Collagen type III resists UVB induced photoaging of HaCaT cells by regulating mTOR signaling pathway

Background

Ultraviolet (UV) is the main factor leading to skin photoaging. In the process of photoaging, the dynamic balance of extracellular matrix is broken, resulting in the increase of reactive oxygen species (ROS), the accumulation of matrix metalloproteinases (MMPs), the decrease of collagen synthesis and the increase of degradation, and the skin becomes loose and wrinkled and pigmented, eventually leading to skin aging.

Objective

To investigate the effect of collagen type III (COLIII) on the autophagy level of human immortalized keratinocytes (HaCaT) induced by ultraviolet B (UVB) and explore whether COLIII can inhibit skin photoaging by changing the autophagy level.

Methods

HaCaT cells were irradiated with UVB to establish a photoaging model, and then the cell migration and repair ability, oxidative stress and inflammation levels, and autophagy levels were detected to explore the effect and mechanism of COLIII on autophagy in photoaged HaCaT cells.

Results

UVB radiation inhibited the cell proliferation and migration repair ability, resulting in the increase of ROS, inflammatory factors IL-6 and MMP-1 in HaCaT cells, while COLIII could attenuate the phototoxicity caused by UVB radiation and resist photoaging. In addition, COLIII can affect the level of autophagy through mTOR signaling pathway and protect HaCaT cells from UVB induced cytotoxicity, thereby attenuating light damage.

Conclusion

COLIII inhibits the autophagy level of UVB irradiated HaCaT cells through mTOR pathway, so as to combat UVB induced skin photoaging.