MA5-13324

antibody from Invitrogen Antibodies

Targeting: CD68 DKFZp686M18236, GP110, LAMP4, macrosialin, SCARD1

Provider product page for MA5-13324

Immunocytochemistry

Immunohistochemistry

Other assay

Antibody data

Antibody Data
Antigen structure
References [113]
Comments [0]
Validations
Immunocytochemistry [2]
Immunohistochemistry [1]
Other assay [18]

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Product number: MA5-13324 - Provider product page
Provider: Invitrogen Antibodies
Product name: CD68 Monoclonal Antibody (KP1)
Antibody type: Monoclonal
Antigen: Other
Description: MA5-13324 targets CD68 in IHC (P) and ICC/IF applications and shows reactivity with Feline, Human, Non-human primate, and Rat samples. Does not react with Canine or Chicken. The MA5-13324 immunogen is subcellular fraction of human alveolar macrophages.
Reactivity: Human, Rat, Feline
Host: Mouse
Isotype: IgG
Antibody clone number: KP1
Vial size: 200 µL
Concentration: 0.5 mg/mL
Storage: 4° C

CD68 protein structure - MA5-13324 shown in red.

Supportive validation

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Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 2 CD68 Semi-quantitative Scoring. CD68 staining in hippocampal sections from animals close to the average for the following groups: (a) Sham, (b) injury, (c) injury + supplement A, and (d) injury + supplement B. Arrows indicate positive staining in the perivascular domain, (e) summary statistics for the semi-quantitative scoring of CD68 pathology ( n >= 5, error bars = standard error. Kruskal-Wallis test p = 0.057).

Supportive validation

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Experimental details: Figure 4. Hepatic MFs promote platelet recruitment. ( A ) Immunohistochemical (IHC) staining for macrophages (CD68 + ) and platelets (CD41 + ) in normal liver biopsies (Normal) and those from patients with AILI (Patient) (n = 10/group). Scale bar, 25 mum. ( B ) Immunofluorescence (IF) staining for intrahepatic platelets (CD41 + ) and Kupffer cells (KCs) (F4/80 + ) in male C57B/6 mice treated with PBS or acetaminophen (APAP) for 3 hr. Scale bar, 25 mum. Arrowheads indicate platelets adherent to KCs. Quantification of platelets adherent to KCs or liver sinusoidal endothelial cells (LSECs). ( C-F ) Male C57B/6 mice were injected with either empty liposomes containing PBS (PBS) or liposomes containing clodronate (CLDN), followed by APAP treatment. ( C, D ) Non-parenchymal cells (NPCs) were isolated and underwent flow cytometry analysis. Indicated cells were gated on single live CD45 + CD146 - cells. IF staining was performed to detect intrahepatic platelets (CD41 + ). Scale bar, 25 mum. ( E ) Serum levels of ALT and ( F ) liver histology with necrotic areas outlined. Scale bar, 250 mum (n = 6 mice/group in B-F ). Two-tailed, unpaired Student's t-test was performed in B-D , F .

Supportive validation

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Experimental details: Figure 3 Decreased PON1 levels associated with an increase in lipid oxidation and accumulation in macrophages in SAH. (A) Plasma oxidized LDL levels in SAH (median, 227; range, 150-430) compared to AC (median, 175; range, 200-100) and HC (median, 172; range, 185-96), and nonsurvivors of SAH (median, 256; range, 183-430) compared to survivors (median, 198; range, 155-310); P < 0.05 is significant. (B) Accumulation of lipid bodies in CD11b+CD163+ macrophages in SAH (median, 4.6%; range, 1.01%-22.7%) compared to AC (median, 3.07%, range, 1.02%-4.51%) and HC (median, 1.85%; range, 1.01%-2.22%), and accumulation of lipid bodies in nonsurvivors of SAH (median, 10.93%; range, 2.44%-22.70%) compared to survivors (median, 2.24%; range, 0.85%-7.62%); P < 0.05 is significant. (C) Accumulation of lipid bodies in CD11b+HLA-DR+ macrophages in SAH (median, 24.55%; range, 4.65%-68.60%) compared to AC (median, 6.38%; range, 3.79%-8.41%) and HC (median, 0.87%; range, 0.10%-2.22%), and accumulation of lipid bodies in nonsurvivors of SAH (median, 45.95%; range, 16.60%-68.60%) compared to survivors (median, 18.70%; range, 4.65%-39.00%); P < 0.05 is significant. (D) Relative expression of linked genes to lipid uptake, transport, metabolism, biosynthesis, macrophage activation, and inflammation in PBMCs of nonsurvivors versus survivors. (E) Immunofluorescent analysis of Nile red staining of healthy MDMs treated with plasma samples of nonsurvivors and survivors of SAH. Mean florescent intensity of

