Wound healing delays in α-Klotho-deficient mice that have skin appearance similar to that in aged humans - Study of delayed wound healing mechanism.
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| Abstract |
Skin atrophy and delayed wound healing are observed in aged humans; however, the molecular mechanism are still elusive. The aim of this study was to analyze the molecular mechanisms of delayed wound healing by aging using α-Klotho-deficient (kl/kl) mice, which have phenotypes similar to those of aged humans. The kl/kl mice showed delayed wound healing and impaired granulation formation compared with those in wild-type (WT) mice. The skin graft experiments revealed that delayed wound healing depends on humoral factors, but not on kl/kl skin tissue. The mRNA expression levels of cytokines related to acute inflammation including IL-1β, IL-6 and TNF-α were higher in wound lesions of kl/kl mice compared with the levels in WT mice by RT-PCR analysis. LPS-induced TNF-α production model using spleen cells revealed that TNF-α production was significantly increased in the presence of FGF23. Thus, higher levels of FGF23 in kl/kl mouse may have a role to increase TNF-α production in would lesion independently of α-Klotho protein, and impair granulation formation and delay wound healing.
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| Authors | Makoto Yamauchi, Yoshihiko Hirohashi, Toshihiko Torigoe, Yoshitaka Matsumoto, Ken Yamashita, Musashi Kayama, Noriyuki Sato, Takatoshi Yotsuyanagi |
| Journal | Biochemical and biophysical research communications (Biochem Biophys Res Commun) Vol. 473 Issue 4 Pg. 845-852 (05 13 2016) ISSN: 1090-2104 [Electronic] United States |
| PMID | 27037022 (Publication Type: Journal Article) |
| Copyright | Copyright © 2016 Elsevier Inc. All rights reserved. |
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