| First Author | Yamauchi M | Year | 2016 |
| Journal | Biochem Biophys Res Commun | Volume | 473 |
| Issue | 4 | Pages | 845-852 |
| PubMed ID | 27037022 | Mgi Jnum | J:234961 |
| Mgi Id | MGI:5792482 | Doi | 10.1016/j.bbrc.2016.03.138 |
| Citation | Yamauchi M, et al. (2016) Wound healing delays in alpha-Klotho-deficient mice that have skin appearance similar to that in aged humans - Study of delayed wound healing mechanism. Biochem Biophys Res Commun 473(4):845-52 |
| abstractText | 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 alpha-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-1beta, IL-6 and TNF-alpha were higher in wound lesions of kl/kl mice compared with the levels in WT mice by RT-PCR analysis. LPS-induced TNF-alpha production model using spleen cells revealed that TNF-alpha 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-alpha production in would lesion independently of alpha-Klotho protein, and impair granulation formation and delay wound healing. |
