Journal: Clinical and Translational Medicine

Article Title: Macrophage Cluster of Differentiation 163 promotes post‐infarction cardiac repair and preserves left ventricular function via osteopontin

doi: 10.1002/ctm2.70662

Figure Lengend Snippet: Higher soluble CD163 (sCD163) levels are associated with more severe left ventricular (LV) dilation and systolic dysfunction in patients with ischaemic cardiomyopathy (ICM). (A) Flowchart of patient enrolment. (B) Plasma concentrations of soluble Cluster of Differentiation 163 (CD163) ( n = 60 and 30), analysed by Mann–Whitney test. Correlations between circulating sCD163 concentration and (C) LV ejection fraction (LVEF), (D) log 10 of N‐terminal pro‐B‐type natriuretic peptide [log 10 (NT‐proBNP)], (E) relative wall thickness (RWT), (F) LV posterior wall thickness at diastole (LVPW, d), (G) LV end‐systolic diameter (LVESD) and (H) LV end‐diastolic diameter (LVEDD) are shown. Each data point represents an individual patient ( n = 30). Statistical analysis was performed using simple linear regression. p values are indicated by asterisks: p < 0.05 (*), p < 0.01 (**), p < 0.001 (***).

Article Snippet: Recombinant mouse CD163 protein (ABclonal) was reconstituted in sterile PBS.

Techniques: Clinical Proteomics, MANN-WHITNEY, Concentration Assay

Journal: Clinical and Translational Medicine

Article Title: Macrophage Cluster of Differentiation 163 promotes post‐infarction cardiac repair and preserves left ventricular function via osteopontin

doi: 10.1002/ctm2.70662

Figure Lengend Snippet: Cluster of Differentiation 163 (CD163) expression was decreased in the infarct zone during the reparative phase after myocardial infarction (MI). (A) Schematic diagram of the mouse study design. (B) Immunohistochemistry staining of CD163 in heart sections at Day 3 and 28 post‐MI. Scale bars, 500 and 50 µm. Boxed areas indicate the regions shown in the zoomed‐in images. Data points represent individual mice ( n = 4) from two independent experiments and analysed by one‐way ANOVA with Tukey's multiple comparisons test. (C) Protein levels of CD163 expression in the heart at Day 3 and 28 post‐MI. Quantification of the CD163/GAPDH ratio is presented ( n = 3). (D–F) Flow cytometric analysis of CD163 + cardiac macrophages (cMacs), defined as CD11b + F4/80 + CD45 + cells, including representative plots (D), percentage of CD163 + cMacs among total cMacs (E) and percentage of CD163 + cMacs among total CD45 + cells (F). Each dot represents one mouse ( n = 5), with data pooled from two independent experiments. Statistical analysis was performed using unpaired t ‐test. See also Figure . WT, wild‐type. p values are indicated by asterisks: p < 0.05 (*), p < 0.01 (**), p < 0.001 (***).

Article Snippet: Recombinant mouse CD163 protein (ABclonal) was reconstituted in sterile PBS.

Techniques: Expressing, Immunohistochemistry, Staining

Journal: Clinical and Translational Medicine

Article Title: Macrophage Cluster of Differentiation 163 promotes post‐infarction cardiac repair and preserves left ventricular function via osteopontin

doi: 10.1002/ctm2.70662

Figure Lengend Snippet: Macrophage Cluster of Differentiation 163 (CD163) protected against myocardial infarction (MI)‐induced systolic dysfunction and left ventricular (LV) dilation. (A) Schematic diagram of the mouse study design by using wild‐type (WT) and Cd163 − / − mice subjected to left anterior descending (LAD) ligation or sham surgery. (B) Representative M‐mode echocardiography images analysed by parasternal long‐axis view (PLAX). Quantification of (C) ejection fraction, (D) fractional shortening, (E) relative wall thickness and (F) global longitudinal strain (GLS). Each dot represents one mouse ( n = 15 for Days 3 and 28; n = 10 for Day 56) pooled from two to three independent experiments. (G) Schematic diagram of the study design using sham‐ or MI‐treated WT and Cd163 − / − mice receiving recombinant mouse CD163 protein (.05 mg/kg/day) or mouse serum albumin (MSA) via intraperitoneal injection three times per week. Quantification of (H) ejection fraction, (I) fractional shortening, (J) relative wall thickness and (K) GLS. Each dot represents one mouse ( n = 10) pooled from two independent experiments. Statistical analysis was performed using two‐way ANOVA followed by Tukey's multiple comparisons test. See also Figures . p values are indicated by asterisks: p < 0.05 (*), p < 0.01 (**), p < 0.001 (***).

