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cd36 pevio770 (Miltenyi Biotec)

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Miltenyi Biotec cd36 pevio770
Flow cytometry antibodies used.

Cd36 Pevio770, supplied by Miltenyi Biotec, used in various techniques. Bioz Stars score: 94/100, based on 25 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/cd36/CD36+Antibody%2C+anti-human%2C+REAfinity/pmc08070390-28-0-2
Average 94 stars, based on 25 article reviews

cd36 pevio770 - by Bioz Stars, 2026-08

94/100 stars

Images

1) Product Images from "Murlentamab, a Low Fucosylated Anti-Müllerian Hormone Type II Receptor (AMHRII) Antibody, Exhibits Anti-Tumor Activity through Tumor-Associated Macrophage Reprogrammation and T Cell Activation"

Article Title: Murlentamab, a Low Fucosylated Anti-Müllerian Hormone Type II Receptor (AMHRII) Antibody, Exhibits Anti-Tumor Activity through Tumor-Associated Macrophage Reprogrammation and T Cell Activation

Journal: Cancers

doi: 10.3390/cancers13081845

Figure Legend Snippet: Flow cytometry antibodies used.

Techniques Used: Flow Cytometry, In Vivo, In Vitro

Figure Legend Snippet: Murlentamab opsonization of SKOV3-R2 + orients naïve macrophages and reprograms TAMs towards an M1-like profile. SKOV3-R2 + ovarian tumor cells were labeled with different 3C23K antibodies (3C23K-FcKO control, 3C23K-CHO normally fucosylated or murlentamab the low fucosylated form) and cultured in the presence of human monocyte-derived macrophages from healthy donors unstimulated (M0) or stimulated with M-CSF and IL-10 (TAMs). ( A ) The proportion of macrophages expressing M1/M2 membrane markers (CD32, CD64, CD80, TLR2, CD163, CD36 and CD206) was determined by flow cytometry after three days of co-culture with SKOV3-R2 + cells. ( B ) The release of cytokines (IL1β, IL12, TNFα, IL6, IFNγ, IL10) and chemokines (CCL2, CCL4, CCL5, CXCL9 and CXCL10) in the culture medium was determined by AlphaLISA after three days of co-culture with SKOV3-R2 + cells. Data shown (boxplots) are the results from three different experiments (performed with three different healthy donors). * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001. p values were determined using one-way ANOVA analysis followed by Tukey’s multiple comparisons test.

Techniques Used: Labeling, Cell Culture, Derivative Assay, Expressing, Membrane, Flow Cytometry, Co-Culture Assay

Image Search Results

Impact of high fat feeding and voluntary exercise on left ventricle morphology in male mice. (A) Representative images of Picrosirius red staining for measurement of interstitial and perivascular fibrosis with 20× magnification. (B) Representative images for Hematoxylin and Eosin for measurement of cardiomyocyte width and area with 40× magnification. (C) Representative images of Oil red O staining for measurement of interstitial lipid deposition with 40× magnification. Quantitative analysis of percent area of (D) interstitial and (E) perivascular fibrosis expressed as fold change from sedentary chow group. Quantitative analysis of (F) cardiomyocyte width and (G) cardiomyocyte area. (H) Quantitative analysis of percent area of lipid deposition expressed as fold change from sedentary chow group left ventricle mRNA expression of fatty acid transporters (I) FABP3, (J) CD36, and hypertrophy markers (K) β-MHC and (L) ANP in male VET or sedentary mice fed an HFD or chow diet. Values were calculated relative to 18S housekeeper. Analysis was performed using two-way analysis of variance with Tukey’s post hoc test for multiple comparisons. Data are expressed as mean ± standard error of the mean. (D–H) n : 8–12 per group. (I–L) n : 8–9 per group. * p < 0.05, **** p < 0.0001. ANP = atrial natriuretic peptide; β-MHC = beta myosin heavy chain; CD36 = platelet glycoprotein 4; FABP3 = fatty acid-binding protein 3; HFD = high fat diet; Myh7 = moysin heavy chain 7; VET = voluntary exercise training.

