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Новая страница: «C-C chemokine receptor type 1 (C-C CKR-1) (CC-CKR-1) (CCR-1) (CCR1) (HM145) (LD78 receptor) (Macrophage inflammatory protein 1-alpha receptor) (MIP-1alpha-R) (RAN...»

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C-C chemokine receptor type 1 (C-C CKR-1) (CC-CKR-1) (CCR-1) (CCR1) (HM145) (LD78 receptor) (Macrophage inflammatory protein 1-alpha receptor) (MIP-1alpha-R) (RANTES-R) (CD191 antigen) [CMKBR1] [CMKR1] [SCYAR1]

==Publications==

{{medline-entry
|title=Myocardial Infarction Superimposed on Aging: MMP-9 Deletion Promotes M2 Macrophage Polarization.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/25878031
|abstract=In this study, we examined the combined effect of aging and myocardial infarction on left ventricular remodeling, focusing on matrix metalloproteinase (MMP)-9-dependent mechanisms. We enrolled 55 C57BL/6J wild type (WT) and 85 MMP-9 Null (Null) mice of both sexes at 11-36 months of age and evaluated their response at Day 7 post-myocardial infarction. Plasma MMP-9 levels positively linked to age in WT mice (r = .46, p = .001). MMP-9 deletion improved survival (76% for WT vs 88% for Null, p = .021). Post-myocardial infarction, there was a progressive increase in left ventricular dilation with age in WT but not in Null mice. By inflammatory gene array analysis, WT mice showed linear age-dependent increases in three different proinflammatory genes (C3, CCl4, and CX3CL1; all p < .05), whereas Null mice showed increases in three proinflammatory genes (CCL5, CCL9, and CXCL4; all p < .05) and seven anti-inflammatory genes (CCL1, CCL6, [[CCR1]], [[IL11]], IL1r2, IL8rb, and Mif; all p < .05). Compared with WT, macrophages isolated from Null left ventricle infarct demonstrated enhanced expression of anti-inflammatory M2 markers [[CD163]], [[MRC1]], TGF-β1, and YM1 (all p < .05), without affecting proinflammatory M1 markers. In conclusion, MMP-9 deletion stimulated anti-inflammatory polarization of macrophages to attenuate left ventricle dysfunction in the aging post-myocardial infarction.
|mesh-terms=* Aging
* Animals
* Cytokines
* Echocardiography
* Female
* Gene Expression
* Immunohistochemistry
* Ligation
* Male
* Matrix Metalloproteinase 9
* Mice
* Mice, Inbred C57BL
* Myocardial Infarction
* Real-Time Polymerase Chain Reaction
* Survival Analysis
* Ventricular Remodeling
|keywords=* Aging
* Cardiac remodeling
* M2 phenotype.
* Macrophage polarization
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5175450
}}
{{medline-entry
|title=The role of [[CCR1]] expression in the retinal degeneration in rd mice.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/21275605
|abstract=Chemokine receptors are reported to be involved in neuronal cell death and CNS neurodegenerative diseases. The aim of the current study was to investigate the expression of [[CCR1]], a major chemokine receptor for CC chemokines in retinal dystrophy in rd (retinal degeneration) mice and further explore its role in photoreceptor degeneration. The expression levels of [[CCR1]] mRNA in the whole control and rd retinas at postnatal days (P) 8, 10, 12, 14, 16, and 18 were determined by RT-PCR assay. Location of [[CCR1]] in the retina of rd mice at each age group was studied by immunohistochemical analysis. Expression of [[CCR1]] in the photoreceptor cells and apoptotic cells was determined by double labeling. Expression of [[CCR1]] mRNA was noted in both control and rd retinas at each age group. [[CCR1]]-positive cells started to emerge in the outer nuclear layer (ONL) in rd retinas at P8 and reached a peak at P12 and P14. Double labeling of [[CCR1]] with rhodopsin, CD11b, or TUNEL staining showed expression of [[CCR1]] in the photoreceptor cells, rather than in the microglial cells. Partial [[CCR1]] expression was observed in some of the apoptotic photoreceptor cells. Expression of [[CCR1]] in the photoreceptor cells was increased with the progress of retinal degeneration in rd mice. Activation of [[CCR1]] may play a role in the photoreceptor apoptosis.
|mesh-terms=* Aging
* Animals
* Animals, Newborn
* Apoptosis
* CD11b Antigen
* Fluorescent Antibody Technique, Indirect
* Gene Expression Regulation
* In Situ Nick-End Labeling
* Mice
* Mice, Inbred C3H
* Mice, Mutant Strains
* Photoreceptor Cells, Vertebrate
* RNA, Messenger
* Receptors, CCR1
* Retinal Degeneration
* Reverse Transcriptase Polymerase Chain Reaction
* Rhodopsin

