1. Academic Validation
  2. ANXA2 promotes osteogenic differentiation and inhibits cellular senescence of periodontal ligament cells (PDLCs) in high glucose conditions

ANXA2 promotes osteogenic differentiation and inhibits cellular senescence of periodontal ligament cells (PDLCs) in high glucose conditions

  • PeerJ. 2024 Sep 18:12:e18064. doi: 10.7717/peerj.18064.
Yanlin Huang 1 2 Jiaye Wang 1 2 Chunhui Jiang 1 2 Minghe Zheng 3 Mingfang Han 1 2 Qian Fang 1 2 Yizhao Liu 1 2 Ru Li 1 2 Liangjun Zhong 1 2 Zehui Li 1 2
Affiliations

Affiliations

  • 1 Hangzhou Normal University, Zhejiang, China.
  • 2 Department of Stomatology, The Affiliated Hospital of Hangzhou Normal University, Zhejiang, China.
  • 3 Department of Stomatology, No.904 Hospital of the Joint Logistics Support Force of the Chinese People's Liberation Army, Jiangsu Province, Wuxi, China.
Abstract

Background: Periodontal ligament cells (PDLCs) are a major component of the periodontal ligament and have an important role in the regeneration of periodontal tissue and maintenance of homeostasis. High glucose can affect the activity and function of PDLCs in a variety of ways; therefore, it is particularly important to find ways to alleviate the effects of high glucose on PDLCs. Annexin A2 (ANXA2) is a calcium- and phospholipid-binding protein involved in a variety of cellular functions and processes, including cellular cytokinesis, cytophagy, migration, and proliferation.

Aim: The aim of this study was to exploring whether ANXA2 attenuates the deleterious effects of high glucose on PDLCs and promotes osteogenic differentiation capacity.

Methods and results: Osteogenic differentiation potential, cellular senescence, oxidative stress, and cellular Autophagy were detected. Culturing PDLCs with medium containing different glucose concentrations (CTRL, 8 mM, 10 mM, 25 mM, and 40 mM) revealed that high glucose decreased the protein expression of ANXA2 (p < 0.0001). In addition, high glucose decreased the osteogenic differentiation potential of PDLCs as evidenced by decreased calcium deposition (p = 0.0003), lowered ALP activity (p = 0.0010), and a decline in the expression of osteogenesis-related genes (p = 0.0008). Moreover, β-Galactosidase staining and expression of p16, p21 and p53 genes showed that it increased cellular senescence in PDLCs (p < 0.0001). Meanwhile high glucose increased oxidative stress in PDLCs as shown by ROS (p < 0.0001). However, these damages caused by high glucose were inhibited after the addition of 1 µM recombinant ANXA2 (rANXA2), and we found that rANXA2 enhanced Autophagy in PDLCs under high glucose conditions.

Conclusions and discussion: Therefore, our present study demonstrates that alterations in ANXA2 under high glucose conditions may be a factor in the decreased osteogenic differentiation potential of PDLCs. Meanwhile, ANXA2 is associated with Autophagy, oxidative stress, and cellular senescence under high glucose conditions.

Keywords

ANXA2; Autophagy; Cellular senescence; Oxidative stress; Periodontal ligament cells; Periodontitis.

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