Journal: Journal of Sport and Health Science

Article Title: Influence of diet-induced obesity and voluntary exercise training on cardiac lipids and mitochondrial function in mice

doi: 10.1016/j.jshs.2025.101095

Figure Lengend Snippet: Impact of high fat feeding and voluntary exercise on left ventricle morphology in male mice. (A) Representative images of Picrosirius red staining for measurement of interstitial and perivascular fibrosis with 20× magnification. (B) Representative images for Hematoxylin and Eosin for measurement of cardiomyocyte width and area with 40× magnification. (C) Representative images of Oil red O staining for measurement of interstitial lipid deposition with 40× magnification. Quantitative analysis of percent area of (D) interstitial and (E) perivascular fibrosis expressed as fold change from sedentary chow group. Quantitative analysis of (F) cardiomyocyte width and (G) cardiomyocyte area. (H) Quantitative analysis of percent area of lipid deposition expressed as fold change from sedentary chow group left ventricle mRNA expression of fatty acid transporters (I) FABP3, (J) CD36, and hypertrophy markers (K) β-MHC and (L) ANP in male VET or sedentary mice fed an HFD or chow diet. Values were calculated relative to 18S housekeeper. Analysis was performed using two-way analysis of variance with Tukey’s post hoc test for multiple comparisons. Data are expressed as mean ± standard error of the mean. (D–H) n : 8–12 per group. (I–L) n : 8–9 per group. * p < 0.05, **** p < 0.0001. ANP = atrial natriuretic peptide; β-MHC = beta myosin heavy chain; CD36 = platelet glycoprotein 4; FABP3 = fatty acid-binding protein 3; HFD = high fat diet; Myh7 = moysin heavy chain 7; VET = voluntary exercise training.

Article Snippet: The following TaqMan assay gene transcripts were used: fatty acid-binding protein 3 (FABP3, Mm02342495_m1), platelet glycoprotein 4 (CD36, Mm00432403_m1), beta myosin heavy chain (β-MHC, Mm00600555_m1), atrial natriuretic peptide (ANP, Mm01255747_g1), OPA1 (Mm01349707_g1), DRP1 (Mm01342903_m1), robosomal18S (18S, Mm03928990_g1).

Techniques: Staining, Expressing, Binding Assay

Preparation and anti‐atherosclerotic mechanisms of the CuPB@HA nanozyme. (A) Synthesis procedure of CuPB@HA. PB nanoparticles were prepared through a PVP/HCl‐assisted thermal reaction using K 3 [Fe(CN) 6 ] as the precursor, followed by Cu incorporation to obtain CuPB and subsequent HA functionalization to form CuPB@HA. (B) Therapeutic mechanisms. Systemically administered CuPB@HA selectively targets lesional CD44 + macrophages. Upon internalization, it synergistically remodels the plaque microenvironment by scavenging ROS to promote a shift toward an anti‐inflammatory macrophage phenotype and improving macrophage lipid‐handling profiles by downregulating CD36 and upregulating ABCA1/ABCG1‐related cholesterol transport mediators, thereby attenuating foam‐cell lipid accumulation. Some elements in the image were sourced from BioRender ( https://app.biorender.com/illustrations/69c95a7d8bdf29a2ebf6bea4 ).

Journal: Advanced Science

Article Title: Copper‐Doped Prussian Blue Nanozymes With Hyaluronic Acid‐Mediated Targeting Alleviate Oxidative Stress and Regulate Cholesterol Handling for Atherosclerosis Therapy

doi: 10.1002/advs.76976

Figure Lengend Snippet: Preparation and anti‐atherosclerotic mechanisms of the CuPB@HA nanozyme. (A) Synthesis procedure of CuPB@HA. PB nanoparticles were prepared through a PVP/HCl‐assisted thermal reaction using K 3 [Fe(CN) 6 ] as the precursor, followed by Cu incorporation to obtain CuPB and subsequent HA functionalization to form CuPB@HA. (B) Therapeutic mechanisms. Systemically administered CuPB@HA selectively targets lesional CD44 + macrophages. Upon internalization, it synergistically remodels the plaque microenvironment by scavenging ROS to promote a shift toward an anti‐inflammatory macrophage phenotype and improving macrophage lipid‐handling profiles by downregulating CD36 and upregulating ABCA1/ABCG1‐related cholesterol transport mediators, thereby attenuating foam‐cell lipid accumulation. Some elements in the image were sourced from BioRender ( https://app.biorender.com/illustrations/69c95a7d8bdf29a2ebf6bea4 ).

Article Snippet: Subsequently, the samples were incubated overnight at 4°C with specific primary antibodies targeting the M1 marker iNOS (Proteintech, 22226‐1‐AP,1:400), the M2 marker ARG1 (Proteintech, 16001‐1‐AP, 1:400), or the lipid uptake receptor CD36 (MedChemExpress, HY‐P86458, 1:400).

