ADAM Metallopeptidase with Thrombospondin Type 1 Motif, 7 Protéines (ADAMTS7)

Mouse (Murine) ADAM Metallopeptidase with Thrombospondin Type 1 Motif, 7 (ADAMTS7) interaction partners

1. Therefore, these data provided the in vivo evidence, suggesting that ADAMTS-7 may play an important role in the pathogenesis of inflammatory arthritis.

2. Mice lacking Adamts7, Ldlr, Apoe had less lesion formation in aortas and aortic roots vs controls and less neointimal formation after femoral wire injury. Adamts7 expression was induced by injury and hyperlipidemia.

3. Adamts-7 deficiency substantially ameliorated neointima formation in mice at days 14 and 28 after injury. ADAMTS-7 inhibited both endothelial cell proliferation and migration.

4. The overexpression of ADATMTS-7 might contribute to early inflammatory kidney damage associated with aging

5. ADAMTS-7 and TNF-alpha form a positive feedback loop in the regulation of cartilage degradation and osteoarthritis progression.

6. ADAMTS7B has a domain organization with a total of eight thrombospondin type 1 repeats in its ancillary domain. Of these, seven are arranged in two distinct clusters that are separated by a mucin domain

7. Findings demonstrate that ADAMTS-7, a direct target of PTHrP signaling, negatively regulates endochondral bone formation by associating with and inactivating GEP chondrogenic growth factor.

Human ADAM Metallopeptidase with Thrombospondin Type 1 Motif, 7 (ADAMTS7) interaction partners

1. data show that ADAMTS-7 is associated with a vulnerable plaque phenotype in human carotid lesions. These data support previous observations of a potential proatherogenic role of ADAMTS-7.

2. Multivariate analysis showed that DeltaADAMTS-7(day 7 minus day 1) was independently associated with left ventricular reverse remodeling

3. Genetic variation at the ADAMTS7 locus is associated with reduced severity of coronary artery disease.

4. Studied gene expression of genetic variants of ADAMTS7 in atherosclerotic occlusive peripheral arterial disease (PAD). Found mRNA levels of ADAMTS7 to be significantly higher in PAD patients than controls, and that the rs1994016 CC and rs3825807 TT genotypes may upregulate ADAMTS7 mRNA levels and may influence PAD development.

5. The findings suggest that upregulation of ADAMTS-7 and down regulation of COMP are associated with human AA.

6. The native overfunctional ADAMTS7 allele (A) may accelerate VSMC migration and lead to neointimal thickening, atherosclerosis progression and acute plaque events.

7. miR-105/Runx2 axis mediates FGF2-induced ADAMTS expression in osteoarthritis cartilage.

8. Allelic variation that associates with reduced ADAMTS7 expression confers stronger coronary heart disease protection in never-smokers than in ever-smokers.

9. During inflammatory conditions, AP-1 and Sp1 sustained the expression of ADAMTS7, and ADAMTS7 sustained the expression of catabolic genes in nucleus pulposus cells

10. ADAMTS7 and LPA single nucleotide polymorphisms are related to a 24-h ambulatory systolic-diastolic pressure regression index.

11. Expression of miR-26a and miR-29a was significantly down regulated in leukoplakia and cancer tissues but up regulated in lichen planus tissues. Expression of target genes such as, ADAMTS7, ATP1B1, COL4A2, CPEB3, CDK6, DNMT3a and PI3KR1 was significantly down regulated in at least two of three disease types with respect to normal tissues.

12. Our results indicate the presence of ADAMTS-7 in human NP cells and imply its potential role in disc degeneration.

13. The main contribution of this study is the proposal of a pharmacophore for ADAMTS7.

14. The significant associations observed between this coding variant in ADAMTS7 and the risk of CAD development.

15. Logistic regression analysis indicated that the association between ADAMTS-7 and heart failure after AMI was independent from traditional cardiovascular risk factors and other biomarkers

16. Data conclude that ADAMTS-7 level appears to be positively associated with expression of TNF-alpha and Phospho-NF-kappaB P65 in cartilage, which may imply its association with cartilage destruction of ONFH.

17. ADAMTS7 localized to cells having smooth muscle cell markers in human coronary artery disease lesions. Cultured vascular smooth muscle cells had ADAMTS7 at the cytoplasm and cell membrane, where it colocalized with markers of podosomes.

18. There was a reduction in the amount of cleaved ADAMTS7 prodomain in media conditioned by VSMCs of the G/G genotype.

19. statistically significant increase in mRNA expression of ADAMTS-7 and ADAMTS-12 was observed in the endplate cells in degenerative discs compared with nondegenerative discs

20. identified ADAMTS7 as novel locus for CAD and association of ABO with MI in the presence of CAD