Article Snippet: Recombinant mouse CD163 protein (ABclonal) was reconstituted in sterile PBS.

Techniques: Ligation, Recombinant, Injection

Journal: Clinical and Translational Medicine

Article Title: Macrophage Cluster of Differentiation 163 promotes post‐infarction cardiac repair and preserves left ventricular function via osteopontin

doi: 10.1002/ctm2.70662

Figure Lengend Snippet: Cluster of Differentiation 163 (CD163) deficiency represses the expression of osteopontin (OPN) in cardiac macrophages (cMacs) during post‐myocardial infarction (MI) cardiac repair. (A) Representative flow cytometry plots showing the distribution of CD163 and CCR2 in cMacs. Percentages of CD163 + CCR2 − cMacs among (B) total cMacs and (C) CD45 + cells. Data points represent individual mice ( n = 5) from two independent experiments and statistics by unpaired t ‐test. (D) Distribution of Tim4 and CD163 in cMacs and (E) distribution of MHC‐II and CD163 in cMacs. Data points represent individual mice ( n = 10) from two independent experiments and statistics by paired t ‐test. (F) CD45 + cells sorted at Day 28 post‐surgery for single‐cell RNA sequencing (scRNA‐seq), with 2483 macrophages and monocytes further subclustered. (G) Proportion of indicated clusters in each group. (H) Distribution of Cd163 in the indicated groups. (I) KEGG pathway analysis of differentially expressed genes between wild‐type (WT) and Cd163 − / − mice in the MI group. (J) Venn diagram showing genes significantly downregulated in Cd163 − / − mice compared to WT in both sham and MI groups. (K) Distribution of Spp1 in the indicated groups. (L) Protein levels of OPN in the indicated groups. Data represent three biological replicates per group. One representative out of three similar experiments is displayed. See also Figures . p values are indicated by asterisks: p < 0.05 (*), p < 0.01 (**), p < 0.001 (***).

Article Snippet: Recombinant mouse CD163 protein (ABclonal) was reconstituted in sterile PBS.

Techniques: Expressing, Flow Cytometry, Single Cell, RNA Sequencing

Journal: Clinical and Translational Medicine

Article Title: Macrophage Cluster of Differentiation 163 promotes post‐infarction cardiac repair and preserves left ventricular function via osteopontin

doi: 10.1002/ctm2.70662

Figure Lengend Snippet: Osteopontin (OPN) administration alleviated systolic dysfunction and ventricular dilation in Cluster of Differentiation 163 (CD163)‐deficient mice after myocardial infarction (MI). (A) Schematic diagram of the mouse study design. Mice received 200 ng OPN, mouse serum albumin (MSA) or an equal volume of phosphate‐buffered saline (PBS) injected directly into the infarct zone during surgery. (B) Representative M‐mode echocardiography images. (C–J) Quantification of ejection fraction, fractional shortening, relative wall thickness and global longitudinal strain (GLS) at Day 3 and 28 post‐MI. Data points represent individual mice ( n = 11 or 10 for MSA‐treatment) from two independent experiments. Statistical analysis was performed using two‐way ANOVA with Tukey's multiple comparisons test. See also Figure . WT, wild‐type. p values are indicated by asterisks: p < 0.05 (*), p < 0.01 (**), p < 0.001 (***).

Article Snippet: Recombinant mouse CD163 protein (ABclonal) was reconstituted in sterile PBS.

