2. Academic Validation
  3. Collagen I protects human keratinocytes HaCaT against UVB injury via restoring PINK1/parkin-mediated mitophagy

Collagen I protects human keratinocytes HaCaT against UVB injury via restoring PINK1/parkin-mediated mitophagy

  • Arch Biochem Biophys. 2024 Jan 26:109905. doi: 10.1016/j.abb.2024.109905.
Yuying Zhu 1,  Wendie Xiang 1,  Sijun He 1,  Zhao San 1,  Weiwei Liu 1,  Jin Wu 1,  Toshihiko Hayashi 2,  Kazunori Mizuno 3,  Shunji Hattori 3,  Hitomi Fujisaki 3,  Takashi Ikejima 4
Affiliations

Affiliations

  • 1 Wuya College of Innovation, Shenyang Pharmaceutical University, Shenyang, 110016, Liaoning, China.
  • 2 Wuya College of Innovation, Shenyang Pharmaceutical University, Shenyang, 110016, Liaoning, China; Nippi Research Institute of Biomatrix, Toride, Ibaraki, 302-0017, Japan.
  • 3 Nippi Research Institute of Biomatrix, Toride, Ibaraki, 302-0017, Japan.
  • 4 Wuya College of Innovation, Shenyang Pharmaceutical University, Shenyang, 110016, Liaoning, China; Key Laboratory of Computational Chemistry-Based Natural Antitumor Drug Research & Development, Liaoning, China. Electronic address: [email protected].
PMID: 38281543 DOI: 10.1016/j.abb.2024.109905
Abstract

Collagen I is a major component of extracellular matrix in human skin, and is also widely used in a variety of skin-care products. In this study, we investigated the modulatory roles of collagen I on human immortalized keratinocytes HaCaT, especially when cells were irradiated with UVB. Interestingly, the cells grown on plates coated by molecular collagen I, but not fibrillar collagen I, acquired certain resistance against UVB damages, as shown by increased survival and reduced Apoptosis. The accumulation of dysfunctional mitochondria in UVB-treated cells was attenuated by molecular collagen I-coating. Interestingly, molecular collagen I rescued the loss of mitochondrial biogenesis in cells treated with UVB. Loss of PINK1/parkin-mediated Mitophagy was dominant for the accumulation of dysfunctional mitochondria after UVB irradiation. Of note, cells cultured on molecular collagen I-precoated plates exhibited reserved Mitophagy after UVB irradiation, as reflected by the enhanced protein level of PINK1/parkin, increased mitochondrial ubiquitin and the co-localization of lysosomes and mitochondria. Moreover, in UVB-treated cells, inhibiting Mitophagy by Cyclosporin A, or by silencing PINK1 or parkin, disturbed the resolution of mitochondrial stress and reduced the protective effect of molecular collagen I, indicating that Mitophagy is pivotal for the protection of collagen I against UVB damage in keratinocytes HaCaT. Collectively, this study reveals an unexpected protective role of collagen I, which facilitates Mitophagy to rescue cells under UVB irradiation, providing a new direction for clinical application of collagen products.

Keywords

Apoptosis; Collagen I; HaCaT cells; Mitophagy; UVB.

Figures
Products