Techniques:

Single‐cell transcriptomics identifies CD44 as a potential targeting receptor on pathogenic macrophages in atherosclerotic lesions. (A) UMAP projection of the human carotid plaque single‐cell transcriptomic dataset ( GSE253903 ), illustrating the distinct clustering of major immune and stromal cell lineages. (B) Dot plot depicting the expression profiles of cell‐type‐specific marker genes across all identified clusters. (C) Density Plot showing the high expression of CD44. (D) Violin plots demonstrate significantly elevated CD44 expression in macrophages from symptomatic patients compared to asymptomatic patients. (E) UMAP sub‐clustering of the macrophage population into distinct functional subsets. (F) Bar graph showing an increased proportion of inflammatory macrophages and a decreased proportion of Foamy_Trem2 macrophages in symptomatic lesions. (G) Violin plots detailing the differential expression of CD44 across macrophage subtypes between the two clinical groups. (H) Density Plot illustrating the strong co‐expression of CD44 with pathogenic markers (IL1B, NFE2L2, and CD36).

Journal: Advanced Science

Article Title: Copper‐Doped Prussian Blue Nanozymes With Hyaluronic Acid‐Mediated Targeting Alleviate Oxidative Stress and Regulate Cholesterol Handling for Atherosclerosis Therapy

doi: 10.1002/advs.76976

Figure Lengend Snippet: Single‐cell transcriptomics identifies CD44 as a potential targeting receptor on pathogenic macrophages in atherosclerotic lesions. (A) UMAP projection of the human carotid plaque single‐cell transcriptomic dataset ( GSE253903 ), illustrating the distinct clustering of major immune and stromal cell lineages. (B) Dot plot depicting the expression profiles of cell‐type‐specific marker genes across all identified clusters. (C) Density Plot showing the high expression of CD44. (D) Violin plots demonstrate significantly elevated CD44 expression in macrophages from symptomatic patients compared to asymptomatic patients. (E) UMAP sub‐clustering of the macrophage population into distinct functional subsets. (F) Bar graph showing an increased proportion of inflammatory macrophages and a decreased proportion of Foamy_Trem2 macrophages in symptomatic lesions. (G) Violin plots detailing the differential expression of CD44 across macrophage subtypes between the two clinical groups. (H) Density Plot illustrating the strong co‐expression of CD44 with pathogenic markers (IL1B, NFE2L2, and CD36).

Techniques: Single-cell Transcriptomics, Single Cell, Expressing, Marker, Functional Assay, Quantitative Proteomics

CuPB@HA nanozymes accumulate in atherosclerotic plaques and synergistically remodel lipid metabolism, oxidative stress, and inflammatory polarization in macrophages. (A) Representative in vivo fluorescence images of HFD‐fed ApoE −/− atherosclerotic mice after intravenous administration of Cy5.5‐labeled CuPB or CuPB@HA at 12 and 24 h post‐injection. (B) Ex vivo fluorescence images of major organs, including heart, liver, spleen, lung, and kidney, harvested at corresponding time points after nanozyme administration. (C) Representative confocal fluorescence images of atherosclerotic plaque sections from HFD‐fed ApoE −/− mice showing the spatial association of Cy5.5‐labeled CuPB@HA with CD68‐positive macrophage‐rich regions and CD44‐positive regions. Cy5.5‐labeled CuPB@HA is pseudo‐colored red, CD68 or CD44 is shown in green. (D) Fluorescence microscopy images showing the time‐dependent cellular uptake of FITC‐labeled CuPB and CuPB@HA by macrophages, with or without excess free HA pre‐incubation. FITC‐labeled nanozymes are shown in green, and nuclei are stained with DAPI in blue. (E) Western blot analysis of proteins related to lipid metabolism, oxidative stress, and inflammatory polarization in RAW264.7 macrophages after different treatments. (F) RT‐qPCR analysis of genes related to lipid metabolism, oxidative stress, and inflammatory polarization in RAW264.7 macrophages after different treatments. (G) Representative Oil Red O staining images showing intracellular lipid accumulation in RAW264.7 macrophages after different treatments. (H–J) Representative immunofluorescence images showing the expression of ARG1 (H), iNOS (I), and CD36 (J) in RAW264.7 macrophages after different treatments. (K) Quantitative analysis of cellular uptake fluorescence intensity in Figure 4D. (L) Quantitative analysis of Oil Red O‐positive areas in Figure 4G (n = 3). (M–O) Quantitative fluorescence analysis of ARG1 (M), iNOS (N), and CD36 (O) staining in Figure 4H–J ( n = 5). Quantitative data are presented as the mean ± SD. Statistical significance was assessed via one‐way ANOVA (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001).

