Lasers in Medical Science

, Volume 33, Issue 3, pp 581–588 | Cite as

Potential role of S100A8 in skin rejuvenation with the 1064-nm Q-switched Nd:YAG laser

Original Article
  • 93 Downloads

Abstract

The 1064-nm Q-switched Nd:YAG laser is demonstrated to be effective for non-ablative skin rejuvenation, but the molecular mechanism by which dermis responses to laser-induced damage and initiates skin remodeling is still unclear. HaCaT cells and 3T3 skin fibroblasts were irradiated with the 1064-nm Q-switched Nd:YAG laser at the different doses. Then, cells were collected and lysed for PCR and Western blot analysis. Cell viability was detected by Cell Counting Kit-8 (CCK-8) before and after laser irradiation. The expressions of S100A8, advanced glycosylation end product-specific receptor (RAGE) and inflammatory cytokines in two cell lines were markedly upregulated after laser treatments. The PCR, Western blot, and ELISA analysis showed the significant increase of type I and III procollagen in the 3T3 cells treated with the 1064-nm laser. Interestingly, si S100A8 effectively inhibited the expression of cytokines and collagen, while S100A8 treatments significantly increased them. P-p38 and p-p65 levels were also elevated after the 1064-nm laser irradiation, which is positively related with S100A8. Cell viability and reactive oxygen species (ROS) levels were not changed, while the content of superoxidase dismutase (SOD) in two cells was increased after laser irradiation. Our results demonstrated that the overexpression of S100A8 induced by the 1064-nm laser irradiation triggered inflammatory reactions in skin cells. The inflammatory microenvironment and improvement of skin antioxidant capacity contribute to new collagen synthesis in the skin cells. Thus, S100A8 was required for laser-induced new collagen synthesis in skin cells. p38/MAPK and NF-κB signal pathways were involved in S100A8-mediated inflammatory reactions in response to laser irradiation.

Keywords

The 1064-nm Q-switched Nd:YAG laser S100A8 Skin inflammatory reactions Collagen 

Notes

Acknowledgements

This work was supported by the National Natural Science Foundation of China (No.81271742).

Compliance with ethical standards

Conflict of interest

The authors declare that they have no conflict of interest.

