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Novus Biologicals anti abca1 pe
Anti Abca1 Pe, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 90/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/abca1/ABCA1+Antibody+%5BPE%5D/pm42021392-181-49-50
Average 90 stars, based on 2 article reviews

anti abca1 pe - by Bioz Stars, 2026-09

90/100 stars

Images

Incubation:

Article Title: Imeglimin Inhibits Macrophage Foam Cell Formation and Atherosclerosis in Streptozotocin-Induced Diabetic ApoE-Deficient Mice.
Article Snippet: Equal amounts of protein (20 μg) were loaded onto NuPAGETM 4–12% Bis-Tris gradient gels (NOVEX by Life Technologies, Winston-Salem, NC, USA) and electrophoresed before being transferred onto nitrocellulose membranes. .. Membranes were blocked using 5% bovine serum albumin at room temperature for 1 h, followed by overnight incubation at 4 ◦C with primary antibodies targeting CD36 (PA1-16813, 1:1000, Thermo Fisher Scientific), ABCA1 (NB400-105, 1:1000, Novus Biologicals, Littleton, CO, USA), ABCG1 (NB400-132, 1:1000, Novus Biologicals), AMPK (2532, 1:1000, Cell Signaling Technology), phosphorylated AMPK (pAMPK, 2535, 1:1000, Cell Signaling Technology), and β-actin (ab8227, 1:10,000, Abcam, Cambridge, UK). .. After washing, membranes were incubated with horseradish peroxidase-conjugated secondary antibodies at room temperature for 1 h. Protein bands were visualized using an enhanced chemiluminescence (ECL) detection reagent (Thermo Fisher Scientific) and quantified using ImageJ software (version 1.53g, NIH, Bethesda, MD, USA).

Article Title: Luteolin Nanomedicine with Stimulus-Driven Traceless Release for Targeting Treatment of Atherosclerosis by Enhancing Lipid Efflux
Article Snippet: .. The membranes were blocked with 5% bovine serum albumin (BSA) in PBS for 1 h at room temperature and subsequently incubated overnight at 4 °C with specific primary antibodies, such as ABCA1 (Novus, USA) and ABCG1 (Novus, USA). ..

Article Title: Imeglimin Inhibits Macrophage Foam Cell Formation and Atherosclerosis in Streptozotocin-Induced Diabetic ApoE-Deficient Mice
Article Snippet: Equal amounts of protein (20 μg) were loaded onto NuPAGETM 4–12% Bis-Tris gradient gels (NOVEX by Life Technologies, Winston-Salem, NC, USA) and electrophoresed before being transferred onto nitrocellulose membranes. .. Membranes were blocked using 5% bovine serum albumin at room temperature for 1 h, followed by overnight incubation at 4 °C with primary antibodies targeting CD36 (PA1-16813, 1:1000, Thermo Fisher Scientific), ABCA1 (NB400-105, 1:1000, Novus Biologicals, Littleton, CO, USA), ABCG1 (NB400-132, 1:1000, Novus Biologicals), AMPK (2532, 1:1000, Cell Signaling Technology), phosphorylated AMPK (pAMPK, 2535, 1:1000, Cell Signaling Technology), and β-actin (ab8227, 1:10,000, Abcam, Cambridge, UK). .. After washing, membranes were incubated with horseradish peroxidase-conjugated secondary antibodies at room temperature for 1 h. Protein bands were visualized using an enhanced chemiluminescence (ECL) detection reagent (Thermo Fisher Scientific) and quantified using ImageJ software (version 1.53g, NIH, Bethesda, MD, USA).

Article Title: The Regulation of COX-2, ABCA1 and ABCG1 by the lncRNA PACERR links the inflammatory response and cholesterol homeostasis
Article Snippet: Protein was extracted in RIPA buffer (Cell Signaling) with protease and phosphatase inhibitors (Roche) and subsequently normalized with a Pierce BCA Protein Assay Kit (Thermo Fisher Scientific). .. Samples (30 μg per well) were electrophoresed on 4–20% TGX-gradient gels (Bio-Rad Laboratories) and transferred to nitrocellulose membranes at 125 V for 2 h. Membranes were incubated overnight with the specified antibodies directed against COX-2 (Cayman 160106) ABCA1 (Novus Biologicals, NB400-105), ABCG1 (Novus NB400-132) and ß-actin (Sigma A5441). .. Proteins were visualized by using appropriate secondary antibodies and scanned with an Odyssey Imaging System (Li-Cor Biosciences).

other:

Article Title: RER1 regulates lipid metabolism in monocytes and macrophages
Article Snippet: ABCA1 , Novus Biologicals , Cat#NB400-105 , .

Western Blot:

Article Title: Loss of ADAM17 in smooth muscle cells enhances their transformation to macrophage-like cells leading to more severe atherosclerosis in mice.
Article Snippet: Total protein concentration was determined with a BCA kit (BioRad). .. Western blotting was performed on aortic tissue, SMC or macrophage protein extracts as before [7] using the following antibodies: CD68 (BioRad), Calponin 1 (Abcam), ADAM17 (Sigma for human, Kerafast for mouse), Caspase 3 (Cell Signaling), αSMA (Abcam), Galectin 3 (Abcam), SM22α/Transgelin (Abcam), ABCA1 (Novus Bio), CD36 (Novus Bio), SR-A1 (Novus Bio), LAL (Abcam), TNFR1 (Santa Cruz), TNFR2 (Cell Signaling), LXR (Abcam), NFκB (p65) (Santa Cruz), Phospho- and total IKKα/β (Cell Signaling). .. The intensity of bands on immunoblots was quantified using the Image-Quant TL software (Cytiva), and normalized to total protein (memcode-stained membrane).