|full-text-url=https://sci-hub.do/10.3109/02713683.2010.535133
}}
{{medline-entry
|title=Aging is associated with increased human T cell CC chemokine receptor gene expression.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/14585197
|abstract=Leukocyte chemokine receptors (CR) are central to the pathogenesis of many human diseases, including human immunodeficiency virus-1 (HIV-1) infection. Elderly individuals infected with the HIV-1 virus have a shorter disease-free interval and worse clinic outcome. However, the reasons for this are unclear. We recently reported increased CC chemokine receptor (CCR) expression in CD4 T cells in aged mice, but it is not known if similar changes occur in humans. In addition, it is unclear if the observed differences are related to aged-related expansion in the memory T cell compartment. In this report, we examined the effects of aging on CCR gene expression in human peripheral blood mononuclear cells (PBMCs), CD4 T cells, and naive/memory T cells. Aging is found to be associated with increased [[CCR1]]-5 expression in PBMCs and CD4 T cells. In addition, although the age-related increases in CCR expression occurred in both naive and memory T cells, the greatest changes were seen in the memory T cell subset. We propose that the observed aging-associated increase in T cell chemokine receptor expression may contribute to the worse clinical outcome of T cell chemokine receptor-dependent disease, such as HIV-1 infection, in the elderly.
|mesh-terms=* Adolescent
* Adult
* Aged
* Aged, 80 and over
* Aging
* CD4-Positive T-Lymphocytes
* Chemokines, CC
* Humans
* Immunologic Memory
* Middle Aged
* Receptors, Chemokine

|full-text-url=https://sci-hub.do/10.1089/107999003322485071
}}
{{medline-entry
|title=T cell chemokine receptor expression in aging.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/12517955
|abstract=Changes in chemokine receptor expression are important in determining T cell migration and the subsequent immune response. To better understand the contribution of the chemokine system in immune senescence we determined the effect of aging on CD4( ) T cell chemokine receptor function using microarray, RNase protection assays, Western blot, and in vitro chemokine transmigration assays. Freshly isolated CD4( ) cells from aged (20-22 mo) mice were found to express a higher level of [[CCR1]], 2, 4, 5, 6, and 8 and [[CXCR2]]-5, and a lower level of [[CCR7]] and 9 than those from young (3-4 mo) animals. Caloric restriction partially or completely restored the aging effects on [[CCR1]], 7, and 8 and [[CXCR2]], 4, and 5. The aging-associated differences in chemokine receptor expression cannot be adequately explained by the age-associated shift in the naive/memory or Th1/Th2 profile. CD4( ) cells from aged animals have increased chemotactic response to stromal cell-derived factor-1 and macrophage-inflammatory protein-1alpha, suggesting that the observed chemokine receptor changes have important functional consequences. We propose that the aging-associated changes in T cell chemokine receptor expression may contribute to the different clinical outcome in T cell chemokine receptor-dependent diseases in the elderly.
|mesh-terms=* Aging
* Animals
* Blotting, Western
* Caloric Restriction
* Cells, Cultured
* Chemotaxis, Leukocyte
* Mice
* Mice, Inbred C57BL
* Mice, Inbred DBA
* RNA Probes
* RNA Stability
* RNA, Messenger
* Receptors, Chemokine
* Ribonucleases
* T-Lymphocyte Subsets
* Th1 Cells
* Th2 Cells

|full-text-url=https://sci-hub.do/10.4049/jimmunol.170.2.895
}}
{{medline-entry
|title=RANTES and [[MIP]]-1alpha production by T lymphocytes, monocytes and NK cells from nonagenarian subjects.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/11772507
|abstract=While numerous previous studies have investigated age-related changes of cytokine production, little is known about chemokines, the importance of which in regulating immune response is becoming increasingly evident. In this study, a group of healthy subjects over 90 years old is compared to a group of young subjects, we evaluated the ability of monocytes, T lymphocytes and NK cells: (1) to produce RANTES and [[MIP]]-1alpha, either in basal conditions or after stimulation with, respectively, LPS, anti-CD3 MoAb and IL-2; (2) to express the corresponding chemokine receptors ([[CCR1]], [[CCR3]], [[CCR5]]). We demonstrate that: (a) monocytes, T lymphocytes and NK cells spontaneously produced detectable amounts of chemokines, both in young and old subjects; (b) monocyte-dependent RANTES and [[MIP]]-1alpha production induced by LPS was up-regulated in nonagenarian subjects as anti-CD3-induced secretion from T cells; (c) RANTES and [[MIP]]-1alpha production by IL-2 stimulated NK cells was reduced in elderly subjects; (d) [[CCR1]], [[CCR3]] and [[CCR5]] were widely expressed on monocytes, but less expressed on T lymphocytes and NK cells. The diversity within PBMC might reflect their different states of activation and/or responsiveness, influencing the ability to develop rapid innate and long-lasting adaptive immune responses.
|mesh-terms=* Adult
* Aged
* Aged, 80 and over
* Aging
* Cells, Cultured
* Chemokine CCL3
* Chemokine CCL4
* Chemokine CCL5
* Female
* Humans
* Killer Cells, Natural
* Lipopolysaccharides
* Macrophage Inflammatory Proteins
* Male
* Monocytes
* Receptors, CCR1
* Receptors, CCR3
* Receptors, CCR5
* Receptors, Chemokine
* T-Lymphocytes

|full-text-url=https://sci-hub.do/10.1016/s0531-5565(01)00187-5
}}

CCR1 - История изменений

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