期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 22, 期 2, 页码 -出版社
MDPI
DOI: 10.3390/ijms22020936
关键词
PRP; PEPD; prolidase; keratinocytes; HaCaT; proliferation; cell cycle
资金
- European Union funds [POWR.03.02.00-00-I051/16]
- PO WER 2014-2020 [08/IMSD/G/2019]
- National Centre of Science, Poland [2017/25/B/NZ7/02650]
- Medical University of Bialystok [SUB/2/DN/19/001/2227]
PRP activates a complex of growth factors and adhesion receptors that stimulate cell proliferation, migration, and collagen biosynthesis, with PEPD playing a key role in EGFR-dependent keratinocyte proliferation. This study provides a novel mechanism for PRP-dependent wound healing.
Although the role of platelet-rich plasma (PRP) in tissue regeneration has been confirmed in many studies, the mechanism of this process is still not fully understood. Human keratinocytes (HaCaT) cells were used as an experimental model for studies on the effects of PRP on cell proliferation, migration, collagen biosynthesis, prolidase activity, and its expression and anabolic signaling. The activation of epidermal growth factor receptor (EGFR), beta(1)-integrin, and insulin-like growth factor-1 receptor (IGF-1R) by PRP were investigated by western blot and immunocytochemistry. It has been found that PRP induced keratinocytes migration and proliferation through activation of cell cycle progression and EGFR downstream signaling. Similar biological effects were achieved by an addition to the culture medium of prolidase (PEPD), a ligand of EGFR (PRP is a rich source of PEPD-2 ng/mL). PRP-dependent stimulation of collagen biosynthesis was accompanied by an increase in the expression of NF-kappa beta, IGF-1R-downstream signaling proteins, and PEPD activity. The data suggest that PRP activates a complex of growth factors and adhesion receptors that stimulate cell proliferation, migration, and collagen biosynthesis. PRP induces PEPD-dependent human keratinocyte proliferation through activation of the EGFR receptor. Our study provides a novel mechanism of PRP-dependent wound healing.
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