P8 Hydrogen sulfide and SPRC mitigate infarct of myocardial infarction via governing migration and infilitration of macrophages
0
Citation
0
Reference
10
Related Paper
Keywords:
CD163
ABSTRACT Activation of NK1R by SP contributes to increased HIV-1 infection in macrophages. The scavenger receptor CD163 is expressed on cells of monocyte-macrophage origin. Our main goal was to determine if there is interplay among SP, CD163 expression, and HIV infection in macrophages. We showed that SP triggers intracellular calcium elevation and increased CD163 expression in human monocytes in a time- and concentration-dependent manner. The role of CD163 on HIV infection was examined by RT-PCR in sorted monocytes (CD163low and CD163high) and in macrophages having CD163 knocked down using siRNA. We found that the productivity of HIV infection was higher in CD163high cells. Additionally, in macrophages with CD163 expression knocked down, we found a significant decrease of HIV infection. Furthermore, Hb-Hp complexes, which function as an endogenous ligand for CD163, decreased HIV infection in macrophages in a dose-dependent manner. Thus, we demonstrate that SP induces higher levels of CD163 in monocytes and that high expression of CD163 is associated with increases HIV infection in macrophages. Thus, in addition to being a prognostic marker of HIV infection, the expression of CD163 on macrophages may be critical in HIV immunopathogenesis.
CD163
Monocyte
Scavenger Receptor
Cite
Citations (33)
In individuals with diabetes mellitus (DM), the haptoglobin (Hp) genotype is a major determinant of susceptibility to myocardial infarction. We have proposed that this is because of DM and Hp genotype–dependent differences in the response to intraplaque hemorrhage. The macrophage hemoglobin scavenging receptor CD163 plays an essential role in the clearance of hemoglobin released from lysed red blood cells after intraplaque hemorrhage. We sought to test the hypothesis that expression of CD163 is DM and Hp genotype–dependent. CD163 was quantified in plaques by immunohistochemistry, on peripheral blood monocytes (PBMs) by FACS, and as soluble CD163 (sCD163) in plasma by ELISA. In DM plaques, despite an increase in macrophage infiltration, CD163 immunoreactivity was lower, resulting in a dramatic reduction in the percentage of macrophages expressing CD163 (27±2% versus 70±2%, P =0.0001). In individuals with DM as compared with individuals without DM, the percentage of PBMs expressing CD163 was reduced (3.7±0.6% versus 7.1±0.9%, P <0.002) whereas soluble plasma CD163 was increased (2.6±1.1 μg/mL versus 1.6±0.8 μg/mL, P <0.0005). Among DM individuals, the Hp 2-2 genotype was associated with a decrease in the percentage of PBMs expressing CD163 (2.3±0.5% versus 5.6±1.3%, P =0.01) and an increase in plasma soluble CD163 (3.0±0.2 μg/mL versus 2.3±0.2 μg/mL, P =0.04). Taken together, these results demonstrate an impaired hemoglobin clearance capacity in Hp 2-2 DM individuals and may provide the key insight explaining the increased incidence of myocardial infarction in this population.
CD163
Haptoglobin
Scavenger Receptor
Cite
Citations (134)
Macrophages are classified into two phenotypes, M1 and M2, based on their roles. M2 macrophages suppress inflammation and increase in proportion to the malignancy of brain tumors. Recently, macrophage extracellular traps (METs), which change into a network, have been reported as a unique form of macrophage cell death. In this study, immunohistochemical analysis of macrophages in METs in human glioblastoma was performed. To distinguish between M1 and M2 macrophages, multiple immunostainings with Iba1 combined with CD163 or CD204 were performed. M2 macrophages were present in small amounts in normal and borderline areas but showed an increasing trend as they shifted to tumor areas, and most of them were the activated- or phagocytic-type. We also successfully detected METs coexisting with fibrin and lactoferrin near the border between the tumor and necrotic area. M2 macrophages not only suppressed inflammation but also were involved in the formation of METs. This study found that M2 macrophages play various roles in unstable situations.
CD163
M2 Macrophage
Lactoferrin
Cite
Citations (9)
Nanoparticle-based delivery of simvastatin inhibits plaque macrophage proliferation in apolipoprotein E–deficient mice.
Vulnerable plaque
Cite
Citations (199)
CD163 is a member of the scavenger receptor cysteine-rich superfamily restricted to the monocyte/macrophage lineage and is thought to be a useful marker for anti-inflammatory or alternatively activated macrophages. In this study we used mass spectrometric analysis to determine that the antigen recognized by the antibody AM-3K, which we previously generated as a tissue macrophage-specific monoclonal antibody, was CD163. An anti-inflammatory subtype of macrophages stimulated by dexamethasone or interleukin-10 showed strong reactivity for AM-3K and increased expression of CD163 mRNA. Immunohistochemical staining of routinely processed pathological specimens revealed that AM-3K recognized a specialized subpopulation of macrophages. In granulomatous diseases such as tuberculosis, sarcoidosis, or foreign body reactions, tissue macrophages around granulomas, but not component cells of the granulomas such as epithelioid cells and multinucleated giant cells, showed positive staining for AM-3K. In atherosclerotic lesions, scattered macrophages in diffuse intimal lesions were strongly positive for AM-3K, whereas foamy macrophages in atheromatous plaques demonstrated only weak staining. We therefore suggest that, in routine pathological specimens, AM-3K is a useful marker for anti-inflammatory macrophages because these cells can be distinguished from inflammatory or classically activated macrophages. Because AM-3K cross-reacts with macrophage subpopulations in different animal species including rats, guinea pigs, rabbits, cats, dogs, goats, pigs, bovine species, horses, monkeys, and cetaceans, it will have wide application for detection of CD163 in various animals.