Supportive validation

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Experimental details: Fig. 2 Elevated TGF-beta levels in the early inflammatory stage of AS. a Hematoxylin and eosin (H&E) staining and b Safranin O-Fast Green (SOFG) staining of normal and inflamed interspinous ligaments. In the AS group, the right panels show magnified views of the boxed area in the left panels. Scale bar: 100 mum (two panels on the right); 25 mum (left panel). c Immunostaining and d quantitative analysis of CD68-positive cells (brown) in the normal and inflamed interspinous ligaments (sagittal view). The bottom panels show magnified views of the boxed area in the top panels. Scale bar: 100 mum (top panels); 25 mum (bottom panels). e Immunostaining and f quantitative analysis of pSmad2/3-positive cells (brown) in the normal and inflamed interspinous ligaments (sagittal view) in normal ligaments and inflammatory ligaments. The bottom panels show magnified views of the boxed area in the top panels. Scale bar: 100 mum (top panels); 25 mum (bottom panels). g Immunostaining and h quantitative analysis of pSmad1/5/8-positive cells (brown) in the normal and inflamed interspinous ligaments (sagittal view). The bottom panels show magnified views of the boxed area in the top panels. Scale bar: 100 mum (top panels); 25 mum (bottom panels)

Supportive validation

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Experimental details: Fig. 5 Osteoclast resorption of bony interspinous ligaments releases active TGF-beta to drive the progression of ossification in AS patients. a Hematoxylin and eosin (H&E) staining and b Safranin O-Fast Green staining of normal and HO-formed interspinous ligaments. In the AS group, the right panels show magnified views of the boxed area in the left panels. Scale bar: 100 mum (two panels on the right); 25 mum (two panels on the left). c Tartrate-resistant acid phosphatase (TRAP)-positive cells (red) and d quantitative analysis of the TRAP-positive osteoclast surface (OCS) per bone surface. The bottom panels show magnified views of the boxed area in the top panels. Scale bar: 100 mum (top panel); 25 mum (bottom panel). e Immunostaining and f quantitative analysis of CD68-positive cells (brown) in the normal and HO-formed interspinous ligaments (sagittal view). The bottom panels show magnified views of the boxed area in the top panels. Scale bar: 100 mum (top panel); 25 mum (bottom panel). g Immunostaining and h quantitative analysis of pSmad2/3-positive cells in the normal and HO-formed interspinous ligaments (sagittal view). The bottom panels show magnified views of the boxed area in the top panels. Scale bar: 100 mum (top panel); 25 mum (bottom panel). i Immunostaining and j quantitative analysis of Osterix-positive cells (brown) in the normal and HO-formed interspinous ligaments (sagittal view). The bottom panels show magnified views of the boxed area in the top panels. Scal

Supportive validation

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Experimental details: Fig. 5 Dopamine increases the number of cells with high levels of nuclear NF-kappaB. (5A) Representative images of nuclear translocation of NF-kappaB (green) in hMDM in untreated, dopamine-treated or LPS-treated conditions for 60 min. White arrow indicates nuclear NFkappaB staining. (5B) Fold change in the average intensity of nuclear NF-kappaB in control and treated-conditions, [ Fig. 5 B, Wilcoxon test, n = 12, ***p = 0.001, sum of (+,-) ranks 77, -1] (5C) As the increase in average intensity shown in 5B was not the same magnitude as what was seen in Western blot (not shown), the percent of hMDM that expressed high levels of nuclear NF-kappaB increased in dopamine-treated and LPS-treated hMDMs was compared to controls [ Fig. 5 C, Wilcoxon test, n = 12, ***p = 0.001, sum of (+,-) ranks 77, -1]. hMDMs treated with dopamine displayed an increased percentage of cells with a high NFkappaB level. (5D) Representative images of nuclear translocation of NF-kappaB in vehicle or DA treated hMDM from donors with or without CMV infection. Note the increased amount of NF-kappaB in the dopamine-treated cells with CMV. (5E) Percentage of cells with elevated NF-kappaB nuclear expression in hMDM increased when pre-existing CMV infection was present [ Fig. 8 B, mixed effects model (REML), n = 7 without CMV, n = 6 with CMV; CMV, **p = 0.0037, F(1,11) = 13.44; DA, **p = 0.0020, F (1,11) = 16.18]. (For interpretation of the references to colour in this figure legend, the reader is referred to th

