A Disintegrin and Metalloprotease 15 is Expressed on Rheumatoid Arthritis Synovial Tissue Endothelial Cells and may Mediate Angiogenesis

Nishimi, Shinichiro; Isozaki, Takeo; Wakabayashi, Kuninobu; Takeuchi, Hiroko; Kasama, Tsuyoshi

doi:10.3390/cells8010032

Cited by 10 publications

(11 citation statements)

References 23 publications

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“…ADAM15 is involved in the response to hypoxia, proteolytic ectodomain processing of cytokines, cell adhesion signaling, and angiogenesis in endothelial cells(Horiuchi et al 2003; Nishimi et al 2019). In addition, the silencing of ADAM15 can inhibit the expression of proinflammatory cytokines in rheumatoid angiogenesis(Nishimi et al 2019). Moreover, systemic proinflammatory cytokines are associated with the development of AMS and high-altitude pulmonary edema(B.…”

Section: Discussionmentioning

confidence: 99%

“…The downregulation of ADAM15 may play a protective role in individuals without AMS ADAM15 was identified as a candidate protective biomarker of individuals without AMS and was selected by the machine learning-based model with high accuracy to distinguish nAMS1k and nAMS4k. ADAM15 is involved in the response to hypoxia, proteolytic ectodomain processing of cytokines, cell adhesion signaling, and angiogenesis in endothelial cells (Horiuchi et al 2003;Nishimi et al 2019). In addition, the silencing of ADAM15 can inhibit the expression of proinflammatory cytokines in rheumatoid angiogenesis (Nishimi et al 2019).…”

Section: The Downregulation Of S100a12 May Not Prevent Amsmentioning

confidence: 99%

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Proteomic and clinical biomarkers for acute mountain sickness diagnosis, prognosis, protection, and pathogenesis in a longitudinal cohort

Yang

Jia

Song

et al. 2021

Preprint

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Acute mountain sickness (AMS) is frequently experienced by non-high-altitude natives at high altitudes, which affects the quality of health and productivity of humans. The diagnosis of the disease mainly depends on a self-questionnaire, which reveals our insufficient understanding of AMS and the necessity of developing reliable biomarkers for AMS. In addition to 65 clinical indexes and 22 AMS symptom phenotypes, we profiled the plasma proteomic profiles of AMS via a combination of proximity extension assay with multiple reaction monitoring for a longitudinal cohort of 53 individuals divided into discovery and validation stages. Through differential analysis, machine learning models with high accuracy and protein-symptom-clinical index functional network analysis, we identified proteomic and clinical biomarkers for AMS diagnosis, prognosis, protection, and pathogenesis. RET, a top-weighted protein in the pathogenesis model, showed opposite regulations between individuals with AMS and those without AMS ascending to a high altitude. The downregulation of ADAM15 may play a protective role at high altitude in individuals without AMS. These results suggest that RET and ADAM15 could be promising therapeutic targets for AMS. Moreover, PHGDH and TRAF2 could be candidate predictive and diagnostic biomarkers for AMS, respectively. Additionally, C-peptide was found to be actively involved in the pathogenesis and could aid the assistant diagnosis of AMS. Notably, individuals with AMS showed higher gluconeogenesis activity at the plain than those without AMS. Our findings shed light on the proteomic and clinical biomarkers of AMS, provide a wealth of biological insights into AMS, and thereby promote precision medicine for AMS.

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Section: Discussionmentioning

confidence: 99%

Section: The Downregulation Of S100a12 May Not Prevent Amsmentioning

confidence: 99%

Proteomic and clinical biomarkers for acute mountain sickness diagnosis, prognosis, protection, and pathogenesis in a longitudinal cohort

Yang

Jia

Song

et al. 2021

Preprint

View full text Add to dashboard Cite

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“…Proteins within ADAM and ADAMTS families may also contribute to the regulation of angiogenesis and adipogenesis [ 8 ]. For example, endothelial cell tube formation is decreased in ADAM15 small interfering RNA-treated endothelial cells, and an overexpression of ADAM17 in endothelial cells downregulates TSP-1 expression [ 101 , 102 ], suggesting that both ADAM15 and ADAM17 can stimulate angiogenesis.…”

