VEGF promotes cartilage angiogenesis by phospho-ERK1/2 activation of Dll4 signaling in temporomandibular joint osteoarthritis caused by chronic sleep disturbance in Wistar rats

Dong, Yabing; Wu, Gaoyi; Zhu, Ting; Chen, Hongyu; Zhu, Yong; Zhu, Guoqiang; Han, Fabin; Zhao, Hongxia

doi:10.18632/oncotarget.14874

Cited by 19 publications

(22 citation statements)

References 31 publications

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“…It is worth noting that there is a significant positive correlation between VEGF and miR-21-5p in vitro. Moreover, according to many studies, miR-21-5p can regulate the phosphorylation of ERK-MAPK signalling pathway components by targeting Spry1 in a variety of cells [15,34,38,39] and based on the close correlation between VEGF and the ERK-MAPK signalling pathway [7,27,38], we speculate that miR-21-5p can promote angiogenesis in TMJ, and this effect is likely related to the degree of phosphorylation of ERK-MAPK signalling pathway components. Finally, the experimental results of the chicken embryo angiogenesis assay and Western blotting showed that miR-21-5p has a pro-angiogenic effect, which was significantly mediated by the ERK-MAPK signalling pathway.…”

Section: Discussionmentioning

confidence: 76%

“…It has been confirmed that when VEGF is combined with its signal receptor VEGF2, downstream kinases such as MAPK can be phosphorylated to activate the ERK-MAPK signalling pathway [26]. Moreover, ERK-MAPK signalling pathway activated by VEGF can induce the activation of MMPs [27]. Because VEGF, MMPs and the ERK-MAPK pathways are closely related to the development of OA and there is a close relationship between MicroRNAs determine cell fate by participating in the regulation of extracellular signalling pathways and expression of certain molecules [28], and miR-21-5p has been reported to play an important role in cell apoptosis, pathological growth and stress [29,30], processes that are closely related to OA cartilage lesions.…”

Section: Discussionmentioning

confidence: 97%

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MiR-21-5p regulates extracellular matrix degradation and angiogenesis in TMJOA by targeting Spry1

Zhang

et al. 2020

Arthritis Res Ther

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Background: Due to the lack of research on the pathological mechanism of temporomandibular joint osteoarthritis (TMJOA), there are few effective treatment measures in the clinic. In recent years, microRNAs (miRs) have been demonstrated to play an important role in the pathogenesis of osteoarthritis (OA) by regulating a variety of target genes, and the latest evidence shows that miR-21-5p is specifically overexpressed in OA. The purpose of this project was to clarify whether miR-21-5p can regulate the TMJOA process by targeting Spry1. Methods: TMJOA was induced by a unilateral anterior crossbite (UAC) model, and the effect of miR-21-5p knockout on TMJOA was evaluated by toluidine blue (TB), immunohistochemical (IHC) staining, Western blotting (WB) and RT-qPCR. Primary mouse condylar chondrocytes (MCCs) were isolated, cultured and transfected with a series of mimics, inhibitors, siRNA-Spry1 or cDNA Spry1. WB, RT-qPCR, IHC and TB were used to detect the effect of miR-21-5p and its target gene Spry1 on the expression of MMP-13, VEGF and p-ERK1/2 in TMJOA. The effect of miR-21-5p on angiogenesis was evaluated by chick embryo chorioallantoic membrane (CAM) assay and WB.

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Section: Discussionmentioning

confidence: 76%

Section: Discussionmentioning

confidence: 97%

MiR-21-5p regulates extracellular matrix degradation and angiogenesis in TMJOA by targeting Spry1

Zhang

et al. 2020

Arthritis Res Ther

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“…Blood vessels not only transport oxygen and nutrients throughout the human body but also nourish tumors and other disease conditions [ 2 ]. To date, the precise mechanisms of angiogenesis remain to be defined but a large number of studies have shown that mechanical and chemical stimulation could regulate expression of different cytokine and growth factors to promote endothelial cell proliferation, while angiogenesis is also the key process in cancer development and progression [ 3 ]. Malignant cells are rapidly dividing cells and grow uncontrollably due to activation of oncogenes and/or inactivation of tumor suppressor genes [ 4 ].…”

Section: Introductionmentioning

confidence: 99%

Knockdown of MALAT1 expression inhibits HUVEC proliferation by upregulation of miR-320a and downregulation of FOXM1 expression

