Cellular and physiological upregulation of inducible nitric oxide synthase, arginase, and inducible cyclooxygenase in wound healing

Wound repair is regulated by overlapping cellular, physiological and biochemical events. Prostaglandins and nitric oxide have been a focus for inflammation research particularly since the discovery of their inducible isoforms nitric oxide synthase (iNOS) and cyclooxygenase‐2 (COX‐2). Study of the ce...

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Bibliographic Details
Published in:Journal of cellular physiology 2019-12, Vol.234 (12), p.23618-23632
Main Authors: Abd El‐Aleem, Seham A., Abdelwahab, Soha, AM‐Sherief, Hany, Sayed, Ahmed
Format: Article
Language:English
Subjects:
Arginase
chronic wound
cyclooxygenase
Enzymes
Immunocytochemistry
inducible nitric oxide synthase
Inflammation
Isoforms
keloid
Macrophages
Nitric oxide
Nitric-oxide synthase
Physiology
Prostaglandin endoperoxide synthase
Prostaglandins
Proteins
Repair
Rodents
Skin
Substrates
ulcer
Up-regulation
Wound healing
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Summary:Wound repair is regulated by overlapping cellular, physiological and biochemical events. Prostaglandins and nitric oxide have been a focus for inflammation research particularly since the discovery of their inducible isoforms nitric oxide synthase (iNOS) and cyclooxygenase‐2 (COX‐2). Study of the cellular expression of iNOS and COX‐2 and arginase which competes with iNOS for its substrate, in an in vivo model of wound healing could reveal important roles for these enzymes in the physiological progression of wound repair. Adult male rats received full thickness dermal wounds which were harvested at different times. Protein levels and activities of the enzymes were assessed by western blot and biochemical assays respectively. The cellular distribution and the colocalization were assessed by immunostaining. The protein levels and activities of iNOS, arginase, and COX‐2 increased only during the inflammatory phase of wound. Immunocytochemistry showed that the three enzymes were coexpressed and the main cellular source was inflammatory cells mainly macrophages. iNOS was induced at the wound site and was the earliest to increase significantly (p 
ISSN:0021-9541
1097-4652
DOI:10.1002/jcp.28930