Impaired Healing of a Cutaneous Wound in an Inducible Nitric Oxide Synthase-Knockout Mouse

Background. We investigated the effects of loss of inducible nitric oxide synthase (iNOS) on the healing process of cutaneous excisional injury by using iNOS-null (KO) mice. Population of granulation tissue-related cell types, that is, myofibroblasts and macrophages, growth factor expression, and re...

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Main Authors: Takashi Kitano, Hiroshi Yamada, Maki Kida, Yuka Okada, Shizuya Saika, Munehito Yoshida
Format: Article
Language:English
Published: Wiley 2017-01-01
Series:Dermatology Research and Practice
Online Access:http://dx.doi.org/10.1155/2017/2184040
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author Takashi Kitano
Hiroshi Yamada
Maki Kida
Yuka Okada
Shizuya Saika
Munehito Yoshida
author_facet Takashi Kitano
Hiroshi Yamada
Maki Kida
Yuka Okada
Shizuya Saika
Munehito Yoshida
author_sort Takashi Kitano
collection DOAJ
description Background. We investigated the effects of loss of inducible nitric oxide synthase (iNOS) on the healing process of cutaneous excisional injury by using iNOS-null (KO) mice. Population of granulation tissue-related cell types, that is, myofibroblasts and macrophages, growth factor expression, and reepithelialization were evaluated. Methods. KO and wild type (WT) mice of C57BL/6 background were used. Under general anesthesia two round full-thickness excision wounds of 5.0 mm in diameter were produced in dorsal skin. After specific intervals of healing, macroscopic observation, histology, immunohistochemistry, and real-time reverse transcription-polymerase chain reaction (RT-PCR) were employed to evaluate the healing process. Results. The loss of iNOS retards granulation tissue formation and reepithelialization in excision wound model in mice. Detailed analyses showed that myofibroblast appearance, macrophage infiltration, and mRNA expression of transforming growth factor b and of collagen 1α2 were all suppressed by lacking iNOS. Conclusions. iNOS is required in the process of cutaneous wound healing. Lacking iNOS retards macrophage invasion and its expression of fibrogenic components that might further impair fibrogenic behaviors of fibroblasts.
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spelling doaj-art-058afba3f0ea43a1b737c6efceeee56f2025-02-03T01:24:21ZengWileyDermatology Research and Practice1687-61051687-61132017-01-01201710.1155/2017/21840402184040Impaired Healing of a Cutaneous Wound in an Inducible Nitric Oxide Synthase-Knockout MouseTakashi Kitano0Hiroshi Yamada1Maki Kida2Yuka Okada3Shizuya Saika4Munehito Yoshida5Department of Orthopedic Surgery, Wakayama Medical University School of Medicine, 811-1 Kimiidera, Wakayama 641-0012, JapanDepartment of Orthopedic Surgery, Wakayama Medical University School of Medicine, 811-1 Kimiidera, Wakayama 641-0012, JapanDepartment of Ophthalmology, Wakayama Medical University School of Medicine, 811-1 Kimiidera, Wakayama 641-0012, JapanDepartment of Critical Care Medicine, Wakayama Medical University School of Medicine, 811-1 Kimiidera, Wakayama 641-0012, JapanDepartment of Critical Care Medicine, Wakayama Medical University School of Medicine, 811-1 Kimiidera, Wakayama 641-0012, JapanDepartment of Orthopedic Surgery, Wakayama Medical University School of Medicine, 811-1 Kimiidera, Wakayama 641-0012, JapanBackground. We investigated the effects of loss of inducible nitric oxide synthase (iNOS) on the healing process of cutaneous excisional injury by using iNOS-null (KO) mice. Population of granulation tissue-related cell types, that is, myofibroblasts and macrophages, growth factor expression, and reepithelialization were evaluated. Methods. KO and wild type (WT) mice of C57BL/6 background were used. Under general anesthesia two round full-thickness excision wounds of 5.0 mm in diameter were produced in dorsal skin. After specific intervals of healing, macroscopic observation, histology, immunohistochemistry, and real-time reverse transcription-polymerase chain reaction (RT-PCR) were employed to evaluate the healing process. Results. The loss of iNOS retards granulation tissue formation and reepithelialization in excision wound model in mice. Detailed analyses showed that myofibroblast appearance, macrophage infiltration, and mRNA expression of transforming growth factor b and of collagen 1α2 were all suppressed by lacking iNOS. Conclusions. iNOS is required in the process of cutaneous wound healing. Lacking iNOS retards macrophage invasion and its expression of fibrogenic components that might further impair fibrogenic behaviors of fibroblasts.http://dx.doi.org/10.1155/2017/2184040
spellingShingle Takashi Kitano
Hiroshi Yamada
Maki Kida
Yuka Okada
Shizuya Saika
Munehito Yoshida
Impaired Healing of a Cutaneous Wound in an Inducible Nitric Oxide Synthase-Knockout Mouse
Dermatology Research and Practice
title Impaired Healing of a Cutaneous Wound in an Inducible Nitric Oxide Synthase-Knockout Mouse
title_full Impaired Healing of a Cutaneous Wound in an Inducible Nitric Oxide Synthase-Knockout Mouse
title_fullStr Impaired Healing of a Cutaneous Wound in an Inducible Nitric Oxide Synthase-Knockout Mouse
title_full_unstemmed Impaired Healing of a Cutaneous Wound in an Inducible Nitric Oxide Synthase-Knockout Mouse
title_short Impaired Healing of a Cutaneous Wound in an Inducible Nitric Oxide Synthase-Knockout Mouse
title_sort impaired healing of a cutaneous wound in an inducible nitric oxide synthase knockout mouse
url http://dx.doi.org/10.1155/2017/2184040
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