Sun

Zhao

et al. 2017

Oncotarget

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Regulation of cancer angiogenesis could be a useful strategy in cancer therapy. Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a long non-coding RNA (lncRNA), and can induce cancer cell proliferation, while lncRNAs, generally are able to act as microRNA (miRNA) sponges. The latter is a type of competitive endogenous RNA (ceRNA) that regulates expression of the targeting miRNAs and protein-coding genes. This study investigated the proliferative role of MALAT1 in human umbilical vein endothelial cells (HUVECs) and the underlying molecular events. The data showed that knockdown of MALAT1 expression using MALAT1 siRNA inhibited HUVEC proliferation and also significantly decreased levels of FOXM1 mRNA and protein in vitro, while knockdown of FOXM1 expression reduced HUVEC proliferation. Annotation of HUVEC microarray data revealed that seven miRNAs, including miR-320a, were upregulated after knockdown of MALAT1 expression in HUVECs. MALAT1 was shown to reciprocally interact with miR-320a, i.e., expression of one negatively regulated levels of the other, whereas knockdown of MALAT1 expression promoted miR-320a levels. Furthermore, miR-320a could directly target and inhibit FOXM1 expression in HUVECs. Knockdown of MALAT1 expression enhanced miR-320a expression but reduced FOXM1 expression resulting in downregulation of HUVEC proliferation. However, such an effect was inhibited by miR-320a depletion. In conclusion, this study demonstrates that miR-320a plays an important role in mediating the effects of MALAT1 on HUVEC proliferation by suppression of FOXM1 expression. Thus, targeting of this gene pathway could be a novel strategy in cancer therapy.

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“…They furtherly indicated that the VEGF binds to its receptor (VEGFR-2), leading to extracellular signal-regulated kinase (ERK1/2) activation. The ERK activation, helped the induction of matrix metalloproteinase (MMP), which aid in the degradation of the extracellular matrix during both the initiation and progression of TMJOA [23]. These previously reported mechanisms concerning the implement of VEGF in the pathogenesis of OA, could elucidate the significance of elevated VEGF expression in the chondrocytes of osteoarthritic mandibular condyle in the present investigation.…”

Section: Discussionmentioning

confidence: 57%

Effects of Locally Delivered Morin Hydrate on Iodoacetate-induced Temporomandibular Joint Osteoarthritis in Rats

Abdelhameed¹,

Hani

Soliman

2020

BDS

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Objectives: morin hydrate has been reported to possess many beneficial pharmacological potentialities including antioxidant and anti-osteoarthritic effects. The antiosteoarthritic properties of locally administrated morin have not been investigated. The objective of this study is to evaluate the locally delivered morin on the temporomandibular joint osteoarthritis in rat. Materials and methods: thirty young adult female Sprague Dawley rats were randomly arranged into three groups; control, osteoarthritis and osteoarthritis with morin. Both the iodoacetate for osteoarthritis induction and morin hydrate therapy were delivered unilaterally via intra-articular route. Results: morin reduced osteoarthritis manifestations with prominent thickening of both condylar fibrous layer and articular disc accompanied with discal cells hypertrophy that ultimately acquired chondrocytes features. The condylar cartilage matrix showed enhancement of extracellular matrix production with morin administration. Discussion: the present study has elucidated antiosteoarthritic effect of intraarticular injection of morin hydrate. Although morin has managed to prevent the propagation and advancing some of the recorded osteoarthritic manifestations; however, it showed some failure in managing others. The administration of morin hydrate modulated the structure of the joint rather than restore it back to its typical configuration. Conclusion: the morin hydrate administration to osteoarthritic animals showed relieve in some of osteoarthritic features and modulated the structure of some joint components to compensate the unhandled manifestations.KEYWORDSIodoacetate; Morin; Osteoarthritis; OARSI Score; Temporomandibular joint.

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VEGF promotes cartilage angiogenesis by phospho-ERK1/2 activation of Dll4 signaling in temporomandibular joint osteoarthritis caused by chronic sleep disturbance in Wistar rats

Cited by 19 publications

References 31 publications

MiR-21-5p regulates extracellular matrix degradation and angiogenesis in TMJOA by targeting Spry1

MiR-21-5p regulates extracellular matrix degradation and angiogenesis in TMJOA by targeting Spry1

Knockdown of MALAT1 expression inhibits HUVEC proliferation by upregulation of miR-320a and downregulation of FOXM1 expression

Effects of Locally Delivered Morin Hydrate on Iodoacetate-induced Temporomandibular Joint Osteoarthritis in Rats

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