Journal: Advanced Science

Article Title: Copper‐Doped Prussian Blue Nanozymes With Hyaluronic Acid‐Mediated Targeting Alleviate Oxidative Stress and Regulate Cholesterol Handling for Atherosclerosis Therapy

doi: 10.1002/advs.76976

Figure Lengend Snippet: CuPB@HA nanozymes accumulate in atherosclerotic plaques and synergistically remodel lipid metabolism, oxidative stress, and inflammatory polarization in macrophages. (A) Representative in vivo fluorescence images of HFD‐fed ApoE −/− atherosclerotic mice after intravenous administration of Cy5.5‐labeled CuPB or CuPB@HA at 12 and 24 h post‐injection. (B) Ex vivo fluorescence images of major organs, including heart, liver, spleen, lung, and kidney, harvested at corresponding time points after nanozyme administration. (C) Representative confocal fluorescence images of atherosclerotic plaque sections from HFD‐fed ApoE −/− mice showing the spatial association of Cy5.5‐labeled CuPB@HA with CD68‐positive macrophage‐rich regions and CD44‐positive regions. Cy5.5‐labeled CuPB@HA is pseudo‐colored red, CD68 or CD44 is shown in green. (D) Fluorescence microscopy images showing the time‐dependent cellular uptake of FITC‐labeled CuPB and CuPB@HA by macrophages, with or without excess free HA pre‐incubation. FITC‐labeled nanozymes are shown in green, and nuclei are stained with DAPI in blue. (E) Western blot analysis of proteins related to lipid metabolism, oxidative stress, and inflammatory polarization in RAW264.7 macrophages after different treatments. (F) RT‐qPCR analysis of genes related to lipid metabolism, oxidative stress, and inflammatory polarization in RAW264.7 macrophages after different treatments. (G) Representative Oil Red O staining images showing intracellular lipid accumulation in RAW264.7 macrophages after different treatments. (H–J) Representative immunofluorescence images showing the expression of ARG1 (H), iNOS (I), and CD36 (J) in RAW264.7 macrophages after different treatments. (K) Quantitative analysis of cellular uptake fluorescence intensity in Figure 4D. (L) Quantitative analysis of Oil Red O‐positive areas in Figure 4G (n = 3). (M–O) Quantitative fluorescence analysis of ARG1 (M), iNOS (N), and CD36 (O) staining in Figure 4H–J ( n = 5). Quantitative data are presented as the mean ± SD. Statistical significance was assessed via one‐way ANOVA (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001).

Techniques: In Vivo, Fluorescence, Labeling, Injection, Ex Vivo, Microscopy, Incubation, Staining, Western Blot, Quantitative RT-PCR, Immunofluorescence, Expressing

Transcriptomic reprogramming of pathogenic macrophages by CuPB@HA nanozymes. (A) Differential expression scatter plot of Model vs. Control, highlighting upregulated DEGs (red, Fold Change > 1.5, FDR < 0.05). (B) GO biological process enrichment of the upregulated DEGs from (A). (C) Differential expression scatter plot of Treat vs. Model, highlighting downregulated DEGs (blue, Fold Change > 1.5, FDR < 0.05). (D) GO biological process enrichment of the downregulated DEGs from (C). (E) Heatmap of representative DEGs for lipid uptake, cholesterol efflux, oxidative stress, and inflammation. (F) Quantitative expression profiles of essential genes selected from (E). Data are mean ± SD ( n = 3). (G) UpSet plot showing the intersection of DEGs between the disease progression and treatment sets. (H) Protein‐protein interaction (PPI) network of the key intersected DEGs. (I) Core PPI sub‐network of highly interconnected hub genes (Cd36, Il1b, Tnf, Il10, Nos2, Arg1, Mmp9).