Section: Angiogenesis and Adipose Tissue Growthmentioning

confidence: 99%

Regulation of Obesity by Antiangiogenic Herbal Medicines

Shin

Yoon

2020

Molecules

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Obesity is the result of an energy imbalance caused by an increased ratio of caloric intake to energy expenditure. In conjunction with obesity, related metabolic disorders, such as dyslipidemia, atherosclerosis, and type 2 diabetes, have become global health problems. Obesity progression is thought to be associated with angiogenesis and extracellular matrix (ECM) remodeling. Angiogenesis occurs in growing adult adipose tissues, which are similar to neoplastic tissues. Adipose tissue is highly vascularized, and each adipocyte is nourished by an extensive capillary network. Adipocytes produce proangiogenic factors, such as vascular endothelial growth factor A and fibroblast growth factor 2, which promote neovascularization within the adipose tissue. Furthermore, matrix metalloproteinases (MMPs), including MMP-2 and MMP-9, play important roles in adipose tissue development and microvessel maturation by modifying the ECM. Thus, modulation of angiogenesis and MMP activity provides a promising therapeutic approach for controlling human obesity and its related disorders. Over the past decade, there has been a great increase in the use of alternative treatments, such as herbal remedies, for these diseases. This review will focus on the role of angiogenesis in adipose tissue growth and the regulation of obesity by antiangiogenic herbal medicines.

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“…It has been shown that ADAM15 induces progression in several cancers including gastric [19], lung [20], colon [21]and prostate [22,23]. ADAM15 as a mediator of angiogenesis is expressed in endothelial cells and up-regulated on the angiogenic endothelial cell surface [24,25]. In addition, ADAM15 promotes cell proliferation, migration and sprouting of endothelial cells and smooth muscle cells [26].…”

Section: Introductionmentioning

confidence: 99%

Targeting the TR4-induced RCC cells-derived exosomally initiated signaling increases Sunitinib efficacy

Wang

Sun

et al. 2022

Preprint

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Sunitinib is the first-line therapy for metastatic clear cell renal cell carcinoma (ccRCC) via suppressing neoangiogenesis and tumor growth. The detailed mechanisms, especially whether and how ccRCC cells can impact endothelial cells sensitivity to Sunitinib, remain unclear. Here, we found that TR4 was commonly upregulated in ccRCC tissue and relative to tumor angiogenesis. Tube formation and Mouse aortic ring assay showed that the overexpression or knockdown of TR4 in ccRCC cells enhanced or reduced the angiogenesis of endothelial cells and their resistance to Sunitinib in vitro. Mechanistically, We found that TR4 transcriptionally increase ADAM15 expression, as a consequence, exosomes carrying relatively large amounts of ADAM15 secreted from ccRCC cell resulted in activating the EGFR phosphorylation and reducing the efficacy of Sunitinib in endothelial cells. Targeting the TR4-induced renal cancers-derived exosomelly initiated signaling with a small molecular, CRM197, increases sunitinib efficacy in vitro and xenograft tumor models. Taken together, our findings indicate a novel function of TR4 in ccRCC blunted the efficacy of sunitinib via exosomal ADAM15-induced activation of EGFR signaling pathway in endothelial cells.

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A Disintegrin and Metalloprotease 15 is Expressed on Rheumatoid Arthritis Synovial Tissue Endothelial Cells and may Mediate Angiogenesis

Cited by 10 publications

References 23 publications

Proteomic and clinical biomarkers for acute mountain sickness diagnosis, prognosis, protection, and pathogenesis in a longitudinal cohort

Proteomic and clinical biomarkers for acute mountain sickness diagnosis, prognosis, protection, and pathogenesis in a longitudinal cohort

Regulation of Obesity by Antiangiogenic Herbal Medicines

Targeting the TR4-induced RCC cells-derived exosomally initiated signaling increases Sunitinib efficacy

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