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牙龈组织和牙龈成纤维细胞培养物衰老分析。

Analysis of senescence in gingival tissues and gingival fibroblast cultures.

机构信息

Department of Oral Disease Research, National Center for Geriatrics and Gerontology, Obu, Japan.

Daiichi Sankyo Healthcare Co., Ltd., Tokyo, Japan.

出版信息

Clin Exp Dent Res. 2022 Aug;8(4):939-949. doi: 10.1002/cre2.581. Epub 2022 May 2.

DOI:10.1002/cre2.581
PMID:35491709
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9382052/
Abstract

OBJECTIVE

To determine senescence-associated changes in the gingival tissues of aged mice and gingival fibroblast cultures.

MATERIALS AND METHODS

The production of senescence-associated β-galactosidase (SA-β-gal) and mRNA expression of p16, p21, interleukin (IL)-1β, and tumor necrosis factor α (TNF-α) were evaluated in gingival tissues, gingival fibroblasts of 10- and 20-month-old C57BL/6NCrl mice, and multiple-passaged and hydrogen peroxide-stimulated human gingival fibroblasts (HGFs). Changes in molecular expression in HGF cultures due to senescent cell elimination by the senolytic drug ABT-263 (Navitoclax) were analyzed.

RESULTS

Compared to 10-week-old mice, the 20-month-old mice had higher numbers of M1 macrophages. The proportion of cells expressing SA-β-gal were also higher in 20- month-old mice than in 10-week-old-mice. Gingival fibroblasts in 20-month-old mice expressed less collagen 1a1, collagen 4a1, and collagen 4a2 mRNA than those in 10-week-old mice. Compared to control cells, H2O2 treated HGF cells expressed higher levels of SA-β-gal and p16, p21, IL-1β, and TNF-α. Furthermore, ABT-263 suppressed HGF cell expression of cytokines after senescence induction.

CONCLUSIONS

Senescence-associated changes were observed in the gingival tissues of aged mice and HGF cultures. In addition, the potential of senolytic drugs to modify aging-related changes in the gingiva was shown.

摘要

目的

确定老年小鼠牙龈组织和牙龈成纤维细胞衰老相关变化。

材料和方法

评估 10 月龄和 20 月龄 C57BL/6NCrl 小鼠的牙龈组织和牙龈成纤维细胞、以及多代传代和过氧化氢刺激的人牙龈成纤维细胞（HGFs）中衰老相关β-半乳糖苷酶（SA-β-gal）的产生和 p16、p21、白细胞介素（IL）-1β和肿瘤坏死因子α（TNF-α）的 mRNA 表达。分析衰老细胞清除剂 ABT-263（Navitoclax）对 HGF 培养物中分子表达变化的影响。

结果

与 10 周龄小鼠相比，20 月龄小鼠的 M1 型巨噬细胞数量更多。20 月龄小鼠 SA-β-gal 表达细胞的比例也高于 10 周龄小鼠。20 月龄小鼠的牙龈成纤维细胞表达的胶原蛋白 1a1、胶原蛋白 4a1 和胶原蛋白 4a2 mRNA 低于 10 周龄小鼠。与对照细胞相比，过氧化氢处理的 HGF 细胞表达更高水平的 SA-β-gal 和 p16、p21、IL-1β和 TNF-α。此外，ABT-263 抑制了衰老诱导后 HGF 细胞细胞因子的表达。

结论

在老年小鼠的牙龈组织和 HGF 培养物中观察到衰老相关变化。此外，还表明了衰老细胞清除药物修饰牙龈与衰老相关变化的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33b4/9382052/9d4bcd6c9e04/CRE2-8-939-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33b4/9382052/5e7b5a8916b5/CRE2-8-939-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33b4/9382052/409db28a6c70/CRE2-8-939-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33b4/9382052/744d483cda1a/CRE2-8-939-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33b4/9382052/c235f40d20dd/CRE2-8-939-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33b4/9382052/57bef1a03ca2/CRE2-8-939-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33b4/9382052/9d4bcd6c9e04/CRE2-8-939-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33b4/9382052/5e7b5a8916b5/CRE2-8-939-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33b4/9382052/409db28a6c70/CRE2-8-939-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33b4/9382052/744d483cda1a/CRE2-8-939-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33b4/9382052/c235f40d20dd/CRE2-8-939-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33b4/9382052/57bef1a03ca2/CRE2-8-939-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33b4/9382052/9d4bcd6c9e04/CRE2-8-939-g005.jpg

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3
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NPJ Aging. 2025 Feb 21;11(1):12. doi: 10.1038/s41514-025-00200-9.
4
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J Dent Res. 2024 Jul;103(8):800-808. doi: 10.1177/00220345241255325. Epub 2024 Jun 14.
5
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