Supportive validation

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Experimental details: Figure 2 Ablation of Pdgfrb + lineage MSCs in dystrophic muscle. ( A ) Representative IF (from n = 5) on gastrocnemius (GM) of Pdgfrb-TK mice showing that GCV treatment depletes PDGFRbeta+ cells associated with CD31+ endothelium. ( B ) Data from ( A ) quantified based on the analysis of n = 10 view fields. ( C ) Representative IF on indicated muscle tissues from mdx/Pdgfrb-TK mice showing that GCV treatment ablates PDGFRbeta+ cells (red arrows) associated with the endothelium stained with isolectin B4 (IB4). ( D ) RT-PCR showing the effect of Pdgfrb + lineage cell ablation on the relative expression of Pdgfrb (normalized to 18S RNA ), n = 3. ( E ) RT-PCR showing the effect of Pdgfrb + lineage cell ablation on the relative expression of Tgfb1 (normalized to 18S RNA ) n = 3. ( F ). Representative IF on indicated muscle tissues from mdx/Pdgfrb-TK mice showing that GCV treatment reduces the frequency of CD68+ macrophages (red arrows) but not CD206+ macrophages (green arrows). * p < 0.05; *** p < 0.01 (Student's t -test). Scale bar: 50 um.

Supportive validation

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Experimental details: Fig. 2 Melatonin treatment reduces morphine-induced inflammasome activation in mouse brain tissues and primary microglia and this effect is mediated by NLRP3. ( A ) mRNA levels of Nlrp3 (n = 6-7 animals per group; F 3,20 = 18.22, P < 0.0001; control group versus morphine group, 95% CI [-1.17 to -0.31], P = 0.0006; morphine group versus group ""melatonin + morphine"", 95% CI [0.57 to 1.43], P = 0.0002), Caspase-1 (n = 5-7 animals per group; F 3,21 = 12.57, P < 0.0001; control group versus morphine group, 95% CI [-2.44 to -0.78], P = 0.0011; morphine group versus group ""melatonin + morphine"", 95% CI [0.72 to 2.45], P = 0.0021) and Il-1beta (n = 7 animals per group; F 3,22 = 13.35, P < 0.0001; control group versus morphine group, 95% CI [-3.06 to -1.06], P = 0.0009; morphine group versus group ""melatonin + morphine"", 95% CI [0.87 to 2.88], P = 0.0012) and ( B ) protein levels of NLRP3, ASC, IL-1beta, Caspase-1 (p20), Pro-IL-1beta and Pro-Caspase-1 in cortex tissues from mice in Fig. 1 A . ( C ) Serum level of IL-1beta in mice treated with morphine and/or melatonin (n = 3 animals per group; F 3,8 = 12.99, P = 0.0019; control group versus morphine group, 95% CI [-66.01 to -17.96], P = 0.0023; morphine group versus group ""melatonin + morphine"", 95% CI [6.58 to 54.63], P = 0.0150). ( D ) Double immunostaining of mouse cerebral cortex brain slices with anti-ASC (red) and anti- TMEM119 (green) antibodies to indicate NLRP3 inflammasome in microglia cells. ( E ) Percentage of micr

Supportive validation

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Experimental details: Figure 5. Immunocytochemistry of retinal sections in the GA borders of donors with AMD stained with inflammatory cell marker antibodies. Immunofluorescence of control and AMD retinal sections labeled with antibodies to Iba-1 ( A, B, C, D ) and CD68 ( E, F, G, H ). Non-AMD donor displayed very few Iba-1+ cells in their retinas, with cells mostly localized in the inner retina, but there were a few also localized to the photoreceptor outer segments ( A , white arrowheads ). The AMD donors with small and medium size GA atrophy ( B, C ) displayed infiltration of Iba-1+ cells in the outer retina; these cells displayed an amoeboid phenotype. However, fewer Iba-1+ cells were present in the retinas of AMD donors with big size GA atrophy ( D ). Non-AMD donor ( E ) displayed very few CD68+ cells in their retinas. The AMD donors with small and medium size GA atrophy displayed increased presence of CD68+ cells in the inner retina ( F, G, white arrowheads ). However, CD68+ cells were mostly absent from AMD donors with big size GA atrophy ( D ). For all images, the atrophy was located at the left edge of the picture. Scale bar: 200 um.