Techniques: Saline, Injection

Journal: Clinical and Translational Medicine

Article Title: Macrophage Cluster of Differentiation 163 promotes post‐infarction cardiac repair and preserves left ventricular function via osteopontin

doi: 10.1002/ctm2.70662

Figure Lengend Snippet: Osteopontin (OPN) administration improved cardiac repair in Cluster of Differentiation 163 (CD163)‐deficient mice following myocardial infarction (MI). (A, B, G) RNA‐seq of infarct and remote zones at Day 28 post‐MI. Mice received 200 ng OPN or phosphate‐buffered saline (PBS) injected into the infarct zone during MI or underwent sham surgery (wild‐type [WT] and Cd163 − / − ). (A) Heatmap showing the average expression of differentially expressed genes (DEGs) in the infarct zone of PBS‐treated Cd163 − / − MI mice (cut‐off: p < .05). Sample sizes: n = 3, 3, 3, 3, 2, 2, with each sample pooled from two to three mice. (B) Heatmap showing the average expression of DEGs in the remote zone compared with PBS‐treated Cd163 − / − MI mice (cut‐off: p < .05); n = 3, 3, 3, 3, 3, 2, with each sample pooled from two to three mice. (C) GO biological pathway enrichment analysis of Cluster 3 genes identified in (A). (D) Masson's trichrome staining of heart sections from the indicated mice at Day 28 post‐surgery. Scale bar: 500 and 50 µm. Boxed areas indicate the regions shown in the zoomed‐in images. (E) Percentage of fibrotic scar area in the left ventricle. Data points represent individual mice ( n = 3) from two independent experiments. Statistical analysis was performed using one‐way ANOVA with Holm‐Šídák's multiple comparisons test. (F) Relative scar thickness was normalized to the mean scar thickness of PBS‐treated WT mice following MI. Each data point represents an individual region ( n = 24) collected from three mice across two independent experiments. Statistical significance was assessed using the Kruskal–Wallis test with Dunn's multiple comparisons. (G) Verhoeff's elastin–Van Gieson (EVG) staining showing elastin (black) and collagen (red) in heart sections from the indicated mice at Day 28 post‐surgery. Scale bar: 500 and 50 µm. Boxed areas indicate the regions shown in the zoomed‐in images. (H) Quantification of the elastin‐to‐collagen area ratio after excluding nuclear areas. Data points represent individual fields of view ( n = 30) from three mice across two independent experiments. Statistical analysis was performed using the Kruskal–Wallis test followed by Dunn's multiple comparisons. See also Figure . p values are indicated by asterisks: p < 0.05 (*), p < 0.01 (**), p < 0.001 (***).

Article Snippet: Recombinant mouse CD163 protein (ABclonal) was reconstituted in sterile PBS.

Techniques: RNA Sequencing, Saline, Injection, Expressing, Staining

Journal: Journal of Inflammation Research

Article Title: Increased CD163+ Macrophage Activation and High Expression of CD163 Promote Granulosa Cell Apoptosis in Polycystic Ovary Syndrome

doi: 10.2147/JIR.S532920

Figure Lengend Snippet: Increased macrophages and elevated CD163 expression in macrophages in the ovary and uterus of PCOS mice. ( a ) Representative immunofluorescence images of CD163 and F4/80 in ovaries and uteri of control and PCOS mice (scale bar = 100 μm). ( b ) Quantification of CD163 + , F4/80 + , and F4/80 + CD163 + cell proportions in the ovaries and uteri of control and PCOS mice. * p < 0.05, ** p < 0.01, ns: p > 0.05.

Article Snippet: CD163 protein was acquired from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Expressing, Immunofluorescence, Control

Journal: Journal of Inflammation Research

Article Title: Increased CD163+ Macrophage Activation and High Expression of CD163 Promote Granulosa Cell Apoptosis in Polycystic Ovary Syndrome

doi: 10.2147/JIR.S532920

Figure Lengend Snippet: Increased M1 and M2 macrophages and elevated CD163 expression in M1 and M2 macrophages in the ovary and uterus of PCOS mice. ( a ) Representative immunofluorescence images of CD163, F4/80, iNOS, and Arg1 in the ovaries of control and PCOS mice (scale bar = 50 μm). ( b ) Representative immunofluorescence images of CD163, F4/80, iNOS, and Arg1 in the uterus of control and PCOS mice (scale bar = 50 μm). ( c ) Quantification of F4/80 + iNOS + CD163 + and F4/80 + Arg1 + CD163 + cell proportions in the ovaries. ( d ) Quantification of F4/80 + iNOS + CD163 + and F4/80 + Arg1 + CD163 + cell proportions in the uterus. * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: CD163 protein was acquired from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Expressing, Immunofluorescence, Control

