Hypoxia-inducible factor expression is related to apoptosis and cartilage degradation in temporomandibular joint osteoarthritis
© 2022. The Author(s)..
BACKGROUND: It remains unclear etiology of cartilaginous tissues in osteoarthritis (OA) lesions. In this study, we hypothesized the accumulation of hypoxia-inducible factor (HIF) and activated apoptosis relate to condylar cartilage degeneration in vivo.
METHODS: Malocclusion stress was applied for 2 weeks, 4 weeks and 8 weeks to induce an OA-like lesion animal model in rats. Histological analysis was performed by H&E staining and Safranin O/fast green staining. The expression levels of protein in condylar cartilage were examined by immunostaining to evaluate cartilage degeneration.
RESULTS: We found apparent histological phenotypes associated with degeneration in the occlusion disorder (OD) stress group. The OD group at 4 weeks and 8 weeks had obviously reduced expression of Aggrecan (Acan) and type II collagen (Col II) in cartilage. In contrast, the OD groups had higher levels of ADAM metallopeptidase with thrombospondin type 5 (ADAMTS5) and matrix metallopeptidase 13 (MMP13) in the condylar cartilage than the control group. Moreover, the OD group cartilage had prominent degenerative changes with reduced levels of hypoxia inducible factor 1 alpha (HIF1α) and increased levels of hypoxia inducible factor 2 alpha (HIF2α) and the apoptosis factor Caspase3 in condylar cartilage at 8 weeks.
CONCLUSION: Thus, abnormal hypoxic conditions inducing Occlusion disorder stress results in cartilage degeneration. opposite expression patterns of HIF1α and HIF2α could be involved in the pathogenesis of condylar cartilage degeneration and chondrocyte apoptosis. HIF2α may provide a potential negative feedback mechanism for HIF1α during cartilage damage.
| Medienart: |
E-Artikel |
|---|
| Erscheinungsjahr: |
2022 |
|---|---|
| Erschienen: |
2022 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:23 |
|---|---|
| Enthalten in: |
BMC musculoskeletal disorders - 23(2022), 1 vom: 16. Juni, Seite 583 |
| Sprache: |
Englisch |
|---|
| Beteiligte Personen: |
Zhang, Jun [VerfasserIn] |
|---|
| Links: |
|---|
| Themen: |
Apoptosis |
|---|
| Anmerkungen: |
Date Completed 20.06.2022 Date Revised 16.07.2022 published: Electronic Citation Status MEDLINE |
|---|
| doi: |
10.1186/s12891-022-05544-x |
|---|
| funding: |
|
|---|---|
| Förderinstitution / Projekttitel: |
|
| PPN (Katalog-ID): |
NLM342317040 |
|---|
| LEADER | 01000naa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLM342317040 | ||
| 003 | DE-627 | ||
| 005 | 20231226013829.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 231226s2022 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1186/s12891-022-05544-x |2 doi | |
| 028 | 5 | 2 | |a pubmed24n1141.xml |
| 035 | |a (DE-627)NLM342317040 | ||
| 035 | |a (NLM)35710352 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 100 | 1 | |a Zhang, Jun |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Hypoxia-inducible factor expression is related to apoptosis and cartilage degradation in temporomandibular joint osteoarthritis |
| 264 | 1 | |c 2022 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a ƒaComputermedien |b c |2 rdamedia | ||
| 338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
| 500 | |a Date Completed 20.06.2022 | ||
| 500 | |a Date Revised 16.07.2022 | ||
| 500 | |a published: Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a © 2022. The Author(s). | ||
| 520 | |a BACKGROUND: It remains unclear etiology of cartilaginous tissues in osteoarthritis (OA) lesions. In this study, we hypothesized the accumulation of hypoxia-inducible factor (HIF) and activated apoptosis relate to condylar cartilage degeneration in vivo | ||
| 520 | |a METHODS: Malocclusion stress was applied for 2 weeks, 4 weeks and 8 weeks to induce an OA-like lesion animal model in rats. Histological analysis was performed by H&E staining and Safranin O/fast green staining. The expression levels of protein in condylar cartilage were examined by immunostaining to evaluate cartilage degeneration | ||
| 520 | |a RESULTS: We found apparent histological phenotypes associated with degeneration in the occlusion disorder (OD) stress group. The OD group at 4 weeks and 8 weeks had obviously reduced expression of Aggrecan (Acan) and type II collagen (Col II) in cartilage. In contrast, the OD groups had higher levels of ADAM metallopeptidase with thrombospondin type 5 (ADAMTS5) and matrix metallopeptidase 13 (MMP13) in the condylar cartilage than the control group. Moreover, the OD group cartilage had prominent degenerative changes with reduced levels of hypoxia inducible factor 1 alpha (HIF1α) and increased levels of hypoxia inducible factor 2 alpha (HIF2α) and the apoptosis factor Caspase3 in condylar cartilage at 8 weeks | ||
| 520 | |a CONCLUSION: Thus, abnormal hypoxic conditions inducing Occlusion disorder stress results in cartilage degeneration. opposite expression patterns of HIF1α and HIF2α could be involved in the pathogenesis of condylar cartilage degeneration and chondrocyte apoptosis. HIF2α may provide a potential negative feedback mechanism for HIF1α during cartilage damage | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Apoptosis | |
| 650 | 4 | |a Cartilage degradation | |
| 650 | 4 | |a Condyle | |
| 650 | 4 | |a Osteoarthritis | |
| 650 | 7 | |a Matrix Metalloproteinase 13 |2 NLM | |
| 650 | 7 | |a EC 3.4.24.- |2 NLM | |
| 700 | 1 | |a Hu, Yu |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Zihan |e verfasserin |4 aut | |
| 700 | 1 | |a Wu, Xuelian |e verfasserin |4 aut | |
| 700 | 1 | |a Yang, Chun |e verfasserin |4 aut | |
| 700 | 1 | |a Yang, Hefeng |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t BMC musculoskeletal disorders |d 2000 |g 23(2022), 1 vom: 16. Juni, Seite 583 |w (DE-627)NLM111431875 |x 1471-2474 |7 nnns |
| 773 | 1 | 8 | |g volume:23 |g year:2022 |g number:1 |g day:16 |g month:06 |g pages:583 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.1186/s12891-022-05544-x |3 Volltext |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a GBV_NLM | ||
| 951 | |a AR | ||
| 952 | |d 23 |j 2022 |e 1 |b 16 |c 06 |h 583 | ||