Supportive validation

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Experimental details: FIGURE 1 Prkaa1 upregulation is associated with macrophage metabolism in mice fed a high-fat diet. (A) Schema illustrating leukocyte sorting from adipose tissues by CD45-positive staining. (B) Real-time PCR analysis and quantification of mRNA levels of Prkaa1 and Prkaa2 in leukocytes sorted from stromal vascular cells in HFD- and CD-fed mice. n = 8. (C,D) Real-time PCR analysis and quantification of mRNA levels of Slc2a1 , Pfkfb3 , Cd36 , and Cpt1 in leukocytes sorted from stromal vascular cells in HFD- and CD-fed mice. n = 8. (E,F) Representative images and quantification data of Prkaa1, Slc2a1, and CD36 co-staining with F4/80 or CD68 (macrophage markers) in adipose tissues from HFD- and CD-fed mice. n = 4, Scale bars, 20 mum. All data were expressed as mean +- SEM. Statistical significance was determined by unpaired Student's t -test. * p < 0.05 was considered significant, ** p < 0.01, *** p < 0.001.

Supportive validation

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Experimental details: 10.1371/journal.pone.0260554.g001 Fig 1 Left ventricular remote cardiac and renal cortical interstitial fibrosis and associated myofibroblast and macrophage infiltration, from hypertensive animals (H), hypertensive animals treated with daily oral spironolactone (H+SP), hypertensive animals with a myocardial infarction (H+MI) and hypertensive animals with a myocardial infarction and daily oral treatment with spironolactone (H+MI+SP) after four weeks. (a) Representative images of cardiac fibrosis, myofibroblasts and macrophage from the inferior segment of the left ventricle. The top panels show histological sections (Picrosirius red) of the whole heart (transverse section taken 6mm from the apex), with higher powered images (x100) of the inferior myocardium in the panels below. The lower panels show representative pictures (x100 magnification) taken from the remote inferior segment of myofibroblasts (stained positive with alpha smooth muscle actin; alphaSMA, and shown by the arrows) and macrophage (stained positive with Cluster of Differentiation 68; CD68, and shown by arrows). (b) Quantitative assessment of remote cardiac (left) and renal cortical (right) interstitial fibrosis (as assessed by Picrosirius red, top panels), myofibroblasts (as assessed by alphaSMA, middle panels) and macrophage infiltration (as assessed by CD68, bottom panels). The red dashed line represents the mean normotensive values (data not shown). Values are expressed as mean +- standard deviation. * indic

Supportive validation

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Experimental details: Figure 11. Deficiency of Ces1d in adipose tissue causes local unhealthy microenvironment in adipose tissue and the liver, ultimately leading to systemic insulin resistance. (A) qPCR analysis for the mRNA levels of adipogenesis-related genes including Pdgfa , Pdgfb , Zfp243 , and Dlk1 in the sWAT of WT and FKO mice fed on regular chow or HFD (n = 5 in each group, each point represents a biology replicate, representative of three repeats). Data are represented as mean +- SEM, one-way ANOVA , * P < 0.05, ** P < 0.01, *** P < 0.001. (B) qPCR analysis for the mRNA levels of fibrosis related genes including Col1a1 , Col2a1 , Clo3a1 , Clo6a3 , and Lox in the sWAT from WT and FKO mice fed on regular chow or HFD (n = 5 in each group, each point represents a biology replicate, representative of three repeats). Data are represented as mean +- SEM, one-way ANOVA , * P < 0.05, ** P < 0.01, *** P < 0.001. (C) qPCR analysis for the mRNA levels of inflammation related genes including Tlr4 , Tnf , and Adgre1 in the sWAT of WT and FKO mice fed on regular chow or HFD (n = 5 in each group, each point represents a biology replicate, representative of three repeats). Data are represented as mean +- SEM, one-way ANOVA , * P < 0.05, ** P < 0.01. (D) IF staining with alpha-Mac-2 antibody on the eWAT of WT and FKO mice fed on HFD (representative of six fields, experiments were repeated for three times; scale bars: 200 mum). (E) Co-IF staining with alpha-CD68 (green) and alpha-CD206 (red) antibodies on

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 1 CtBP mRNA and protein levels were significantly increased in OA biopsies . (A and B) The relative mRNA levels of CtBP1 and CtBP2. Total RNA from biopsies of 48 OA patients and 48 controls was used to determine the mRNA levels of CtBP1 (A) and CtBP2 (B) by qRT-PCR analyses. The expression of CtBP1 and CtBP2 in a healthy control was defined as one-fold. **P