Journal: Advanced Science

Article Title: Copper‐Doped Prussian Blue Nanozymes With Hyaluronic Acid‐Mediated Targeting Alleviate Oxidative Stress and Regulate Cholesterol Handling for Atherosclerosis Therapy

doi: 10.1002/advs.76976

Figure Lengend Snippet: Transcriptomic reprogramming of pathogenic macrophages by CuPB@HA nanozymes. (A) Differential expression scatter plot of Model vs. Control, highlighting upregulated DEGs (red, Fold Change > 1.5, FDR < 0.05). (B) GO biological process enrichment of the upregulated DEGs from (A). (C) Differential expression scatter plot of Treat vs. Model, highlighting downregulated DEGs (blue, Fold Change > 1.5, FDR < 0.05). (D) GO biological process enrichment of the downregulated DEGs from (C). (E) Heatmap of representative DEGs for lipid uptake, cholesterol efflux, oxidative stress, and inflammation. (F) Quantitative expression profiles of essential genes selected from (E). Data are mean ± SD ( n = 3). (G) UpSet plot showing the intersection of DEGs between the disease progression and treatment sets. (H) Protein‐protein interaction (PPI) network of the key intersected DEGs. (I) Core PPI sub‐network of highly interconnected hub genes (Cd36, Il1b, Tnf, Il10, Nos2, Arg1, Mmp9).

Techniques: Quantitative Proteomics, Control, Expressing, Biomarker Discovery

CuPB@HA attenuates atherosclerotic plaque burden and promotes plaque stability in HFD‐fed ApoE −/− mice. (A) Schematic of the in vivo experimental design and treatment timeline. (B–E) Serum lipid profiles of mice in different treatment groups, including (B) total cholesterol (TC), (C) triglycerides (TG), (D) low‐density lipoprotein cholesterol (LDL‐C), and (E) high‐density lipoprotein cholesterol (HDL‐C). Data are mean ± SD ( n = 6). Significance was assessed via one‐way ANOVA with Tukey's post hoc test (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001). (F–J) Representative histological and immunohistochemical images of aortic root cross‐sections (scale bars: 100 µm): (F) Representative Oil Red O (ORO) staining of aortas. (G) ORO staining for lipid accumulation; (H) H&E staining for necrotic core and plaque morphology; (I) Masson's trichrome staining for collagen deposition; and (J) IHC staining for CD36 expression. (K–O) Quantification of lesional characteristics across treatment groups: (K) relative plaque area ( en face ORO), (L) lipid area (aortic root ORO), (M) necrotic core area (H&E), (N) collagen‐to‐plaque ratio (Masson's trichrome), and (O) CD36‐positive area (IHC). Data are presented as the mean ± SD ( n = 6). Significance was assessed via one‐way ANOVA with Tukey's post hoc test (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001).

Journal: Advanced Science

Article Title: Copper‐Doped Prussian Blue Nanozymes With Hyaluronic Acid‐Mediated Targeting Alleviate Oxidative Stress and Regulate Cholesterol Handling for Atherosclerosis Therapy

doi: 10.1002/advs.76976

Figure Lengend Snippet: CuPB@HA attenuates atherosclerotic plaque burden and promotes plaque stability in HFD‐fed ApoE −/− mice. (A) Schematic of the in vivo experimental design and treatment timeline. (B–E) Serum lipid profiles of mice in different treatment groups, including (B) total cholesterol (TC), (C) triglycerides (TG), (D) low‐density lipoprotein cholesterol (LDL‐C), and (E) high‐density lipoprotein cholesterol (HDL‐C). Data are mean ± SD ( n = 6). Significance was assessed via one‐way ANOVA with Tukey's post hoc test (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001). (F–J) Representative histological and immunohistochemical images of aortic root cross‐sections (scale bars: 100 µm): (F) Representative Oil Red O (ORO) staining of aortas. (G) ORO staining for lipid accumulation; (H) H&E staining for necrotic core and plaque morphology; (I) Masson's trichrome staining for collagen deposition; and (J) IHC staining for CD36 expression. (K–O) Quantification of lesional characteristics across treatment groups: (K) relative plaque area ( en face ORO), (L) lipid area (aortic root ORO), (M) necrotic core area (H&E), (N) collagen‐to‐plaque ratio (Masson's trichrome), and (O) CD36‐positive area (IHC). Data are presented as the mean ± SD ( n = 6). Significance was assessed via one‐way ANOVA with Tukey's post hoc test (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001).

