cellular response to UV-A

Definition

Target type: biologicalprocess

Any process that results in a change in state or activity of a cell (in terms of movement, secretion, enzyme production, gene expression, etc.) as a result of a UV-A radiation stimulus. UV-A radiation (UV-A light) spans the wavelengths 315 to 400 nm. [GOC:mah]

Cellular response to UV-A is a complex process involving multiple signaling pathways and molecular mechanisms that ultimately lead to the repair of DNA damage and the maintenance of cellular homeostasis. UV-A radiation, with wavelengths ranging from 315 to 400 nm, penetrates deeper into the skin than UVB and can cause a variety of cellular effects.

Upon exposure to UV-A, various cellular components, including DNA, proteins, and lipids, can be directly or indirectly affected. The primary mechanism of UV-A-induced DNA damage is the generation of reactive oxygen species (ROS), particularly singlet oxygen (¹O2). These ROS can directly damage DNA, leading to the formation of various lesions, including cyclobutane pyrimidine dimers (CPDs) and 6-4 photoproducts (6-4PPs). However, UV-A is less efficient at directly inducing CPDs and 6-4PPs compared to UVB.

UV-A can also cause indirect damage to DNA through the activation of signaling pathways involving the MAPK (mitogen-activated protein kinase) and NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) pathways. These pathways are activated by the generation of ROS and the activation of various signaling molecules, such as p38 MAPK and JNK (c-Jun N-terminal kinase). Activation of these pathways leads to the expression of various genes involved in DNA repair, cell cycle arrest, and apoptosis.

One of the key mechanisms involved in cellular response to UV-A is DNA repair. Cells have evolved sophisticated mechanisms to repair UV-A-induced DNA damage. The major DNA repair pathways involved in repairing UV-A-induced damage include nucleotide excision repair (NER), base excision repair (BER), and mismatch repair (MMR). NER is the primary pathway responsible for repairing CPDs and 6-4PPs, which are the most prevalent UV-A-induced DNA lesions. BER is involved in repairing oxidative damage to DNA bases caused by ROS generated by UV-A.

In addition to DNA repair, cells can also activate other responses to mitigate the damaging effects of UV-A, including cell cycle arrest and apoptosis. Cell cycle arrest allows time for DNA repair to occur before cells progress through the cell cycle and potentially replicate damaged DNA, leading to mutations. Apoptosis, or programmed cell death, eliminates severely damaged cells, preventing the propagation of damaged cells.

Cellular response to UV-A is a dynamic process that involves multiple cellular signaling pathways and molecular mechanisms. The specific response of a cell to UV-A depends on various factors, including the dose of UV-A exposure, the type of cell, and the cell's repair capacity. Understanding the intricate mechanisms involved in cellular response to UV-A is crucial for developing strategies to prevent and treat UV-A-induced skin damage and cancer.'
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Proteins (6)

Compounds (152)