CD163
CD68
Granulation tissue
Monocyte
Cite
Citations (165)
Abstract Although macrophages are important players in the injury/repair processes in animal models of acute kidney injury (AKI), their roles in human AKI remains uncertain owing to a paucity of human biopsy studies. We investigated the role of macrophages in 72 cases of biopsy-proven acute tubular necrosis (ATN) and six cases of healthy kidney. Macrophages were identified by CD68 and CD163 immunohistochemistry and analyzed for their effect on renal outcomes. CD163+ M2 macrophages outnumbered CD68+ cells in the healthy kidneys, suggesting that CD163+ macrophages are resident macrophages. The infiltration of both subtypes of macrophages increased significantly in ATN. The density of the CD68+ macrophages was significantly higher in advanced-stage AKI, whereas CD163+ M2 macrophages was not. Eighty percent of patients exhibited renal functional recovery during follow-up. Older age and a higher density of CD163+ macrophages predicted non-recovery, whereas the AKI stage, tubular injury score, and density of CD68+ cells did not. The density of CD163+ M2 macrophages was an independent predictor of low eGFR at 3 months in advanced-stage AKI. This is the first human study demonstrating the possible role of macrophages in the injury and repair phases of AKI.
CD163
CD68
Infiltration (HVAC)
Acute tubular necrosis
Cite
Citations (21)
CD163
Haptoglobin
Monocyte
Hemopexin
Scavenger Receptor
Cite
Citations (22)
Background The macrophage hemoglobin scavenging receptor CD163 plays a major role in the clearance of hemoglobin (Hb) released from lysed red blood cells after intraplaque hemorrhage (IPH). We hypothesize that impairment in CD163 expression may alter HO‐1 and ferritin defense mechanism in the clearance of Hb in diabetic (DM) plaques inducing atherothrombosis. Methods Human DM atherosclerotic plaques (33) and no‐DM plaques (49) were characterized using H&E. The macrophage (CD68) and CD163 protein expressions were quantified by double label immunochemistry and gene expression in serial sections by real time PCR. The HO‐1 and ferritin protein expression was graded by immunohistochemistry. Results The mean percentage of macrophages expressing CD163 was significantly decreased in DM plaques (DM 26.2 % ± 2 vs No‐DM 66.9 % ± 2, p=0.0001). The CD163 and HO‐1 mRNA expressions were down regulated in DM (DM 0.0689±0.017 vs No‐DM 0.3078±0.055, p=0.002, and DM 0.002±0.0006 vs No‐DM 0.0369±0.012, P =0.005) respectively. The protein expression of ferritin was also decreased in DM plaques (DM 0.7±0.1 vs no‐DM 2.6±0.2, p=0.0001). Conclusion CD163 may have a functional role in the induction of HO‐1 and ferritin expression. Thus, impairment in CD163 expression may alter HO‐1 and ferritin defense mechanism leading to atherothrombosis in DM plaques.
CD163
Scavenger Receptor
CD68
Haptoglobin
Cite
Citations (0)
Abstract The scavenger receptor CD163 is exclusively expressed by monocyte/macrophages and is shed by matrix metalloproteinases (MMPs) and neutrophil elastase (ELA2) as soluble CD163 (sCD163). Monocyte phenotype is altered in diabetes, but the relationship among monocyte CD163, sCD163, and diabetic complications is not known and was investigated in this study. Blood was obtained from patients with diabetes for >10 yr and mice with diabetes for ≤20 wk. Blood from people and mice without diabetes acted as controls. The percentage of CD163+ monocytes and monocyte CD163 mRNA was determined by flow cytometry and qRT-PCR, respectively. Plasma sCD163, MMPs, and ELA2 were measured by ELISA. The ability of glucocorticoids to stimulate isolated monocyte CD163 expression was also investigated. The percentage of CD163+ monocytes was significantly decreased and sCD163 significantly increased (both P < 0.05) in patients with diabetes with complications compared to those without complications. Plasma ELA2 and MMP-3 were also increased (P < 0.05), but CD163 mRNA was unaltered. sCD163 correlated with worsening renal function, as determined by eGFR (r = −0.48, P < 0.05). In diabetic mice, increased sCD163 at wk 5 and decreased percentage of CD163+ monocytes at wk 10 preceded alteration in kidney collagen IV mRNA at wk 20 (all P < 0.05). In vitro incubation of monocytes in anti-inflammatory glucocorticoid increased the percentage of CD163+ monocytes (P < 0.05). In people, higher sCD163 and decreased percentage of CD163+ monocytes were consistent with increased monocyte activation and shedding. The murine data indicated that these changes preceded the development of diabetic complications. Taken together, these results suggest that higher circulating percentage of CD163+ monocytes may have anti-inflammatory effects and may protect from development of diabetic complications.
CD163
Monocyte
Cite
Citations (27)
<p>The phenotype of macrophages in WT and CD163-/- mice. The expression of CD163 and CD204 was detected in peritoneal macrophages by western blot analysis (A). The expressions of EMR1, CD163, CD204, and CD206 were tested in several tissues by immunohistochemistry (B).</p>
CD163
M2 Macrophage
Cite
Citations (0)