances in wound care · 2019Review
- Article
- Wound-Healing Markers Revealed by Proximity Extension Assay in Tears of Patients following Glaucoma Surgery.International journal of molecular sciences · 2018Article
- The clinically used PARP inhibitor olaparib improves organ function, suppresses inflammatory responses and accelerates wound healing in a murine model of third-degree burn injury.British journal of pharmacology · 2018Article
- Redox Profiling Reveals Clear Differences between Molecular Patterns of Wound Fluids from Acute and Chronic Wounds.Oxidative medicine and cellular longevity · 2018Article
- Topical 11β-Hydroxysteroid Dehydrogenase Type 1 Inhibition Corrects Cutaneous Features of Systemic Glucocorticoid Excess in Female Mice.Endocrinology · 2018Article
- Trial watch - inhibiting PARP enzymes for anticancer therapy.Molecular & cellular oncology · 2016Review
- Inhibition of poly(ADP-ribose) polymerase 1 protects against acute myeloid leukemia by suppressing the myeloproliferative leukemia virus oncogene.Oncotarget · 2015Article
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Poly(ADP-ribosyl)ation (PARylation) is a protein modification reaction regulating various diverse cellular functions ranging from metabolism, DNA repair and transcription to cell death. We set out to investigate the role of PARylation in wound healing, a highly complex process involving various cellular and humoral factors. We found that topically applied poly[ADP-ribose] polymerase (PARP) inhibitors 3-aminobenzamide and PJ-34 accelerated wound closure in a mouse model of excision wounding. Moreover, wounds also closed faster in PARP-1 knockout mice as compared with wild-type littermates. Immunofluorescent staining for poly(ADP-ribose) (PAR) indicated increased PAR synthesis in scattered cells of the wound bed. Expression of interleukin (IL)-6, tumor necrosis factor (TNF)-α, inducible nitric oxide synthase and matrix metalloproteinase-9 was lower in the wounds of PARP-1 knockout mice as compared with control, and expression of IL-1β, cyclooxygenase-2, TIMP-1 and -2 also were affected. The level of nitrotyrosine (a marker of nitrating stress) was lower in the wounds of PARP-1 knockout animals as compared with controls. In vitro scratch assays revealed significantly faster migration of keratinocytes treated with 3-aminobenzamide or PJ34 as compared with control cells. These data suggest that PARylation by PARP-1 slows down the wound healing process by increasing the production of inflammatory mediators and nitrating stress and by slowing the migration of keratinocytes.
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