Photoaging: why “Bad” Collagen builds up.

UV-mediated downregulation of the endocytic collagen receptor, Endo180, contributes to accumulation of extracellular collagen fragments in photoaged skin.
Tang S, Lucius R, Wenck H, Gallinat S, Weise JM.
J Dermatol Sci. 2013 Apr;70(1):42-8. doi: 10.1016/j.jdermsci.2013.01.008. Epub 2013 Feb 4.

• Skin aging can be divided into two parts:
  • intrinsic aging or the passing of years. Nothing much we can do about this and it mainly depends on genetic factors ! It mostly appears as fine wrinkles.
  • extrinsic aging or aging caused by the environment. Ultraviolet-light (UV) is an important cause and photoaged skin is typically thickened with the presence of deep wrinkles.

• Photoaged skin is thickened and is named solar elastosis in histological terms. Under the microscope, broken elastin fibers can be seen and and even at higher magnification collagen bundles are found to be of abnormal structure and arrangement.
• This accumulation of collagen appears to be the result of the impossibility of fibroblasts (main cells responsible for the structural elements in the dermis and produce for example hyaluronic acid and collagen) to re-uptake and degrade collagen fibers.
• The authors show in cell cultures done on fibroblasts from skin biopsies that:
  • The endocytic collagen receptor, Endo180:
    • is needed for reuptake of collagen reuptake
    • its expression is reduced with UV irradiation and collagen accumulates as a result (immunostaining)
  • alpha-2 integrin expression is also altered with UV-irradiation and it plays an important role to bing collagen initially.

• To conclude: photoaging appears to be mediated through specific mechanisms triggered by ultraviolet irradiation. It would be interesting to see this in lesions linked with photoaging such as non-melanoma skin cancers (NMSC, Basal Cell and Squamous Cell Carcinomas), melanomas and precancerous skin lesions (actinic keratosis).

Contributors

Dr Christophe Hsu – dermatologist. Geneva, Switzerland