Techniques: In Vivo, Immunohistochemical staining, Staining, Immunohistochemistry, Expressing

Cluster of differentiation 36 (CD36) mediates the uptake of DHA into the myocytes of grass carp. (A) The internalization of CD36 in human embryonic kidney 293T (HEK 293T) cells transfected with CD36 after treated for 2 h. Green fluorescence indicated CD36 and 4′,6-diamidino-2-phenylindole (DAPI) staining marked the nucleus, scale bar = 8 μm. (B) Protein levels of CD36 expression in myoblasts treated with CD36 inhibitor. (C) Quantitative results of CD36 protein levels in myoblasts treated with CD36 inhibitor. Control, untreated; DHA, treated with 50 μmol/L DHA; DHA + SSO, co-treated with 50 μmol/L DHA and 200 μmol/L SSO. DHA = docosahexaenoic acid; SSO = sulfosuccinimidyl oleate sodium (a CD36 inhibitor); GAPDH = glyceraldehyde-3-phosphate dehydrogenase. P -value less than 0.05 indicates a significant difference, n = 3.

Journal: Animal Nutrition

Article Title: PPARα-CD36-CAV1-mediated docosahexaenoic acid (DHA) uptake promotes muscle fiber development in grass carp ( Ctenopharyngodon idellus )

doi: 10.1016/j.aninu.2025.10.011

Figure Lengend Snippet: Cluster of differentiation 36 (CD36) mediates the uptake of DHA into the myocytes of grass carp. (A) The internalization of CD36 in human embryonic kidney 293T (HEK 293T) cells transfected with CD36 after treated for 2 h. Green fluorescence indicated CD36 and 4′,6-diamidino-2-phenylindole (DAPI) staining marked the nucleus, scale bar = 8 μm. (B) Protein levels of CD36 expression in myoblasts treated with CD36 inhibitor. (C) Quantitative results of CD36 protein levels in myoblasts treated with CD36 inhibitor. Control, untreated; DHA, treated with 50 μmol/L DHA; DHA + SSO, co-treated with 50 μmol/L DHA and 200 μmol/L SSO. DHA = docosahexaenoic acid; SSO = sulfosuccinimidyl oleate sodium (a CD36 inhibitor); GAPDH = glyceraldehyde-3-phosphate dehydrogenase. P -value less than 0.05 indicates a significant difference, n = 3.

Article Snippet: To investigate whether DHA promotes myoblast proliferation via the CD36-mediated absorption pathway, this study utilized DHA (HY-B2167) and the CD36 inhibitor sulfosuccinimidyl oleate sodium (SSO; HY-112847A), both from MedChem Express LLC (Monmouth Junction, NJ, USA).

Techniques: Transfection, Fluorescence, Staining, Expressing, Control

Docosahexaenoic acid (DHA) enhances the proliferation of grass carp myoblasts through the cluster of differentiation 36 (CD36)-mediated uptake mechanism. (A and B) The relative mRNA expression levels of proliferation-related genes (cyclin D1 and cyclin E) in myoblasts treated with DHA for 24 h. (C) Percentage of 5-ethynyl-2′-deoxyuridine (EdU)-positive myoblastsrelative to the total myoblasts. (D) EdU (red fluorescence) and Hoechst (blue fluorescence, nuclei) staining. Scale bar, 200 μm. Control, untreated; DHA, treated with 50 μmol/L DHA; DHA + SSO, co-treated with 50 μmol/L DHA and 200 μmol/L SSO. SSO = sulfosuccinimidyl oleate sodium (a CD36 inhibitor). P -value less than 0.05 indicates a significant difference, n = 3.

Journal: Animal Nutrition

Article Title: PPARα-CD36-CAV1-mediated docosahexaenoic acid (DHA) uptake promotes muscle fiber development in grass carp ( Ctenopharyngodon idellus )

doi: 10.1016/j.aninu.2025.10.011

Figure Lengend Snippet: Docosahexaenoic acid (DHA) enhances the proliferation of grass carp myoblasts through the cluster of differentiation 36 (CD36)-mediated uptake mechanism. (A and B) The relative mRNA expression levels of proliferation-related genes (cyclin D1 and cyclin E) in myoblasts treated with DHA for 24 h. (C) Percentage of 5-ethynyl-2′-deoxyuridine (EdU)-positive myoblastsrelative to the total myoblasts. (D) EdU (red fluorescence) and Hoechst (blue fluorescence, nuclei) staining. Scale bar, 200 μm. Control, untreated; DHA, treated with 50 μmol/L DHA; DHA + SSO, co-treated with 50 μmol/L DHA and 200 μmol/L SSO. SSO = sulfosuccinimidyl oleate sodium (a CD36 inhibitor). P -value less than 0.05 indicates a significant difference, n = 3.

