Kartogenin potentially protects temporomandibular joints from collagenase-induced osteoarthritis via core binding factor β and runt-related transcription factor 1 binding - A rat model study
© 2023 Association for Dental Sciences of the Republic of China. Publishing services by Elsevier B.V..
Background/purpose: Temporomandibular joint (TMJ) osteoarthritis (TMJOA) is a chronic disease with progressive destruction of articular cartilage. This study aimed to explore the therapeutic effects of kartogenin on TMJOA via promoting the binding of core binding factor β (CBFβ) and runt-related transcription factor 1 (RUNX1).
Materials and methods: Type II collagenase was injected into 35 8-week-old male Sprague Dawley rat TMJs to establish the TMJOA model. Kartogenin, or the CBFβ-RUNX1 complex inhibitor (Ro5-3335), was also delivered via intra-articular injection. Subchondral bone was analyzed by MicroCT. The hematoxylin-eosin, Safranin O, and toluidine blue O staining were used to observe histopathology. Immunohistochemical staining of proliferating cell nuclear antigen (PCNA), caspase-3 (CASP3), interleukin-1β (IL-1β), and collagen II (COL2) was performed.
Results: TMJOA was established in rats by intra-articular injection of type II collagenase. The condylar cartilage and subchondral bone were damaged, with decreased PCNA and COL2 and increased CASP3 and IL-1 (P < .001). Compared with the OA group, kartogenin alleviated the destruction of cartilage and subchondral bone, rescued the expression of PCNA and COL2, and decreased the expression of CASP3 and IL-1β (P < .01). Ro5-3335 did not aggravate the pathology of TMJOA but neutralized the therapeutic effects of kartogenin on TMJOA.
Conclusion: Kartogenin has a potential therapeutic effect on TMJOA via promoting the CBFβ-RUNX1 binding.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2023 |
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| Erschienen: |
2023 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:18 |
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| Enthalten in: |
Journal of dental sciences - 18(2023), 4 vom: 02. Okt., Seite 1553-1560 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Ye, Li [VerfasserIn] |
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| Links: |
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| Themen: |
CBFβ |
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| Anmerkungen: |
Date Revised 26.10.2023 published: Print-Electronic Citation Status PubMed-not-MEDLINE |
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| doi: |
10.1016/j.jds.2023.03.002 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM362935157 |
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| 245 | 1 | 0 | |a Kartogenin potentially protects temporomandibular joints from collagenase-induced osteoarthritis via core binding factor β and runt-related transcription factor 1 binding - A rat model study |
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| 500 | |a Date Revised 26.10.2023 | ||
| 500 | |a published: Print-Electronic | ||
| 500 | |a Citation Status PubMed-not-MEDLINE | ||
| 520 | |a © 2023 Association for Dental Sciences of the Republic of China. Publishing services by Elsevier B.V. | ||
| 520 | |a Background/purpose: Temporomandibular joint (TMJ) osteoarthritis (TMJOA) is a chronic disease with progressive destruction of articular cartilage. This study aimed to explore the therapeutic effects of kartogenin on TMJOA via promoting the binding of core binding factor β (CBFβ) and runt-related transcription factor 1 (RUNX1) | ||
| 520 | |a Materials and methods: Type II collagenase was injected into 35 8-week-old male Sprague Dawley rat TMJs to establish the TMJOA model. Kartogenin, or the CBFβ-RUNX1 complex inhibitor (Ro5-3335), was also delivered via intra-articular injection. Subchondral bone was analyzed by MicroCT. The hematoxylin-eosin, Safranin O, and toluidine blue O staining were used to observe histopathology. Immunohistochemical staining of proliferating cell nuclear antigen (PCNA), caspase-3 (CASP3), interleukin-1β (IL-1β), and collagen II (COL2) was performed | ||
| 520 | |a Results: TMJOA was established in rats by intra-articular injection of type II collagenase. The condylar cartilage and subchondral bone were damaged, with decreased PCNA and COL2 and increased CASP3 and IL-1 (P < .001). Compared with the OA group, kartogenin alleviated the destruction of cartilage and subchondral bone, rescued the expression of PCNA and COL2, and decreased the expression of CASP3 and IL-1β (P < .01). Ro5-3335 did not aggravate the pathology of TMJOA but neutralized the therapeutic effects of kartogenin on TMJOA | ||
| 520 | |a Conclusion: Kartogenin has a potential therapeutic effect on TMJOA via promoting the CBFβ-RUNX1 binding | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a CBFβ | |
| 650 | 4 | |a Kartogenin | |
| 650 | 4 | |a Osteoarthritis | |
| 650 | 4 | |a Proliferation | |
| 650 | 4 | |a Temporomandibular joint | |
| 700 | 1 | |a Cao, Zhiwei |e verfasserin |4 aut | |
| 700 | 1 | |a Tan, Xing |e verfasserin |4 aut | |
| 700 | 1 | |a Zhao, Chengzhi |e verfasserin |4 aut | |
| 700 | 1 | |a Cao, Yubin |e verfasserin |4 aut | |
| 700 | 1 | |a Pan, Jian |e verfasserin |4 aut | |
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