The Annexin A1 Protein Mimetic Peptide Ac2‐26 prevents cellular senescence of CHON‐001 chondrocytes against tumor necrosis factor‐α via the Nrf2/NF‐κB pathway.
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| Title: | The Annexin A1 Protein Mimetic Peptide Ac2‐26 prevents cellular senescence of CHON‐001 chondrocytes against tumor necrosis factor‐α via the Nrf2/NF‐κB pathway. |
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| Authors: | Yang, Lei1 (AUTHOR), Gong, Kaijian1 (AUTHOR), Ren, Guoxing1 (AUTHOR), Chen, Bo2 (AUTHOR) chenboo211@163.com |
| Source: | Biotechnology & Applied Biochemistry. Jun2025, Vol. 72 Issue 3, p755-765. 11p. |
| Subjects: | Telomerase reverse transcriptase, Cellular aging, Peptides, p53 protein, Gene expression |
| Abstract: | Osteoarthritis (OA) is a degenerative joint disorder characterized by progressive cartilage degradation. Excessive oxidative stress (OS), inflammatory responses, extracellular matrix breakdown, and cellular senescence of chondrocytes play crucial roles in the pathological development of OA. Currently, curing OA remains a significant challenge. In this study, we aimed to elucidate the protective effects of Annexin A1 protein Mimetic Peptide (Ac2‐26) against tumor necrosis factor‐α (TNF‐α)‐induced damage in CHON‐001 chondrocytes by assessing cellular senescence, OS, and the expression levels of matrix metalloproteinase‐13 (MMP‐13) and a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS)‐4. Our results show that Ac2‐26 mitigated the reduction of telomerase activity and the exacerbation of cellular senescence induced by TNF‐α in CHON‐001 chondrocytes. Treatment with TNF‐α led to decreased expression of the human telomerase reverse transcriptase gene and increased expression of the telomeric repeat‐binding factor 2 gene, which were reversed by Ac2‐26 treatment. The TNF‐α‐induced increases in the gene and protein expressions of p53 and p16 were restored by Ac2‐26 in a dose‐dependent manner. Additionally, we found that TNF‐α caused elevations in the mRNA and protein levels of MMP‐13 and ADAMTS‐4, which were reduced by Ac2‐26 in a dose‐dependent fashion. Furthermore, TNF‐α triggered the activation of nuclear factor κ‐B (NF‐κB) by increasing the levels of phosphorylated NF‐κB p65 and the luciferase activity of NF‐κB. Notably, Ac2‐26 alleviated OS by reducing mitochondrial reactive oxygen species levels and promoting the activation of NF‐E2‐related factor 2 (Nrf2) in TNF‐α‐challenged CHON‐001 chondrocytes. Silencing Nrf2 abolished the Ac2‐26‐induced activation of NF‐κB and cellular senescence in CHON‐001 chondrocytes. Collectively, these findings offer new insights into the potential therapeutic use of Ac2‐26 for treating OA. [ABSTRACT FROM AUTHOR] |
| Copyright of Biotechnology & Applied Biochemistry is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.) | |
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| Header | DbId: egs DbLabel: Engineering Source An: 185839105 AccessLevel: 6 PubType: Academic Journal PubTypeId: academicJournal PreciseRelevancyScore: 0 |
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| Items | – Name: Title Label: Title Group: Ti Data: The Annexin A1 Protein Mimetic Peptide Ac2‐26 prevents cellular senescence of CHON‐001 chondrocytes against tumor necrosis factor‐α via the Nrf2/NF‐κB pathway. – Name: Author Label: Authors Group: Au Data: <searchLink fieldCode="AR" term="%22Yang%2C+Lei%22">Yang, Lei</searchLink><relatesTo>1</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Gong%2C+Kaijian%22">Gong, Kaijian</searchLink><relatesTo>1</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Ren%2C+Guoxing%22">Ren, Guoxing</searchLink><relatesTo>1</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Chen%2C+Bo%22">Chen, Bo</searchLink><relatesTo>2</relatesTo> (AUTHOR)<i> chenboo211@163.com</i> – Name: TitleSource Label: Source Group: Src Data: <searchLink fieldCode="JN" term="%22Biotechnology+%26+Applied+Biochemistry%22">Biotechnology & Applied Biochemistry</searchLink>. Jun2025, Vol. 72 Issue 3, p755-765. 