Techniques: Expressing, Fluorescence, Staining, Control

Cluster of differentiation 36 (CD36) facilitates the uptake of docosahexaenoic acid (DHA) in grass carp myoblasts via a CAV1-dependent endocytic pathway. (A-D) The mRNA expression of endocytosis-related genes in myoblasts treated with DHA for 24 h. (E) The colocalization and internalization of CD36 (green fluorescence) and CAV1 (red fluorescence) were observed in human embryonic kidney 293T (HEK 293T) cells transfected with plasmid after being treated with DHA for different time. Scale bar, 8 μm. Control, untreated; DHA, treated with 50 μmol/L DHA. P -value less than 0.05 indicates a significant difference, n = 3.

Journal: Animal Nutrition

Article Title: PPARα-CD36-CAV1-mediated docosahexaenoic acid (DHA) uptake promotes muscle fiber development in grass carp ( Ctenopharyngodon idellus )

doi: 10.1016/j.aninu.2025.10.011

Figure Lengend Snippet: Cluster of differentiation 36 (CD36) facilitates the uptake of docosahexaenoic acid (DHA) in grass carp myoblasts via a CAV1-dependent endocytic pathway. (A-D) The mRNA expression of endocytosis-related genes in myoblasts treated with DHA for 24 h. (E) The colocalization and internalization of CD36 (green fluorescence) and CAV1 (red fluorescence) were observed in human embryonic kidney 293T (HEK 293T) cells transfected with plasmid after being treated with DHA for different time. Scale bar, 8 μm. Control, untreated; DHA, treated with 50 μmol/L DHA. P -value less than 0.05 indicates a significant difference, n = 3.

Techniques: Expressing, Fluorescence, Transfection, Plasmid Preparation, Control

Docosahexaenoic acid (DHA) promotes myoblast proliferation in grass carp via cluster of differentiation 36 (CD36) and CAV1. (A) Protein levels of CAV1 expression in myoblasts treated with CAV1 inhibitor. (B) Quantitative results of CAV1 protein levels in myoblasts treated with CAV1 inhibitor. (C) Percentage of 5-ethynyl-2′-deoxyuridine (EdU)-positive myoblasts relative to the total myoblasts. (D) EdU (red fluorescence) and Hoechst (blue fluorescence, nuclei) staining. Scale bar, 200 μm. (E and F) The mRNA expression levels of proliferation-related genes (cyclin D1 and cyclin E) in myoblasts treated with DHA for 24 h. (G) Overexpression of cav1 in myoblasts. Control, untreated; DHA, treated with 50 μmol/L DHA; DHA + Nys, co-treated with 50 μmol/L DHA and 75 μmol/L Nys; DHA + Nys + SSO, co-treated with 50 μmol/L DHA, 75 μmol/L Nys, and 200 μmol/L SSO; CAV1 OE, myoblasts were transfected with a CAV1-overexpression plasmid; DHA + CAV1 OE, CAV1-overexpressing myoblasts were treated with 50 μmol/L DHA. SSO = sulfosuccinimidyl oleate sodium (a CD36 inhibitor); Nys = nystatin (a CAV1 inhibitor); CAV1 OE = CAV1-overexpressing; GAPDH = glyceraldehyde-3-phosphate dehydrogenase. P -value less than 0.05 indicates a significant difference, n = 3.

Journal: Animal Nutrition

Article Title: PPARα-CD36-CAV1-mediated docosahexaenoic acid (DHA) uptake promotes muscle fiber development in grass carp ( Ctenopharyngodon idellus )

