4.1 Article

Denatured Collagen Could Increase the Autophagy Level and Inhibit Apoptosis of Fibroblasts to Help Cell Survival and Influence Wound Healing

Journal

Publisher

SAGE PUBLICATIONS INC
DOI: 10.1177/1534734620925942

Keywords

denatured collagen; fibroblast; autophagy; apoptosis

Funding

  1. National Natural Science Foundation of China [81971832]
  2. Natural Science Foundation of Shanghai [19ZR1432100]

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This study investigated the regulatory role of denatured collagen on autophagy and apoptosis in fibroblasts. The results showed that denatured collagen stimulation enhanced autophagy and inhibited apoptosis in fibroblasts. This suggests that denatured collagen promotes cell survival and influences wound healing.
When exposed to thermal factors, collagen in the dermis denatures, which could affect the biological behavior of cells. Previous studies have demonstrated that denatured collagen could influence the activity of fibroblasts and induce fibroblasts differentiate into myofibroblasts. However, information on the regulation of fibroblasts by denatured collagen-modulated autophagy and apoptosis during the wound healing process is limited. In this article, we researched the effect of denatured collagen-modulated autophagy and apoptosis on fibroblasts. An in vitro model comprising fibroblasts and denatured collagen was established to identify the potential ability of denatured collagen to modulate autophagy and apoptosis. Western blotting, quantitative polymerase chain reaction, transmission electron microscopy, TUNEL assay, and immunofluorescence staining were used to examine the changes induced by denatured collage. Protein and mRNA levels of LC3 and beclin-1 were significantly increased after stimulated by denatured collagen, while those of caspase-3 were reduced. Unlike stimulation with normal collagen, denatured collagen enhanced autophagy and inhibited apoptosis of fibroblasts. After blocking autophagy using 3-methyladenine, the apoptotic function was increased. Denatured collagen could increase autophagy and inhibit apoptosis of the fibroblasts to promote cell survival and influence wound healing.

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