ArticleJournal of cellular and molecular medicine2018
HMGB1-induced angiogenesis in perforated disc cells of human temporomandibular joint.
Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 27 citations in OpenAlex.
- The role of HMGB1 in vascular endothelial cells.Apoptosis : an international journal on programmed cell death · 2026Review
- Histological and Immunohistochemical Insights into Disc Perforation in the Temporomandibular Joint: A Case Report.Journal of functional morphology and kinesiology · 2025Article
- The relationship of ALPK1, hyaluronic acid and M1 macrophage polarization in the temporomandibular joint synovitis.Journal of cellular and molecular medicine · 2024Article
- Inflammation and coagulation abnormalities via the activation of the HMGB1‑RAGE/NF‑κB and F2/Rho pathways in lung injury induced by acute hypoxia.International journal of molecular medicine · 2023Article
- Various Three-Dimensional Culture Methods and Cell Types for Exosome Production.Tissue engineering and regenerative medicine · 2023Review
- Potential pathological and molecular mechanisms of temporomandibular joint osteoarthritis.Journal of dental sciences · 2023Review
- Temporomandibular Joint Osteoarthritis: Pathogenic Mechanisms Involving the Cartilage and Subchondral Bone, and Potential Therapeutic Strategies for Joint Regeneration.International journal of molecular sciences · 2022Review
- Morphological changes of TMJ disc in surgically treated ADDwoR patients: a retrospective study.BMC oral health · 2022Article
- Glycyrrhizin regulates rat TMJOA progression by inhibiting the HMGB1-RAGE/TLR4-NF-κB/AKT pathway.Journal of cellular and molecular medicine · 2022Article
- Pathological mechanism of chondrocytes and the surrounding environment during osteoarthritis of temporomandibular joint.Journal of cellular and molecular medicine · 2021Review
- Exosomal HMGB1 derived from hypoxia-conditioned bone marrow mesenchymal stem cells increases angiogenesis via the JNK/HIF-1α pathway.FEBS open bio · 2021Article
- miR-300 mitigates cancer-induced bone pain through targeting HMGB1 in rat models.Genes & genomics · 2020Article
- Tissue Engineering for the Temporomandibular Joint.Advanced healthcare materials · 2019Review
- HMGB1/RAGE axis mediates the apoptosis, invasion, autophagy, and angiogenesis of the renal cell carcinoma.OncoTargets and therapy · 2018Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High mobility group 1 protein (HMGB1), a highly conserved nuclear DNA-binding protein and inflammatory mediator, has been recently found to be involved in angiogenesis. Our previous study has demonstrated the elevation of HMGB1 in the tissue of perforated disc of temporomandibular joint (TMJ). Here, we investigated a novel mediator of HMGB1 in regulating hypoxia-inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) to mediate angiogenesis in perforated disc cells of TMJ. HMGB1 increased the expression of HIF-1α and VEGF in a dose- and time-dependent manner in these cells. Moreover, immunofluorescence assay exhibits that the HIF-1α were activated by HMGB1. In addition, HMGB1 activated extracellular signal-related kinase 1/2 (Erk1/2), Jun N-terminal kinase (JNK), but not P38 in these cells. Furthermore, both U0126 (ErK inhibitor) and SP600125 (JNK inhibitor) significantly suppressed the enhanced production of HIF-1α and VEGF induced by HMGB1. Tube formation of human umbilical vein endothelial cells (HUVECs) was significantly increased by exposure to conditioned medium derived from HMGB1-stimulated perforated disc cells, while attenuated with pre-treatment of inhibitors for VEGF, HIF-1α, Erk and JNK, individually. Therefore, abundance of HMGB1 mediates activation of HIF-1α in disc cells via Erk and JNK pathway and then, initiates VEGF secretion, thereby leading to disc angiogenesis and accelerating degenerative change of the perforated disc.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.