References

  1. 1.
    Goldberg DJ, Whitworth J (1997) Laser skin resurfacing with the Q-switched Nd: YAG laser. Dermatol Surg 23(10):903–906CrossRefPubMedGoogle Scholar
  2. 2.
    MC LEE, Hu S, MC CHEN, YC SHIH, YL HUANG, SH LEE (2009) Skin rejuvenation with 1,064-nm Q-switched Nd: YAG laser in Asian patients. Dermatol Surg 35(6):929–932CrossRefGoogle Scholar
  3. 3.
    Gold MH, Sensing W, Biron J (2014) Fractional Q-switched 1,064-nm laser for the treatment of photoaged-photodamaged skin. J Cosmet Laser Ther 16(2):69–76CrossRefPubMedGoogle Scholar
  4. 4.
    Yongqian C, Li L, Jianhai B, Ran H, Li G, Hao W, Xining W, Shigang X, Yibing W (2017) A split-face comparison of Q-switched Nd: YAG 1064-nm laser for facial rejuvenation in nevus of Ota patients. Lasers Med Sci:1–5Google Scholar
  5. 5.
    Ye X, Wang L, Dang Y, Liu B, Zhao D (2012) Investigation of the 1064 nm Q-switched Nd: YAG laser on collagen expression in an animal model. Photomed Laser Surg 30(10):604–609CrossRefPubMedGoogle Scholar
  6. 6.
    Dang Y, Ye X, Weng Y, Tong Z, Ren Q (2010) Effects of the 532-nm and 1,064-nm Q-switched Nd: YAG lasers on collagen turnover of cultured human skin fibroblasts: a comparative study. Lasers Med Sci 25(5):719–726CrossRefPubMedGoogle Scholar
  7. 7.
    Dang Y, Ren Q, Li W, Yang Q, Zhang J (2006) Comparison of biophysical properties of skin measured by using non-invasive techniques in the KM mice following 595 nm pulsed dye, 1064 nm Q-switched Nd: YAG and 1320 nm Nd: YAG laser non-ablative rejuvenation. Skin Res Technol 12(2):119–125CrossRefPubMedGoogle Scholar
  8. 8.
    Dessing MC, Butter LM, Teske GJ, Claessen N, Van Der Loos CM, Vogl T, Roth J, Van Der Poll T, Florquin S, Leemans JC (2010) S100A8/A9 is not involved in host defense against murine urinary tract infection. PLoS One 5(10):e13394CrossRefPubMedPubMedCentralGoogle Scholar
  9. 9.
    Ehrchen JM, Sunderkötter C, Foell D, Vogl T, Roth J (2009) The endogenous Toll-like receptor 4 agonist S100A8/S100A9 (calprotectin) as innate amplifier of infection, autoimmunity, and cancer. J Leukoc Biol 86(3):557–566CrossRefPubMedGoogle Scholar
  10. 10.
    Kwon CHMH, Park HJ, Choi JH, Park DY (2013) S100A8 and S100A9 promote invasion and migration through p38 mitogen-activated protein kinase-dependent NF-κB activation in gastric cancer cells. Mol Cells 35(3):226–234CrossRefPubMedPubMedCentralGoogle Scholar
  11. 11.
    Sunahori K, Yamamura M, Yamana J, Takasugi K, Kawashima M, Yamamoto H, Chazin WJ, Nakatani Y, Yui S, Makino H (2006) The S100A8/A9 heterodimer amplifies proinflammatory cytokine production by macrophages via activation of nuclear factor kappa B and p38 mitogen-activated protein kinase in rheumatoid arthritis. Arthritis Res Ther 8(3):R69CrossRefPubMedPubMedCentralGoogle Scholar
  12. 12.
    Ren X, Ge M, Qin X, Xu P, Zhu P, Dang Y, Gu J, Ye X (2016) S100a8/NF-κB signal pathway is involved in the 800-nm diode laser-induced skin collagen remodeling. Lasers Med Sci 31(4):673–678CrossRefPubMedGoogle Scholar
  13. 13.
    Yan Y-Y, Bai J-P, Xie Y, J-Z Y, Ma C-G (2013) The triterpenoid pristimerin induces U87 glioma cell apoptosis through reactive oxygen species-mediated mitochondrial dysfunction. Oncol Lett 5(1):242–248CrossRefPubMedGoogle Scholar
  14. 14.
    Ghavami S, Rashedi I, Dattilo BM, Eshraghi M, Chazin WJ, Hashemi M, Wesselborg S, Kerkhoff C, Los M (2008) S100A8/A9 at low concentration promotes tumor cell growth via RAGE ligation and MAP kinase-dependent pathway. J Leukoc Biol 83(6):1484–1492CrossRefPubMedPubMedCentralGoogle Scholar
  15. 15.
    Preissig J, Hamilton K, Markus R Current laser resurfacing technologies: a review that delves beneath the surface. In: Seminars in plastic surgery, 2012. vol 03. Thieme Medical Publishers, pp 109–116Google Scholar
  16. 16.
    Silva EJ, Argyris PP, Zou X, Ross KF, Herzberg MC (2014) S100A8/A9 regulates MMP-2 expression and invasion and migration by carcinoma cells. Int J Biochem Cell Biol 55:279–287CrossRefPubMedPubMedCentralGoogle Scholar
  17. 17.
    Schieven GL (2005) The biology of p38 kinase: a central role in inflammation. Curr Top Med Chem 5(10):921–928CrossRefPubMedGoogle Scholar
  18. 18.
    Lawrence T (2009) The nuclear factor NF-κB pathway in inflammation. Cold Spring Harb Perspect Biol 1(6):a001651CrossRefPubMedPubMedCentralGoogle Scholar
  19. 19.
    Pandel R, Poljšak B, Godic A, Dahmane R (2013) Skin photoaging and the role of antioxidants in its prevention. ISRN Dermatology 2013Google Scholar

Copyright information

© Springer-Verlag London Ltd., part of Springer Nature 2017

Authors and Affiliations

  1. 1.Institute of Biomedical Sciences, School of Life SciencesEast China Normal UniversityShanghaiChina
  2. 2.Department of Dermatology, Changhai HospitalSecond Military Medical UniversityShanghaiChina

Personalised recommendations