Редактирование: CCR10 (раздел)

==Publications==

{{medline-entry
|title=Cardiac aging is initiated by matrix metalloproteinase-9-mediated endothelial dysfunction.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/24658018
|abstract=Aging is linked to increased matrix metalloproteinase-9 (MMP-9) expression and extracellular matrix turnover, as well as a decline in function of the left ventricle (LV). Previously, we demonstrated that C57BL/6J wild-type (WT) mice > 18 mo of age show impaired diastolic function, which was attenuated by MMP-9 deletion. To evaluate mechanisms that initiate the development of cardiac dysfunction, we compared the LVs of 6-9- and 15-18-mo-old WT and MMP-9 null (Null) mice. All groups showed similar LV function by echocardiography, indicating that dysfunction had not yet developed in the older group. Myocyte nuclei numbers and cross-sectional areas increased in both WT and Null 15-18-mo mice compared with young controls, indicating myocyte hypertrophy. Myocyte hypertrophy leads to an increased oxygen demand, and both WT and Null 15-18-mo mice showed an increase in angiogenic signaling. Plasma proteomic profiling and LV analysis revealed a threefold increase in von Willebrand factor and fivefold increase in vascular endothelial growth factor in WT 15-18-mo mice, which were further elevated in Null mice. In contrast to the upregulation of angiogenic stimulating factors, actual LV vessel numbers increased only in the 15-18-mo Null LV. The 15-18-mo WT showed amplified expression of inflammatory genes related to angiogenesis, including C-C chemokine receptor (CCR)7, [[CCR10]], interleukin (IL)-1f8, IL-13, and IL-20 (all, P < 0.05), and these increases were blunted by MMP-9 deletion (all, P < 0.05). To measure vascular permeability as an index of endothelial function, we injected mice with FITC-labeled dextran. The 15-18-mo WT LV showed increased vascular permeability compared with young WT controls and 15-18-mo Null mice. Combined, our findings revealed that MMP-9 deletion improves angiogenesis, attenuates inflammation, and prevents vascular leakiness in the setting of cardiac aging.
|mesh-terms=* Aging
* Animals
* Endothelium, Vascular
* Female
* Heart
* Hypertrophy
* Male
* Matrix Metalloproteinase 9
* Mice, Inbred C57BL
* Mice, Knockout
* Models, Animal
* Myocytes, Cardiac
* Neovascularization, Physiologic
* Phenotype
* Ventricular Dysfunction, Left
* Ventricular Remodeling
|keywords=* MMP-9
* aging
* angiogenesis
* extracellular matrix
* inflammation
* proteomics
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4024719
}}