A study conducted by researchers at Boston University School of Medicine (BUSM) provides new evidence that long-wave ultraviolet light (UVA) induces a protein that could result in premature skin ageing. The findings demonstrate that aspects of photoageing, the process of skin ageing by chronic exposure to ultraviolet radiation, could be linked to genetic factors that accelerate the ageing process when induced by the environment.

The study, published in the Journal of Investigative Dermatology, was led by BUSM co-authors Thomas M. Ruenger, Professor and Vice Chair of the department of dermatology, and Hirotaka Takeuchi, MS.


Photoageing is attributed to continuous exposure to UVA and shortwave ultraviolet light (UVB) rays over a long period of time, and affects skin surfaces most often exposed to sunlight, including the face, ears, hands and neck. The UVA or UVB rays can be from the sun or from synthetic sources, such as tanning beds.

Progerin is a protein that has been associated with both normal and abnormal ageing. In Hutchinson Gilford Progeria syndrome, a genetic disorder characterised by a vast acceleration of ageing of most organs, expression and accumulation of progerin is caused by a mutation in the Lamin A gene.

In this study, skin cells were cultured and exposed to UVB or UVA rays and then examined for expression and accumulation of progerin. The results showed that progerin is induced by ultraviolet light, specifically UVA rays, and that this induction is mediated by reactive oxygen species causing alternative splicing of the LaminA gene pre-mRNA.

The researchers also note that some aspects of photoageing should be regarded as a process of damage-accelerated intrinsic ageing and that intrinsic and extrinsic ageing are interdependent.