CIDeRGeneral Information:
| Id: | 4,953 |
| Diseases: |
Atherosclerosis
Cardiovascular disease |
| Mus musculus | |
| chow- or HCD fed ldr (-/-) mice | |
| article | |
| Reference: | Miyazaki T et al.(2011) m-Calpain induction in vascular endothelial cells on human and mouse atheromas and its roles in VE-cadherin disorganization and atherosclerosis Circulation 124: 2522-2532 [PMID: 22064597] |
Interaction Information:
| Comment | The expression levels of m-calpain (CAPN2) were significantly increased in the aorta and lung in ldr(-/-) mice during 12 weeks of HCD-feeding (high cholesterol diet) compared with those in chow feeding. |
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Formal Description Interaction-ID: 48934 |
environment high cholesterol diet increases_expression of gene/protein |
| Comment | Confocal immunohistochemistry showed that the density of m-calpain‚Äďpositive ECs (endothelial cells) was clearly increased in aortic intima in HCD-fed (high cholesterol diet) ldlr (-/-) mice compared with chow-fed mice. |
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Formal Description Interaction-ID: 48935 |
environment high cholesterol diet increases_quantity of gene/protein |
| Comment | Administration of each calpain inhibitor, calpeptin or ALLM, to ldlr (-/-) mice led to suppression of HCD (high cholesterol diet)-induced atherosclerosis in the aortic tree and root, whereas plasma levels of LPC and total, LDL, and high-density lipoprotein cholesterol were unaffected. |
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Formal Description Interaction-ID: 48940 |
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| Comment | Administration of each calpain inhibitor, calpeptin or ALLM, to ldlr (-/-) mice led to suppression of HCD (high cholesterol diet)-induced atherosclerosis in the aortic tree and root, whereas plasma levels of LPC and total, LDL, and high-density lipoprotein cholesterol were unaffected. |
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Formal Description Interaction-ID: 48941 |
drug/chemical compound decreases_activity of phenotype |
| Comment | Administration of each calpain inhibitor, calpeptin or ALLM, to ldlr (-/-) mice led to suppression of HCD (high cholesterol diet)-induced atherosclerosis in the aortic tree and root, whereas plasma levels of LPC and total, LDL, and high-density lipoprotein cholesterol were unaffected. |
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Formal Description Interaction-ID: 48942 |
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| Comment | Administration of each calpain inhibitor, calpeptin or ALLM, to ldlr (-/-) mice led to suppression of HCD (high cholesterol diet)-induced atherosclerosis in the aortic tree and root, whereas plasma levels of LPC and total, LDL, and high-density lipoprotein cholesterol were unaffected. |
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Formal Description Interaction-ID: 48943 |
drug/chemical compound decreases_activity of phenotype |
| Comment | m-Calpain mediates VE-cadherin cleavage and proatherogenic hyperpermeability. VE-cadherin cleavage, which was observed in aorta in HCD (high cholesterol diet)-fed ldlr (-/-) or apoE (-/-) mice, was prevented by the administration of calpeptin or ALLM, the calpain inhibitors. |
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Formal Description Interaction-ID: 48944 |
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| Drugbank entries | Show/Hide entries for CDH5 |
| Comment | VE-cadherin‚Äďmediated AJs (adherence junctions) have an essential role in maintaining EC (endothelial cell) barrier functions. (cited information) |
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Formal Description Interaction-ID: 48946 |
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| Drugbank entries | Show/Hide entries for CDH5 |
| Comment | VE-cadherin‚Äďmediated AJs (adherence junctions) have an essential role in maintaining EC (endothelial cell) barrier functions. (cited information) |
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Formal Description Interaction-ID: 48947 |
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| Drugbank entries | Show/Hide entries for CDH5 |