ADAM Metallopeptidase with Thrombospondin Type 1 Motif, 7 Proteins (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. ADAMTS-7 and TNF-alpha (show TNF Proteins) form a positive feedback loop in the regulation of cartilage degradation and osteoarthritis progression.

5. 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 (show SLC13A2 Proteins) domain

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

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

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

2. 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.

3. The findings suggest that upregulation of ADAMTS-7 and down regulation of COMP (show COMP Proteins) are associated with human AA.

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

5. miR (show MLXIP Proteins)-105/Runx2 (show RUNX2 Proteins) axis mediates FGF2 (show FGF2 Proteins)-induced ADAMTS (show ADAMTS13 Proteins) expression in osteoarthritis cartilage.

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

7. During inflammatory conditions, AP-1 (show FOSB Proteins) and Sp1 (show PSG1 Proteins) sustained the expression of ADAMTS7, and ADAMTS7 sustained the expression of catabolic genes in nucleus pulposus cells

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

9. Expression of miR (show MLXIP Proteins)-26a and miR (show MLXIP Proteins)-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 (show ATP1B1 Proteins), COL4A2 (show COL4a2 Proteins), CPEB3 (show CPEB3 Proteins), CDK6 (show CDK6 Proteins), DNMT3a (show DNMT3A Proteins) and PI3KR1 was significantly down regulated in at least two of three disease types with respect to normal tissues.

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