Transcriptomics analyses of IL-1β-stimulated rat chondrocytes in temporomandibular joint condyles and effect of platelet-rich plasma
The biological mechanism of action of platelet-rich plasma (PRP) in the treatment of temporomandibular joint (TMJ) osteoarthritis remains unclear. This study explored the mechanisms underlying interleukin (IL)-1β-induced inflammation and investigated the effect of PRP on TMJ condylar chondrocytes. P...
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Elsevier
2024-02-01
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author | Shasha Liu Chaolun Wu Yuxin Zhang |
author_facet | Shasha Liu Chaolun Wu Yuxin Zhang |
author_sort | Shasha Liu |
collection | DOAJ |
description | The biological mechanism of action of platelet-rich plasma (PRP) in the treatment of temporomandibular joint (TMJ) osteoarthritis remains unclear. This study explored the mechanisms underlying interleukin (IL)-1β-induced inflammation and investigated the effect of PRP on TMJ condylar chondrocytes. Primary chondrocytes were isolated from the TMJ condyle of 4-week-old rats, and differentially expressed genes among three treatment groups (phosphate-buffered saline [control], IL-1β, and IL-1β + PRP) were identified using RNA-seq and characterized using Gene Ontology and Kyoto Encyclopedia of Genes and Genomes path-enrichment analyses. IL-1β caused inflammatory injury to chondrocytes by upregulating the TNF, NF-κB, and IL-17 signaling pathways and downregulating the MAPK and PI3K/Akt signaling pathways. PRP activated the MAPK and PI3K/Akt signaling pathways, exerting a protective effect on IL-1β-induced chondrocytes. PRP also activated the TNF and IL-17 signaling pathways, producing an inflammatory effect. Additionally, PRP increased the mRNA expression of the matrix catabolism-related genes Mmp3, Mmp9, and Mmp13; the proliferative markers Mki67 and PCNA; and the anti-apoptotic genes of the Bcl-2 family (Bcl2a1 and Bok), while reducing the expression of the pro-apoptotic genes Casp4 and Casp12. The findings suggest that the protective effect of PRP on IL-1β-induced chondrocyte injury is mainly achieved via MAPK-PI3K/Akt signaling, increasing cell proliferation and inhibiting cell apoptosis. |
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spelling | doaj.art-6dff8806379249f0aa3317ef83568d912024-03-09T09:28:54ZengElsevierHeliyon2405-84402024-02-01104e26739Transcriptomics analyses of IL-1β-stimulated rat chondrocytes in temporomandibular joint condyles and effect of platelet-rich plasmaShasha Liu0Chaolun Wu1Yuxin Zhang2Department of Rehabilitation Medicine, The Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200011, China; Department of Rehabilitation Medicine, Sijing Hospital of the Songjiang District of Shanghai, Shanghai, 201600 China; Corresponding author. Department of Rehabilitation Medicine, The Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200011, China.Department of Rehabilitation Medicine, The Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200011, ChinaDepartment of Rehabilitation Medicine, The Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200011, ChinaThe biological mechanism of action of platelet-rich plasma (PRP) in the treatment of temporomandibular joint (TMJ) osteoarthritis remains unclear. This study explored the mechanisms underlying interleukin (IL)-1β-induced inflammation and investigated the effect of PRP on TMJ condylar chondrocytes. Primary chondrocytes were isolated from the TMJ condyle of 4-week-old rats, and differentially expressed genes among three treatment groups (phosphate-buffered saline [control], IL-1β, and IL-1β + PRP) were identified using RNA-seq and characterized using Gene Ontology and Kyoto Encyclopedia of Genes and Genomes path-enrichment analyses. IL-1β caused inflammatory injury to chondrocytes by upregulating the TNF, NF-κB, and IL-17 signaling pathways and downregulating the MAPK and PI3K/Akt signaling pathways. PRP activated the MAPK and PI3K/Akt signaling pathways, exerting a protective effect on IL-1β-induced chondrocytes. PRP also activated the TNF and IL-17 signaling pathways, producing an inflammatory effect. Additionally, PRP increased the mRNA expression of the matrix catabolism-related genes Mmp3, Mmp9, and Mmp13; the proliferative markers Mki67 and PCNA; and the anti-apoptotic genes of the Bcl-2 family (Bcl2a1 and Bok), while reducing the expression of the pro-apoptotic genes Casp4 and Casp12. The findings suggest that the protective effect of PRP on IL-1β-induced chondrocyte injury is mainly achieved via MAPK-PI3K/Akt signaling, increasing cell proliferation and inhibiting cell apoptosis.http://www.sciencedirect.com/science/article/pii/S2405844024027701ChondrocytesInterleukin-1 betaPlatelet-rich plasmaTemporomandibular joint |
spellingShingle | Shasha Liu Chaolun Wu Yuxin Zhang Transcriptomics analyses of IL-1β-stimulated rat chondrocytes in temporomandibular joint condyles and effect of platelet-rich plasma Heliyon Chondrocytes Interleukin-1 beta Platelet-rich plasma Temporomandibular joint |
title | Transcriptomics analyses of IL-1β-stimulated rat chondrocytes in temporomandibular joint condyles and effect of platelet-rich plasma |
title_full | Transcriptomics analyses of IL-1β-stimulated rat chondrocytes in temporomandibular joint condyles and effect of platelet-rich plasma |
title_fullStr | Transcriptomics analyses of IL-1β-stimulated rat chondrocytes in temporomandibular joint condyles and effect of platelet-rich plasma |
title_full_unstemmed | Transcriptomics analyses of IL-1β-stimulated rat chondrocytes in temporomandibular joint condyles and effect of platelet-rich plasma |
title_short | Transcriptomics analyses of IL-1β-stimulated rat chondrocytes in temporomandibular joint condyles and effect of platelet-rich plasma |
title_sort | transcriptomics analyses of il 1β stimulated rat chondrocytes in temporomandibular joint condyles and effect of platelet rich plasma |
topic | Chondrocytes Interleukin-1 beta Platelet-rich plasma Temporomandibular joint |
url | http://www.sciencedirect.com/science/article/pii/S2405844024027701 |
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