ADAM15

Last update 08 May 2025

Basic Info

Synonyms

a disintegrin and metalloproteinase domain 15 (metargidin), ADAM 15, ADAM metallopeptidase domain 15

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Introduction

Active metalloproteinase with gelatinolytic and collagenolytic activity. Plays a role in the wound healing process. Mediates both heterotypic intraepithelial cell/T-cell interactions and homotypic T-cell aggregation. Inhibits beta-1 integrin-mediated cell adhesion and migration of airway smooth muscle cells. Suppresses cell motility on or towards fibronectin possibly by driving alpha-v/beta-1 integrin (ITAGV-ITGB1) cell surface expression via ERK1/2 inactivation. Cleaves E-cadherin in response to growth factor deprivation. Plays a role in glomerular cell migration. Plays a role in pathological neovascularization. May play a role in cartilage remodeling. May be proteolytically processed, during sperm epididymal maturation and the acrosome reaction. May play a role in sperm-egg binding through its disintegrin domain.

100 Clinical Results associated with ADAM15

100 Translational Medicine associated with ADAM15

0 Patents (Medical) associated with ADAM15

236

Literatures (Medical) associated with ADAM15

08 Apr 2025·Modern Rheumatology

VE-cadherin may suppress inflammation depending on the phase of inflammation of rheumatoid arthritis

Article

Author: Miwa, Yusuke ; Wakabayashi, Kuninobu ; Nishimi, Shinichiro ; Isozaki, Takeo ; Fukuse, Sayaka

ABSTRACTObjectivesA disintegrin and metalloproteinase (ADAM)-15 and vascular endothelial (VE)-cadherin are involved in angiogenesis. We investigated the relationship between ADAM-15 and VE-cadherin expressions in rheumatoid arthritis (RA).MethodsVE-cadherin concentrations in the serum of patients with RA were measured using the enzyme linked immunosorbent assay. We stimulated fibroblast-like synoviocytes (RA-FLS) with VE-cadherin and measured the vascular endothelial growth factor (VEGF) and inflammatory cytokine levels using ELISA. We also examined the correlation between serum VE-cadherin levels and DAS-28ESR, and used the Matrigel assay to examine VE-cadherin involvement in angiogenesis.ResultsSerum VE-cadherin levels were significantly higher in patients with RA than in healthy controls. A negative correlation was observed between VE-cadherin and DAS-28ESR. VEGF, chemokine ligand 16, intercellular adhesion molecule-1, and interleukin-8 levels in the supernatant of RA-FLS or human umbilical vein endothelial cells stimulated with VE-cadherin were significantly lower than those in the controls. The number of intercellular bridges formed by endothelial cells using Matrigel significantly decreased in RA synovial fluids from which VE-cadherin had been removed compared to synovial fluids treated with control immunoglobulin G.ConclusionVE-cadherin may have an inhibitory effect on inflammation depending on the phase of RA inflammation.

01 Jan 2025·BIO-PROTOCOL

Profiling the Secretome of Glioblastoma Cells Under Histone Deacetylase Inhibition Using Mass Spectrometry

Article

Author: Carneiro, Katia ; de Abreu Pereira, Denise ; Nogueira, Fábio César Sousa ; Menezes, Aline ; Martins, Yara

Glioblastoma (GBM) is the most aggressive brain tumor, and different efforts have been employed in the search for new drugs and therapeutic protocols for GBM. A label-free, mass spectrometry-based quantitative proteomics has been developed to identify and characterize proteins that are differentially expressed in GBM to gain a better understanding of the interactions and functions that lead to the pathological state focusing on the extracellular matrix (ECM). The main challenge in GBM research has been to identify novel molecular therapeutic targets and accurate diagnostic/prognostic biomarkers. To better investigate the GBM secretome upon in vitro treatment with histone deacetylase inhibitor (iHDAC), we employed a high-throughput label-free methodology of protein identification and quantification based on mass spectrometry followed by in silico studies. Our analysis revealed significant changes in the ECM protein profile, particularly those associated with the angiogenic matrisome. Proteins such as decorin, ADAM10, ADAM12, and ADAM15 were differentially regulated upon in silico analysis. In contrast, key angiogenesis markers such as VEGF and ECM proteins like fibronectin and integrins did not display significant changes. These results suggest that iHDAC inhibitors may modulate or suppress tumor behavior growth by targeting ECM proteins' secretion rather than directly inhibiting angiogenesis. Key features • Analysis of the secretome of U87MG glioblastoma cells. • Studies of mass spectrometry designed to modulate GBM biology and behavior focused on histone deacetylase inhibitors (iHDAC). • Mass spectrometry was developed to identify and characterize proteins that are differentially expressed in GBM.

01 Jan 2025·General physiology and biophysics

TFDP1 overexpression promotes apoptosis of nucleus pulposus cells in intervertebral disc degeneration through regulating ADAM15/MMP9 axis

Article

Author: Xin, Yanxuan ; Xiao, Lijuan ; Tong, Xian

Intervertebral disc degeneration (IVDD) is a common contributor for low back pain, which is featured by loss of extracellular matrix and nucleus pulposus cells (NPCs). Hence, our current study is undertaken to explore the potential mechanism of NPC apoptosis during IVDD. Transcription factor Dp-1 (TFDP1) expression in degenerative and non-degenerative intervertebral disc tissues was analyzed by bioinformatics. After transfection as needed, viability and apoptosis of NPCs were evaluated by cell counting kit-8 assay and flow cytometry, respectively. Western blot or quantitative real-time reverse transcription polymerase chain reaction was applied to assess expressions of TFDP1, matrix metallopeptidase 9 (MMP9), a disintegrin and metalloproteinase 15 (ADAM15), and apoptosis-associated proteins. TFDP1 expression was upregulated in degenerative intervertebral disc tissues. TFDP1 overexpression repressed viability, promoted apoptosis, increased expressions of Bax, Cleaved caspase 3, MMP9 and ADAM15, and decreased Bcl-2 expression in NPCs, while TFDP1 silencing did conversely. ADAM15 silencing promoted viability, inhibited apoptosis, increased Bcl-2 expression, and decreased Bax, Cleaved caspase 3, and MMP9 expressions in NPCs, which were reversed by TFDP1 overexpression. TFDP1 overexpression promotes apoptosis of NPCs in IVDD through regulating ADAM15/MMP9 axis, highlighting its role as a molecular target for the treatment of low back pain.

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ADAM15

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