monoclonal rabbit anti cd36  (Proteintech)

Journal: Nature Communications

Article Title: Loss of embryonically-derived Kupffer cells during hypercholesterolemia accelerates atherosclerosis development

doi: 10.1038/s41467-024-52735-2

Figure Lengend Snippet: A Gene Set Enrichment analysis (GSEA) of the reactome_cholesterol_biosynthesis and foamy plaque macrophages gene signatures in KC from chow- and HC-fed (4 days) Ldlr−/− mice using the Phantasus software. The foamy plaque macrophages gene signature was generated from a previously published dataset (GSE116239). B KCs in HC-fed mice exhibit high granularity (SSC-A hi ) and ( C ) strongly stain for lipids (bodipy; n = 8 chow and n = 7 HC; combined 2 independent experiments; **** p < 0.0001). D Changes in cholesterol content (* p = 0.0115), in cholesteryl-esters (* p = 0.0115) and various CE species in KCs sorted from chow- and HC-fed (4 days) Ldlr−/− mice ( n = 3 chow and n = 4 HC; 1 experiment). E Two-photon laser scanning microscopy images of the liver of chow and HC-fed (4 days) Ldlr−/− mice. Numerous lipid droplets (white spots) are detected by Coherent anti-Stokes Raman Spectroscopy (CARS) in TIMD4 + KCs (red; 3D reconstruction by mask rendering on the right images) and in the hepatocytes (autofluorescence in green) of HC-fed mice as compared to the chow condition. Scale bar = 10 μm. F Calculated amount of total cholesterol (** p = 0.006) and of free cholesterol (FC) and cholesteryl-esters (CE) (**** p < 0.0001) present in the liver of chow- ( n = 6 mice) and HC-fed (4 days; n = 8 mice; 1 experiment) Ldlr−/− mice. G Calculated amount of total cholesterol (**** p < 0.0001) and of FC (** p = 0.003) and CE (** p = 0.003) present in the KC pool of chow- ( n = 3 mice) and HC-fed (4 days; n = 5 mice; 1 experiment) Ldlr −/− mice. H Heatmap generated from the RNA-Seq depicting the level of expression of scavenger receptors in KCs from chow- and HC-fed (4 days) Ldlr−/− mice. I Changes in the granularity (SSC-A; *** p = 0.0002) and lipid content (bodipy; ** p = 0.005) of KCs in mice fed HC diet overnight and injected in vivo either with anti-CD36 blocking antibodies ( n = 8) or isotype control antibodies ( n = 9) (2 independent experiments combined). All data in this figure are presented as mean values ± SEM. Statistical significance has been assessed with a two-sided t -test unless otherwise stated on the corresponding panel legend. Source data are provided as a Source Data File.

Article Snippet: Chow fed Ldlr−/− mice were fasted during the day and administered i.v. 50 μg of anti-CD36 monoclonal antibody (MF3, thermoFisher Scientific) or 50 μg of rat IgG2a isotype (thermoFisher Scientific) before given access to HC diet.

Techniques: Software, Generated, Staining, Laser-Scanning Microscopy, Raman Spectroscopy, RNA Sequencing, Expressing, Injection, In Vivo, Blocking Assay, Control

Journal: Nature Communications

Article Title: Loss of embryonically-derived Kupffer cells during hypercholesterolemia accelerates atherosclerosis development

