Display options
Cite
Boutrand LB, Thépot A, Muther C, et al. Repeated short climatic change affects the epidermal differentiation program and leads to matrix remodeling in a human organotypic skin model. Clin Cosmet Investig Dermatol. 2017;10:43-50doi: 10.2147/CCID.S120800.
Boutrand, L. B., Thépot, A., Muther, C., Boher, A., Robic, J., Guéré, C., Vié, K., Damour, O., & Lamartine, J. (2017). Repeated short climatic change affects the epidermal differentiation program and leads to matrix remodeling in a human organotypic skin model. Clinical, cosmetic and investigational dermatology, 1043-50. https://doi.org/10.2147/CCID.S120800
Boutrand, Laetitia-Barbollat, et al. "Repeated short climatic change affects the epidermal differentiation program and leads to matrix remodeling in a human organotypic skin model." Clinical, cosmetic and investigational dermatology vol. 10 (2017): 43-50. doi: https://doi.org/10.2147/CCID.S120800
Boutrand LB, Thépot A, Muther C, Boher A, Robic J, Guéré C, Vié K, Damour O, Lamartine J. Repeated short climatic change affects the epidermal differentiation program and leads to matrix remodeling in a human organotypic skin model. Clin Cosmet Investig Dermatol. 2017 Feb 13;10:43-50. doi: 10.2147/CCID.S120800. eCollection 2017. PMID: 28243135; PMCID: PMC5315211.
Copy Download .nbib Format: NLM
Share it on

Clin Cosmet Investig Dermatol. 2017 Feb 13;10:43-50. doi: 10.2147/CCID.S120800. eCollection 2017.

Repeated short climatic change affects the epidermal differentiation program and leads to matrix remodeling in a human organotypic skin model.

Clinical, cosmetic and investigational dermatology

Laetitia-Barbollat Boutrand, Amélie Thépot, Charlotte Muther, Aurélie Boher, Julie Robic, Christelle Guéré, Katell Vié, Odile Damour, Jérôme Lamartine

Affiliations

  1. Departement de Biologie, Université Claude Bernard Lyon I.
  2. LabSkinCreations.
  3. CNRS UMR5305, Laboratoire de Biologie Tissulaire et d'Ingénierie Thérapeutique (LBTI), Lyon.
  4. Laboratoires Clarins, Cergy-Pontoise.
  5. Banque de Tissus et Cellules, Hospices Civiles de Lyon, Lyon, France.
  6. Departement de Biologie, Université Claude Bernard Lyon I; CNRS UMR5305, Laboratoire de Biologie Tissulaire et d'Ingénierie Thérapeutique (LBTI), Lyon.

PMID: 28243135 PMCID: PMC5315211 DOI: 10.2147/CCID.S120800

Abstract

Human skin is subject to frequent changes in ambient temperature and humidity and needs to cope with these environmental modifications. To decipher the molecular response of human skin to repeated climatic change, a versatile model of skin equivalent subject to "hot-wet" (40°C, 80% relative humidity [RH]) or "cold-dry" (10°C, 40% RH) climatic stress repeated daily was used. To obtain an exhaustive view of the molecular mechanisms elicited by climatic change, large-scale gene expression DNA microarray analysis was performed and modulated function was determined by bioinformatic annotation. This analysis revealed several functions, including epidermal differentiation and extracellular matrix, impacted by repeated variations in climatic conditions. Some of these molecular changes were confirmed by histological examination and protein expression. Both treatments (hot-wet and cold-dry) reduced the expression of genes encoding collagens, laminin, and proteoglycans, suggesting a profound remodeling of the extracellular matrix. Strong induction of the entire family of late cornified envelope genes after cold-dry exposure, confirmed at protein level, was also observed. These changes correlated with an increase in epidermal differentiation markers such as corneodesmosin and a thickening of the stratum corneum, indicating possible implementation of defense mechanisms against dehydration. This study for the first time reveals the complex pattern of molecular response allowing adaption of human skin to repeated change in its climatic environment.

Keywords: climatic changes; collagen; organotypic tissue; skin; transcriptome

Conflict of interest statement

Disclosure An abstract of this paper was presented at the 46th annual ESDR meeting in Munich (September 2016) as a poster presentation with interim findings. The authors report no conflicts of interes

References

  1. Mol Cell Biochem. 2005 Sep;277(1-2):63-72 - PubMed
  2. J Invest Dermatol. 2008 Dec;128(12):2880-7 - PubMed
  3. J Invest Dermatol. 2005 May;124(5):1062-70 - PubMed
  4. Tissue Eng. 2005 May-Jun;11(5-6):723-33 - PubMed
  5. Am J Pathol. 2011 Apr;178(4):1470-7 - PubMed
  6. Eur J Dermatol. 2016 Aug 1;26(4):350-60 - PubMed
  7. Skin Res Technol. 2008 May;14(2):180-6 - PubMed
  8. Nat Protoc. 2008;3(6):1101-8 - PubMed
  9. Br J Dermatol. 2003 Jun;148(6):1149-52 - PubMed
  10. Br J Dermatol. 2012 Jun;166(6):1245-54 - PubMed
  11. PLoS One. 2014 Feb 05;9(2):e86092 - PubMed
  12. J Korean Med Sci. 2011 Mar;26(3):417-24 - PubMed
  13. J Dermatol Sci. 2000 Dec;24 Suppl 1:S22-8 - PubMed
  14. Int J Cosmet Sci. 2008 Oct;30(5):313-22 - PubMed
  15. PLoS One. 2014 Mar 17;9(3):e92254 - PubMed
  16. Matrix Biol. 2015 Sep;47:85-97 - PubMed
  17. J Cell Biochem. 2005 Jun 1;95(3):620-31 - PubMed
  18. Nat Protoc. 2009;4(1):44-57 - PubMed
  19. J Invest Dermatol. 1998 Nov;111(5):873-8 - PubMed
  20. Br J Dermatol. 2016 Apr;174(4):795-802 - PubMed
  21. Mol Cell Biochem. 2013 Jul;379(1-2):235-41 - PubMed
  22. Photodermatol Photoimmunol Photomed. 2002 Oct;18(5):253-61 - PubMed

Publication Types