A protein called OPN3 may play a role in skin ageing caused by sunlight. (1st May 2020)

• Record Type: Journal Article
• Authors: Lan, Y.; Wang, Y.; Lu, H.
• Is Part Of: British journal of dermatology. Volume 182:Number 5(2020)
• Page Start: e164
• Page End: e164
• Publication Date: 2020-05-01
• Subjects: Dermatology -- Periodicals; Skin -- Diseases -- Periodicals; 616.5
• DOI: 10.1111/bjd.18990
• Languages: English
• ISSNs: 0007-0963

Abstract

Summary: Our skin is regularly exposed to UV radiation from the sun. Chronic, meaning long‐term, exposure to UV radiation (mainly a type of UV called UVA) causes an increase in enzymes called matrix metalloproteinases (MMPs), especially MMP1, MMP2, MMP3 and MMP9, in skin cells called human dermal fibroblasts (HDFs). MMPs can lead to the breakdown of fibrous connective tissue which gives the skin its support and structure, and this is the most important cause of skin photo‐aging (skin aging caused by UV). We don't exactly know how, on a molecular level, fibroblasts sense UVA and trigger signals via cells to MMPs. This study looked at a type of protein in the body called Opsins (OPNs) which can change their signaling pathways (how they communicate with other cells) in response to being hit by light. OPNs play a vital role in our sight, circadian rhythm (our sleep‐wake cycle) and how the eye's pupil responds to light. This study provides evidence that a type of OPNs called OPN3 plays a role in the production of MMP1, MMP2, MMP3 and MMP9 in HDFs following UVA exposure. This provide insights into the understanding of the molecular mechanisms through which human skin cells respond to UVA radiation, and may reveal molecular targets for preventing or treating skin photo‐ageing. This is a summary of the study: Opsin 3 is a key regulator of ultraviolet A‐induced photoageing in human dermal fibroblast cells.