doi: 10.1038/s41467-024-52735-2

Figure Lengend Snippet: A KC numbers before and 4, 8, 13 and 21 days after induction of hypercholesterolemia (0 vs 4 days: **** p < 0.0001 and 0 vs 13 days: * p = 0.04). B Representative flow cytometry of CLEC2 + TIMD4- KCs during prolonged exposure of the mice to hypercholesterolemia. C Frequency of CLEC2 + TIMD4- KCs (0 vs 8 days: ** p = 0.0015, 0 vs 13 days: *** p = 0.0001 and 0 vs 21 days: **** p < 0.0001). D EmKCs and MoKCs numbers before and at 4, 8, 13 and 21 days after induction of hypercholesterolemia (Panels A , C and D : n = 9, 8, 5, 4 and 8 mice for experimental points 0, 4, 8,13, and 21 days; 2 independent experiments combined) (1-way ANOVA and multiple comparison test; EmKCs: 0 vs 4 days: **** p < 0.0001; MoKCs: 0 vs 8 days: ** p = 0.0013, 0 vs 13 days: *** p = 0.0002 and 0 vs 21 days: **** p < 0.0001). E Representative FACS plots showing TIMD4- cells among CLEC2 + KCs in Ldlr −/− and Ccr2 −/− x Ldlr −/− female mice subjected to hypercholesterolemia for 3 weeks. F Fold-change in Csf1 expression (normalized to day 0) in livers of Ldlr−/− mice fed HC diet ( n = 5, 4, 4, 4 and 4 mice for day 0, 4, 7, 13 and 21, respectively; 1-way ANOVA and multiple comparison test; 0 vs 4 days: * p = 0.026, 0 vs 8 days: **** p < 0.0001, 0 vs 13 days: * p = 0.043 and 0 vs 21 days: ** p = 0.007). G Percentage of KI-67 + cells among EmKCs and MoKCs in HC-fed female Ldlr−/− mice for 3 weeks (*** p = 0.0007). H Ly6C+ monocytes and MoDMacs in livers of Ldlr −/− mice fed chow ( n = 4) or HC diet ( n = 4) for 21 days. (Holm-Sidak multiple comparison test; Chow vs HC: Monocytes ** p = 0.002 and MoDMacs ** p = 0.006). I Granularity (**** p < 0.0001) and ( J ) lipid content (**** p < 0.0001) of EmKCs and MoKCs of mice ( n = 9) fed HC diet for 3 weeks. K Lipidomic analysis of sorted EmKCs and MoKCs of mice fed HC diet for 3 weeks ( n = 3 mice; Chow vs HC, FC: * p = 0.04 and CE: *** p < 0.001). L Heatmap of scavenger receptors mRNA expression in sorted EmKCs and MoKCs from Ldlr−/− mice after 3 weeks of HC diet ( n = 4 mice). M CD36 expression (ΔMFI = CD36 MFI minus MFI of non-stained cells) on EmKCs and on VSIG4 − and VSIG4 + MoKCs at 3 weeks of HC diet ( n = 4 mice) showing lower expression on VSIG4 − MoKCs (** p = 0.009). N FITC MFI (bodipy) for EmKCs and for VSIG4 - and VSIG4 + MoKCs after injection of oxidized-LDL labeled with bodipy or not (1-way ANOVA; 2 independent experiments combined; EmKCs vs VSIG4 + MoKCs: * p = 0.031 and EmKCs vs VSIG4 − MoKCs: *** p = 0.0008). All data in this figure are presented as mean values ± SEM. Statistical significance has been assessed with a two-sided t -test (or multiple t -tests) unless otherwise stated on the corresponding panel legend. Source data are provided as a Source Data File.

Article Snippet: Chow fed Ldlr−/− mice were fasted during the day and administered i.v. 50 μg of anti-CD36 monoclonal antibody (MF3, thermoFisher Scientific) or 50 μg of rat IgG2a isotype (thermoFisher Scientific) before given access to HC diet.

Techniques: Flow Cytometry, Comparison, Expressing, Staining, Injection, Labeling

Journal: Journal of Translational Medicine

Article Title: 15,16-Dihydrotanshinone I, a novel β-catenin-targeting inhibitor that inhibits its nuclear translocation and reduces downstream CD36 expression in cancer

doi: 10.1186/s12967-025-07317-1

Figure Lengend Snippet: CD36 is a β-catenin downstream signaling molecule in CRC. ( A ) Western blot showing the expression of β-catenin and CD36 in β-catenin-overexpressed DLD-1 cells (DLD-1- β-catenin) and control cells. ( B ) Immunohistochemical (IHC) staining of CD36 in the human colon cancer tissue and normal colon tissues (US Biomax #CO702b). ( C ) Correlation between the survival probability and CD36 expressions in CRC patients. Western blot showing the protein expressions of CD36 in ( D ) DLD-1 cells, ( E ) HT55 cells and ( F ) β-catenin-overexpressed DLD-1 cells (DLD-1- β-catenin) after 48 h DHTS treatments. The relative intracellular ATP levels in ( G ) DLD-1, ( H ) HT55, ( I ) CD36-overexpressed DLD-1 cells (DLD-1-CD36) and ( J ) β-catenin overexpressed DLD-1 cells (DLD-1-β-catenin) after 48 h DHTS treatments. Shown is the mean ± SEM, n = 3 individual experiments, * p < 0.05, ** p < 0.01 compared to control. DHTS, dihydrotanshinone I; DHTS-L, low dosage of dihydrotanshinone I (1.2 µM for DLD-1, 1 µM for HT55); DHTS-H, high dosage of dihydrotanshinone I (1.6 µM for DLD-1, 2 µM for HT55)

Article Snippet: The TMA sections were incubated with a primary monoclonal rabbit anti-CD36 antibody (catalog number 14347, Cell Signaling Technology) in Tris-buffered saline (TBS) containing 1% bovine serum albumin (BSA) for 1 h. After washing with TBS, the sections were incubated with a horseradish peroxidase-conjugated anti-rabbit secondary antibody (Bio-Rad).