doi: 10.1016/j.aninu.2025.10.011

Figure Lengend Snippet: Docosahexaenoic acid (DHA) promotes myoblast proliferation in grass carp via cluster of differentiation 36 (CD36) and CAV1. (A) Protein levels of CAV1 expression in myoblasts treated with CAV1 inhibitor. (B) Quantitative results of CAV1 protein levels in myoblasts treated with CAV1 inhibitor. (C) Percentage of 5-ethynyl-2′-deoxyuridine (EdU)-positive myoblasts relative to the total myoblasts. (D) EdU (red fluorescence) and Hoechst (blue fluorescence, nuclei) staining. Scale bar, 200 μm. (E and F) The mRNA expression levels of proliferation-related genes (cyclin D1 and cyclin E) in myoblasts treated with DHA for 24 h. (G) Overexpression of cav1 in myoblasts. Control, untreated; DHA, treated with 50 μmol/L DHA; DHA + Nys, co-treated with 50 μmol/L DHA and 75 μmol/L Nys; DHA + Nys + SSO, co-treated with 50 μmol/L DHA, 75 μmol/L Nys, and 200 μmol/L SSO; CAV1 OE, myoblasts were transfected with a CAV1-overexpression plasmid; DHA + CAV1 OE, CAV1-overexpressing myoblasts were treated with 50 μmol/L DHA. SSO = sulfosuccinimidyl oleate sodium (a CD36 inhibitor); Nys = nystatin (a CAV1 inhibitor); CAV1 OE = CAV1-overexpressing; GAPDH = glyceraldehyde-3-phosphate dehydrogenase. P -value less than 0.05 indicates a significant difference, n = 3.

Techniques: Expressing, Fluorescence, Staining, Over Expression, Control, Transfection, Plasmid Preparation

Docosahexaenoic acid (DHA) promotes myofiber proliferation and development in muscle tissue via the PPARα-cluster of differentiation 36 (CD36)-mediated uptake pathway. (A) Site-directed mutagenesis analysis of PPARα binding sites on the pGL3.0-CD36 vector in human embryonic kidney 293T (HEK 293T) cells. (B) The mRNA expression levels of fatty acid absorption ( cd36 and cav1 ) in muscle tissue. (C) Muscle fiber diameter. (D) Muscle fiber density. (E) Representative hematoxylin and eosin (H&E) staining in muscle tissue. Scale bar, 100 μm. (F) The mRNA expression of muscle growth and development related genes ( myog , myod , myhc , mrf4 , and myf5 ) and fiber cell growth factor ( fgf6a and fgf6b ) in muscle tissue. Control, diet without DHA supplementation; DHA, diet supplemented with 0.5% DHA; DHA + GW6471, diet supplemented with 0.5% DHA and GW6471. GW6471 = peroxisome proliferator-activated receptor α inhibitor; Luc = luciferase. P -value less than 0.05 indicates a significant difference, n = 3.

Journal: Animal Nutrition

Article Title: PPARα-CD36-CAV1-mediated docosahexaenoic acid (DHA) uptake promotes muscle fiber development in grass carp ( Ctenopharyngodon idellus )

doi: 10.1016/j.aninu.2025.10.011

Figure Lengend Snippet: Docosahexaenoic acid (DHA) promotes myofiber proliferation and development in muscle tissue via the PPARα-cluster of differentiation 36 (CD36)-mediated uptake pathway. (A) Site-directed mutagenesis analysis of PPARα binding sites on the pGL3.0-CD36 vector in human embryonic kidney 293T (HEK 293T) cells. (B) The mRNA expression levels of fatty acid absorption ( cd36 and cav1 ) in muscle tissue. (C) Muscle fiber diameter. (D) Muscle fiber density. (E) Representative hematoxylin and eosin (H&E) staining in muscle tissue. Scale bar, 100 μm. (F) The mRNA expression of muscle growth and development related genes ( myog , myod , myhc , mrf4 , and myf5 ) and fiber cell growth factor ( fgf6a and fgf6b ) in muscle tissue. Control, diet without DHA supplementation; DHA, diet supplemented with 0.5% DHA; DHA + GW6471, diet supplemented with 0.5% DHA and GW6471. GW6471 = peroxisome proliferator-activated receptor α inhibitor; Luc = luciferase. P -value less than 0.05 indicates a significant difference, n = 3.

Techniques: Mutagenesis, Binding Assay, Plasmid Preparation, Expressing, Staining, Control, Luciferase

Journal: Animal Nutrition

Article Title: PPARα-CD36-CAV1-mediated docosahexaenoic acid (DHA) uptake promotes muscle fiber development in grass carp ( Ctenopharyngodon idellus )

doi: 10.1016/j.aninu.2025.10.011

Techniques: Expressing, Fluorescence, Staining, Control

Journal: Animal Nutrition

Article Title: PPARα-CD36-CAV1-mediated docosahexaenoic acid (DHA) uptake promotes muscle fiber development in grass carp ( Ctenopharyngodon idellus )

doi: 10.1016/j.aninu.2025.10.011

Techniques: Mutagenesis, Binding Assay, Plasmid Preparation, Expressing, Staining, Control, Luciferase

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