11p. – Name: Subject Label: Subjects Group: Su Data: <searchLink fieldCode="DE" term="%22Telomerase+reverse+transcriptase%22">Telomerase reverse transcriptase</searchLink><br /><searchLink fieldCode="DE" term="%22Cellular+aging%22">Cellular aging</searchLink><br /><searchLink fieldCode="DE" term="%22Peptides%22">Peptides</searchLink><br /><searchLink fieldCode="DE" term="%22p53+protein%22">p53 protein</searchLink><br /><searchLink fieldCode="DE" term="%22Gene+expression%22">Gene expression</searchLink> – Name: Abstract Label: Abstract Group: Ab Data: Osteoarthritis (OA) is a degenerative joint disorder characterized by progressive cartilage degradation. Excessive oxidative stress (OS), inflammatory responses, extracellular matrix breakdown, and cellular senescence of chondrocytes play crucial roles in the pathological development of OA. Currently, curing OA remains a significant challenge. In this study, we aimed to elucidate the protective effects of Annexin A1 protein Mimetic Peptide (Ac2‐26) against tumor necrosis factor‐α (TNF‐α)‐induced damage in CHON‐001 chondrocytes by assessing cellular senescence, OS, and the expression levels of matrix metalloproteinase‐13 (MMP‐13) and a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS)‐4. Our results show that Ac2‐26 mitigated the reduction of telomerase activity and the exacerbation of cellular senescence induced by TNF‐α in CHON‐001 chondrocytes. Treatment with TNF‐α led to decreased expression of the human telomerase reverse transcriptase gene and increased expression of the telomeric repeat‐binding factor 2 gene, which were reversed by Ac2‐26 treatment. The TNF‐α‐induced increases in the gene and protein expressions of p53 and p16 were restored by Ac2‐26 in a dose‐dependent manner. Additionally, we found that TNF‐α caused elevations in the mRNA and protein levels of MMP‐13 and ADAMTS‐4, which were reduced by Ac2‐26 in a dose‐dependent fashion. Furthermore, TNF‐α triggered the activation of nuclear factor κ‐B (NF‐κB) by increasing the levels of phosphorylated NF‐κB p65 and the luciferase activity of NF‐κB. Notably, Ac2‐26 alleviated OS by reducing mitochondrial reactive oxygen species levels and promoting the activation of NF‐E2‐related factor 2 (Nrf2) in TNF‐α‐challenged CHON‐001 chondrocytes. Silencing Nrf2 abolished the Ac2‐26‐induced activation of NF‐κB and cellular senescence in CHON‐001 chondrocytes. Collectively, these findings offer new insights into the potential therapeutic use of Ac2‐26 for treating OA. [ABSTRACT FROM AUTHOR] – Name: AbstractSuppliedCopyright Label: Group: Ab Data: <i>Copyright of Biotechnology & Applied Biochemistry is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.) |
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| RecordInfo | BibRecord: BibEntity: Identifiers: – Type: doi Value: 10.1002/bab.2695 Languages: – Code: eng Text: English PhysicalDescription: Pagination: PageCount: 11 StartPage: 755 Subjects: – SubjectFull: Telomerase reverse transcriptase Type: general – SubjectFull: Cellular aging Type: general – SubjectFull: Peptides Type: general – SubjectFull: p53 protein Type: general – SubjectFull: Gene expression Type: general Titles: – TitleFull: The Annexin A1 Protein Mimetic Peptide Ac2‐26 prevents cellular senescence of CHON‐001 chondrocytes against tumor necrosis factor‐α via the Nrf2/NF‐κB pathway. Type: main BibRelationships: HasContributorRelationships: – PersonEntity: Name: NameFull: Yang, Lei – PersonEntity: Name: NameFull: Gong, Kaijian – PersonEntity: Name: NameFull: Ren, Guoxing – PersonEntity: Name: NameFull: Chen, Bo IsPartOfRelationships: – BibEntity: Dates: – D: 01 M: 06 Text: Jun2025 Type: published Y: 2025 Identifiers: – Type: issn-print Value: 08854513 Numbering: – Type: volume Value: 72 – Type: issue Value: 3 Titles: – TitleFull: Biotechnology & Applied Biochemistry Type: main |
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