Journal: Journal of Inflammation Research

Article Title: Increased CD163+ Macrophage Activation and High Expression of CD163 Promote Granulosa Cell Apoptosis in Polycystic Ovary Syndrome

doi: 10.2147/JIR.S532920

Figure Lengend Snippet: Increased apoptosis in CD163 + ovarian cells from PCOS mice. ( a ) Representative images of TUNEL and CD163 in the ovaries of control and PCOS mice via immunofluorescence analysis (scale bar = 50 μm). ( b ) Quantification of TUNEL + and CD163 + TUNEL + cell proportions in the ovaries. ** p < 0.01, *** p < 0.001.

Article Snippet: CD163 protein was acquired from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: TUNEL Assay, Control, Immunofluorescence

Journal: Frontiers in Nutrition

Article Title: High intake of n-6 polyunsaturated fatty acid exacerbates non-alcoholic steatohepatitis by the involvement of multiple metabolic pathways

doi: 10.3389/fnut.2025.1562509

Figure Lengend Snippet: Effects of n-6 PUFA on liver macrophage phenotype in rats with NASH induced by a choline-deficient diet. (A) M1-type Kupffer cells (KCs) identified by double staining: red arrows show CD11c-positive cells, green arrows show CD68-positive cells, and yellow arrows highlight CD11c and CD68 double-positive M1-type KCs (Scale bar – 50 μM). (B) M2-type KCs identified similarly, with red arrows indicating CD163-positive cells, green arrows showing CD68-positive cells, and yellow arrows marking CD163 and CD68 double-positive M2-type KCs (Scale bar – 50 μM). For (A,B) (see ) for full-size photomicrographs. (C) M1/M2 phenotype ratio (unitless), calculated as the proportion of CD68 + CD11c + to CD68 + CD163 + cells. (D) Relative PPAR-γ2 mRNA expression (fold change normalized to GAPDH) in the liver, which is linked to macrophage polarization and inflammation. Data are expressed as mean ±SEM; n = 6/group.

Article Snippet: BCA protein quantitation kit (Boster Bio, Cat # AR0146), RIPA lysis buffer (Boster Bio, Cat # 0105), protease inhibitor cocktails (Boster, Bio Cat # AR1182), phosphatase inhibitor (Boster Bio, Cat # AR1183), color pre-dyed protein marker (Boster Bio, Cat # AR1113), Western-specific primary and secondary antibody diluent (Boster Bio, Cat # AR1017), wash buffer TBS-T (Boster Bio, Cat # AR0195-10), ECL chemiluminescent reagent (Boster Bio, Cat # AR1196), BSA TBS buffer system blocking solution (Boster Bio, Cat # AR0189), NF-κB antibody (Boster Bio, Cat # A01228-1), GAPDH antibody (Boster Bio, Cat # M00227), HRP-conjugated goat anti-rabbit IgG (Boster Bio, Cat # BA1054), CD163 antibody (Boster Bio, Cat # A00812-2), CD11c antibody (Boster Bio, Cat # A00357-3), CD68 antibody (Boster Bio, Cat # BA3638), fluorescent (DyLight 488) labeled goat anti-rabbit IgG (Boster Bio, Cat # BA1127), fluorescent (DyLight 594) labeled goat anti-rabbit IgG (Boster Bio, Cat # BA1142), rat TNF-α ELISA kit (Jiangsu Enzyme Immunoassay Co., Ltd., Cat # MM-0180R1), rat IL-1β ELISA kit (Boster Bio, Cat # EK0393), rat IL-4 ELISA kit (Jiangsu Enzyme Immunoassay Co., Ltd., Cat # MM-0191R1), rat IL-10 ELISA kit (Boster Bio, Cat # EK0418), 25 VD3 assay kit (Roche Diagnostics, Cat # 07028148190), TAOC assay kit (Nanjing Jiancheng, Cat # A015-3-1), MDA assay kit (Nanjing Jiancheng, Cat # A003-1-2), and free fatty acid kit (Kunchuang Biotechnology, Xian, China, Cat # SK125-2).

Techniques: Double Staining, Expressing