Regulation of proliferation and apoptosis of aging periodontal ligament cells by autophagy-related gene 7.

BACKGROUND

Human periodontal ligament cells (hPDLCs) can be applied in periodontal regeneration engineering to repair the tissue defects related to periodontitis. Theoretically, it can affect the vitality of hPDLCs that cell aging increases apoptosis and decreases autophagy. Autophagy is a highly conserved degradation mechanism, which degrades the aging and damaged intracellular organelles through autophagy lysosomes to maintain normal intracellular homeostasis. Meanwhile, autophagy-related gene 7 (ATG7) is a key gene that regulates the level of cellular autophagy.

OBJECTIVE

This study was to explore the effects of autophagic regulation of aging hPDLCs on cell proliferation and cell apoptosis.

METHODS

A cell model of aging hPDLCs overexpressing and silencing ATG7 were respectively constructed by lentiviral vectors in vitro. A series of experiments was performed to confirm relevant senescence phenotype on aging hPDLCs, and to detect the effects of changes in autophagy on their proliferation and apoptosis-related factors in aging hPDLCs.

RESULTS

The results showed that overexpression of ATG7 could motivate autophagy, promoting proliferation of aging hPDLCs and inhibiting apoptosis synchronously (P < 0.05). On the contrary, suppressing autophagy levels by silencing ATG7 would inhibit cell proliferation and accelerate cell senescence (P < 0.05).

CONCLUSION

ATG7 regulates the proliferation and apoptosis of aging hPDLCs. Hence, autophagy may act as a target to delay senescence of hPDLCs, which can be helpful in the future in-depth study on regeneration and functionalization of periodontal supporting tissues.