Techniques: Western Blot, Expressing, Control, Immunohistochemical staining, Immunohistochemistry

Journal: Journal of Translational Medicine

Article Title: 15,16-Dihydrotanshinone I, a novel β-catenin-targeting inhibitor that inhibits its nuclear translocation and reduces downstream CD36 expression in cancer

doi: 10.1186/s12967-025-07317-1

Figure Lengend Snippet: β-catenin/CD36 axis mediates the anti-CRC effect of the DHTS-laden PLGA-co-PEG nanoparticles in vivo. ( A ) Flowchart showing the preparation of DHTS-laden PLGA-co-PEG nanoparticles (DHTS-NP). ( B ) The dissected tumor tissues of the CRC-bearing xenograft mouse models after DHTS-NP or 5-fluorouracil (5-FU) treatments. ( C ) Tumor volume and ( D ) tumor weight of the dissected tumors after DHTS-NP or 5Fu treatments. ( E ) Western blot showing the nuclear expressions of β-catenin in the xenograft tissues. Western blot showing the expressions of ( F ) cytoplasmic β-catenin, ( G ) LEF-1, TCF-4 and CD36 in the xenograft tissues. Shown is the mean ± SEM, n = 6–8 mice in each group, * p < 0.05, ** p < 0.01 compared to control. DHTS, dihydrotanshinone I; DHTS-NP, DHTS-laden PLGA-co-PEG nanoparticles; DHTS-NP-L (15 mg/kg DHTS); DHTS-NP-H (20 mg/kg DHTS); 5Fu, 5-fluorouracil (10 mg/kg)

Article Snippet: The TMA sections were incubated with a primary monoclonal rabbit anti-CD36 antibody (catalog number 14347, Cell Signaling Technology) in Tris-buffered saline (TBS) containing 1% bovine serum albumin (BSA) for 1 h. After washing with TBS, the sections were incubated with a horseradish peroxidase-conjugated anti-rabbit secondary antibody (Bio-Rad).

Techniques: In Vivo, Western Blot, Control

Journal: Redox Biology

Article Title: Radiosensitizing capacity of fenofibrate in glioblastoma cells depends on lipid metabolism

doi: 10.1016/j.redox.2024.103452

Figure Lengend Snippet: Fenofibrate (FF) modulates lipid droplets (LDs) in U87 and LN18 cells. A) Schematic representation of uptake and processing pathways of fatty acids (FAs) in tumor cells. B-i) Percentage of U87 and LN18 cells expressing CD36. B-ii) Mean fluorescent intensity (MFI) of CD36 expression in U87 and LN18 cells. C) U87 and LN18 cells were stained with LipidTOX™ (red) for LD, GPAT4 antibody (green) for lipid enzyme and Hoechst (blue) for nuclei. D) Representative immunoblots and bar graphs (from 3 independent experiments) of basal GPAT4 (D-i) and DGAT1 (D-ii) expression in U87 and LN18 cells. E) Representative confocal images of LDs (red) and nuclei (blue) of U87 and LN18 cells for all treatment groups. F) Graph showing numbers of small and large LDs in U87 (top) and LN18 (bottom) cells per treatment. LD quantification was performed by counting red lipid bodies using ImageJ (minimum of 50 cells per cell line). G) Representative immunoblots and bar graphs showing the expression of DGAT1 in U87 (top) and LN18 (bottom) cells after FF and RTx treatment. H) The normalized value of intracellular GPAT4 in U87 (top) and LN18 (bottom) cells in all treatment groups. Unless stated otherwise, data are shown as means ± SD of at least three independent experiments. P values were calculated using an unpaired t -test (two groups) or a two-way analysis of variance (ANOVA, more than two groups) with Tukey's correction. ∗p < 0.0332, ∗∗p < 0.0021, ∗∗∗p < 0.0002 and ∗∗∗∗p < 0.0001.

Article Snippet: Cells (0.25x10 6 ) were trypsinized, washed twice with ice-cold flow cytometry buffer (phosphate-buffered saline (PBS; Life Technologies)), containing 10 % v/v FBS (Sigma-Aldrich) and incubated with FITC-conjugated CD36 monoclonal antibody (mAb, AC106, 2 μg/mL, Miltenyi Biotec), and membrane Hsp70 mAb (cmHsp70.1, 20 μg/mL, multimmune GmbH) for 30 min in the dark on ice.

Techniques: Expressing, Staining, Western Blot

Journal: Cell Reports Medicine

Article Title: Lipolysis engages CD36 to promote ZBP1-mediated necroptosis-impairing lung regeneration in COPD

doi: 10.1016/j.xcrm.2024.101732

Figure Lengend Snippet:

Article Snippet: Scavenger Receptor B2/CD36 Monoclonal Antibody (Clone JC63.1) , cayman , Cat#10009893; RRID: AB_10613953.

Techniques: Control, Recombinant, Selection, Membrane, Enzyme-linked Immunosorbent Assay, Quantitation Assay, Software