Shear stress preconditioning enhances periodontal ligament stem cell survival

IF 2.2 4区医学 Q2 DENTISTRY, ORAL SURGERY & MEDICINE

Archives of oral biology Pub Date : 2025-03-10 DOI:10.1016/j.archoralbio.2025.106232

Ravipha Suwittayarak , Nuttha Klincumhom , Chaloemrit Phrueksotsai , Nuttapol Limjeerajarus , Chalida Nakalekha Limjeerajarus , Hiroshi Egusa , Thanaphum Osathanon

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引用次数: 0

Abstract

Objective

The study investigated in vitro the influences of shear stress preconditioning on human periodontal ligament stem cells (hPDLSCs) under serum deprivation.

Design

hPDLSCs were subjected to shear stress at 0.5 and 5 dyn/cm², both with and without serum starvation. Cell viability and apoptosis were assessed using the Resazurin assay and flow cytometry analysis, respectively. Gene and protein expressions were analysed by real-time polymerase chain reaction, immunofluorescent staining, and Western blotting.

Results

Our results revealed that shear stress potentially mitigated serum derivation-induced cell death by inducing cell viability, enhancing colony formation, and inhibiting cell apoptosis. The addition of an ERK inhibitor inhibited the shear stress-induced cell apoptosis resistance. Shear stress treatment upregulated cell viability-related gene expression, including SOX2, SOD1 and BIRC5. In particular, shear stress promoted the nuclear translocation of SOX2. Meanwhile, the expression of BIRC5 was not inhibited by cycloheximide. Shear stress-induced SOX2 and BIRC5 expression was attenuated by PI3K and ERK inhibitors, respectively.

Conclusions

Shear stress contributes to promoting SOX2 and BIRC5 expression by hPDLSCs, implicating the promotion of stemness and cell survival under serum starvation.

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剪切应力预处理提高牙周韧带干细胞存活率

目的研究体外剪切应力预处理对血清剥夺条件下人牙周韧带干细胞（hPDLSCs）的影响。设计在血清饥饿和非血清饥饿情况下，pdlscs均承受0.5和5 dyn/cm²的剪切应力。分别用reazurin法和流式细胞术检测细胞活力和凋亡。通过实时聚合酶链反应、免疫荧光染色和Western blotting分析基因和蛋白的表达。结果表明，剪切应力通过诱导细胞活力、增强集落形成和抑制细胞凋亡，可能减轻血清衍生诱导的细胞死亡。ERK抑制剂的加入抑制了剪切应力诱导的细胞凋亡抵抗。剪切应力处理上调细胞活力相关基因表达，包括SOX2、SOD1和BIRC5。特别是剪切应力促进SOX2的核易位。同时，BIRC5的表达不受环己亚胺的抑制。剪切应力诱导的SOX2和BIRC5表达分别被PI3K和ERK抑制剂减弱。结论剪切胁迫可促进hPDLSCs中SOX2和BIRC5的表达，从而促进血清饥饿条件下hPDLSCs的干性和细胞存活。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Archives of oral biology 医学-牙科与口腔外科

CiteScore

5.10

自引率

3.30%

发文量

177

审稿时长

26 days

期刊介绍： Archives of Oral Biology is an international journal which aims to publish papers of the highest scientific quality in the oral and craniofacial sciences. The journal is particularly interested in research which advances knowledge in the mechanisms of craniofacial development and disease, including: Cell and molecular biology Molecular genetics Immunology Pathogenesis Cellular microbiology Embryology Syndromology Forensic dentistry