<scp>IL</scp>‐1β‐regulating angiogenic factors expression in perforated temporomandibular disk cells via <scp>NF</scp>‐κB pathway

Xu, Jie; Cai, Hengxing; Meng, Qinggong; Li, Yingjie; Chen, Guoxin; Fang, Wei; Long, Xing

doi:10.1111/jop.12420

Cited by 12 publications

(12 citation statements)

References 29 publications

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“…VEGF, a potent vascular permeability factor, is pivotal in TMJ pathogenesis . Our previous study demonstrated high expression of VEGF in perforated disc tissue . We also found high expression of HMGB1 in perforated discs vicinity.…”

Section: Discussionsupporting

confidence: 75%

HMGB1‐induced angiogenesis in perforated disc cells of human temporomandibular joint

Feng

Jin

Cao

et al. 2017

J Cellular Molecular Medi

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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-1a (HIF-1a) and vascular endothelial growth factor (VEGF) to mediate angiogenesis in perforated disc cells of TMJ. HMGB1 increased the expression of HIF-1a and VEGF in a dose-and time-dependent manner in these cells. Moreover, immunofluorescence assay exhibits that the HIF-1a 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-1a 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-1a, Erk and JNK, individually. Therefore, abundance of HMGB1 mediates activation of HIF-1a 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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Section: Discussionsupporting

confidence: 75%

HMGB1‐induced angiogenesis in perforated disc cells of human temporomandibular joint

Feng

Jin

Cao

et al. 2017

J Cellular Molecular Medi

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“…Further studies are required to identify and characterize the Chm-1 receptor and its subsequent activity on key downstream signalling pathways. For example, in the perforated disks of temporomandibular joint (TMJ), angiogenesis appears to be regulated by factors that induce the NF-κB pathway [60]. Chm-1 expression was found to be significantly lower in perforated disks as compared to healthy disks, which appears to be regulated via the NF-κB pathway in the presence of interleukin-1β (IL-1β), linking Chm-1 to receptor-mediated NF-κB signaling and pathological angiogenesis of the TMJ [60].…”

Section: Chm-1 Receptor and Signallingmentioning

confidence: 99%

“…For example, in the perforated disks of temporomandibular joint (TMJ), angiogenesis appears to be regulated by factors that induce the NF-κB pathway [60]. Chm-1 expression was found to be significantly lower in perforated disks as compared to healthy disks, which appears to be regulated via the NF-κB pathway in the presence of interleukin-1β (IL-1β), linking Chm-1 to receptor-mediated NF-κB signaling and pathological angiogenesis of the TMJ [60]. Future studies to identify the specific receptor for Chm-1, and to determine the subsequent effect of signalling activation in a cell type dependent manner, are necessary to design therapeutic approaches for the treatment of Chm-1 related conditions, including osteoarthritis, infective endocarditis, and cancer.…”

Section: Chm-1 Receptor and Signallingmentioning

confidence: 99%

Chondromodulin-1 in health, osteoarthritis, cancer, and heart disease

Zhu

Qiu

Bennett

et al. 2019

Cell. Mol. Life Sci.

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The human chondromodulin-1 (Chm-1, Chm-I, CNMD, or Lect1) gene encodes a 334 amino acid type II transmembrane glycoprotein protein with characteristics of a furin cleavage site and a putative glycosylation site. Chm-1 is expressed most predominantly in healthy and developing avascular cartilage, and healthy cardiac valves. Chm-1 plays a vital role during endochondral ossification by the regulation of angiogenesis. The anti-angiogenic and chondrogenic properties of Chm-1 are attributed to its role in tissue development, homeostasis, repair and regeneration, and disease prevention. Chm-1 promotes chondrocyte differentiation, and is regulated by versatile transcription factors, such as Sox9, Sp3, YY1, p300, Pax1, and Nkx3.2. Decreased expression of Chm-1 is implicated in the onset and progression of osteoarthritis and infective endocarditis. Chm-1 appears to attenuate osteoarthritis progression by inhibiting catabolic activity, and to mediate anti-inflammatory effects. In this review, we present the molecular structure and expression profiling of Chm-1. In addition, we bring a summary to the potential role of Chm-1 in cartilage development and homeostasis, osteoarthritis onset and progression, and to the pathogenic role of Chm-1 in infective endocarditis and cancers. To date, knowledge of the Chm-1 receptor, cellular signalling, and the molecular mechanisms of Chm-1 is rudimentary. Advancing our understanding the role of Chm-1 and its mechanisms of action will pave the way for the development of Chm-1 as a therapeutic target for the treatment of diseases, such as osteoarthritis, infective endocarditis, and cancer, and for potential tissue regenerative bioengineering applications.

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“…overexpressed in the injured TMJ. Studies have shown that overexpression of Ang-1 is caused by IL-1β-mediated activation of the MAPK pathway 94,97. Neurovascular interactions are involved in the progression of TMJ osteoarthritis.…”

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confidence: 99%

Pathological mechanism of chondrocytes and the surrounding environment during osteoarthritis of temporomandibular joint

Guan

et al. 2021

J Cellular Molecular Medi

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Temporomandibular joint (TMJ) osteoarthritis is a common chronic degenerative disease of the TMJ. In order to explore its aetiology and pathological mechanism, many animal models and cell models have been constructed to simulate the pathological process of TMJ osteoarthritis. The main pathological features of TMJ osteoarthritis include chondrocyte death, extracellular matrix (ECM) degradation and subchondral bone remodelling. Chondrocyte apoptosis accelerates the destruction of cartilage. However, autophagy has a protective effect on condylar chondrocytes. Degradation of ECM not only changes the properties of cartilage but also affects the phenotype of chondrocytes. The loss of subchondral bone in the early stages of TMJ osteoarthritis plays an aetiological role in the onset of osteoarthritis. In recent years, increasing evidence has suggested that chondrocyte hypertrophy and endochondral angiogenesis promote TMJ osteoarthritis. Hypertrophic chondrocytes secrete many factors that promote cartilage degeneration. These chondrocytes can further differentiate into osteoblasts and osteocytes and accelerate cartilage ossification. Intrachondral angiogenesis and neoneurogenesis are considered to be important triggers of arthralgia in TMJ osteoarthritis. Many molecular signalling pathways in endochondral osteogenesis are responsible for TMJ osteoarthritis. These latest discoveries in TMJ osteoarthritis have further enhanced the understanding of this disease and contributed to the development of molecular therapies. This paper summarizes recent cognition on the pathogenesis of TMJ osteoarthritis, focusing on the role of chondrocyte hypertrophy degeneration and cartilage angiogenesis.

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IL‐1β‐regulating angiogenic factors expression in perforated temporomandibular disk cells via NF‐κB pathway

Abstract: Perforated disk cells secreted more angiogenic factors which might induced via NF-κB pathway.

Cited by 12 publications

References 29 publications

HMGB1‐induced angiogenesis in perforated disc cells of human temporomandibular joint

HMGB1‐induced angiogenesis in perforated disc cells of human temporomandibular joint

Chondromodulin-1 in health, osteoarthritis, cancer, and heart disease

Pathological mechanism of chondrocytes and the surrounding environment during osteoarthritis of temporomandibular joint

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