Flow Cytometry:

Article Title: E3 ubiquitin ligase Listerin regulates macrophage cholesterol efflux and atherosclerosis by targeting ABCA1
Article Snippet: Erythrodiol was purchased from 1 MCE. .. Primary antibodies used for Flow cytometry were Listerin (produced by 2 ABclonal, Project No. WG-059009; immunogen: 3 MGGKNKQRTKGNLRPSNSGRAAELLAKEQGTVPGFIGFGTSQSDLGYVPA-C) 4 and ABCA1 (Novus Cat# NB400-105AF488). ..

Produced:

Image Search Results

A UMAP plot showing human oligodendrocyte (hOlig) subclusters. B Feature plots of marker genes in hOlig. C Proportion of each hOlig subcluster across sTBI groups, relative to the entire cortex (left) and hOligs (right). D Boxplots of hOlig-ABCA1 and hOlig-FOS proportions across sTBI groups, with significant P- values (< 0.05) from two-sided Mann–Whitney U test indicated ( n = 4 control, 4 for < 24 h, 9 for 24–49 h, 5 for 72–94 h). Center line: median; box: interquartile range; whiskers: 1.5×IQR. E RNA velocity analysis of hOlig subtypes across sTBI stages. F Scatter plots show the temporal dynamics of ABCA1 expression (left) and hOlig-ABCA1 proportion (right) across time post sTBI, with solid lines representing LOESS-fitted values, shaded areas indicating 95% confidence intervals. G Representative electron microscopy images of human sTBI tissue. Arrows indicate disrupted myelin. n = 3 independent samples per group, with similar results. Scale bars: 5 μm (top), 500 nm (bottom). H Co-expression network of the hOlig-ABCA1 module showing hub gene connectivity (kME) and GO biological processes identified by one-sided hypergeometric tests with BH correction. I Representative immunofluorescence images of ABCA1 and OLIG2 across sTBI stages. Boxed regions are shown as insets with corresponding single-channel images. Scale bars: 50 μm (main), 20 μm (insets, single-channel). J Quantification of OLIG2⁺ABCA1⁺ cell density and integrated ABCA1 intensity within OLIG2-defined regions. n = 4/group. K Representative immunofluorescence images of MBP and CNP in differentiated MO3.13 under each condition. Scale bar: 25 μm. L Fluorescence intensity of MBP (top) and CNP (bottom); n = 3/group. M Right: hierarchical clustering of proteins upregulated compared with control (log₂FC > 0.25) and correlated with ABCA1 (Spearman r > 0.6) using the Relapsing-Remitting Multiple Sclerosis proteomic dataset. GO processes enriched in cluster 2 are shown. Left: Expression of the same proteins, grouped according to the clusters on the right, across hOlig subclusters. Proteins enriched in processes on the right are highlighted. J , L Data are mean ± s.e.m., using one-way ANOVA with Tukey’s multiple comparison test. Only significant P- values (< 0.05) are shown. Source data are provided as a Source Data file.

Journal: Nature Communications

Article Title: Single-nucleus analysis reveals human-specific oligodendrocyte polarization and conserved neuronal responses after severe traumatic brain injury

doi: 10.1038/s41467-026-73036-w

Figure Lengend Snippet: A UMAP plot showing human oligodendrocyte (hOlig) subclusters. B Feature plots of marker genes in hOlig. C Proportion of each hOlig subcluster across sTBI groups, relative to the entire cortex (left) and hOligs (right). D Boxplots of hOlig-ABCA1 and hOlig-FOS proportions across sTBI groups, with significant P- values (< 0.05) from two-sided Mann–Whitney U test indicated ( n = 4 control, 4 for < 24 h, 9 for 24–49 h, 5 for 72–94 h). Center line: median; box: interquartile range; whiskers: 1.5×IQR. E RNA velocity analysis of hOlig subtypes across sTBI stages. F Scatter plots show the temporal dynamics of ABCA1 expression (left) and hOlig-ABCA1 proportion (right) across time post sTBI, with solid lines representing LOESS-fitted values, shaded areas indicating 95% confidence intervals. G Representative electron microscopy images of human sTBI tissue. Arrows indicate disrupted myelin. n = 3 independent samples per group, with similar results. Scale bars: 5 μm (top), 500 nm (bottom). H Co-expression network of the hOlig-ABCA1 module showing hub gene connectivity (kME) and GO biological processes identified by one-sided hypergeometric tests with BH correction. I Representative immunofluorescence images of ABCA1 and OLIG2 across sTBI stages. Boxed regions are shown as insets with corresponding single-channel images. Scale bars: 50 μm (main), 20 μm (insets, single-channel). J Quantification of OLIG2⁺ABCA1⁺ cell density and integrated ABCA1 intensity within OLIG2-defined regions. n = 4/group. K Representative immunofluorescence images of MBP and CNP in differentiated MO3.13 under each condition. Scale bar: 25 μm. L Fluorescence intensity of MBP (top) and CNP (bottom); n = 3/group. M Right: hierarchical clustering of proteins upregulated compared with control (log₂FC > 0.25) and correlated with ABCA1 (Spearman r > 0.6) using the Relapsing-Remitting Multiple Sclerosis proteomic dataset. GO processes enriched in cluster 2 are shown. Left: Expression of the same proteins, grouped according to the clusters on the right, across hOlig subclusters. Proteins enriched in processes on the right are highlighted. J , L Data are mean ± s.e.m., using one-way ANOVA with Tukey’s multiple comparison test. Only significant P- values (< 0.05) are shown. Source data are provided as a Source Data file.

Article Snippet: After primary human oligodendrocytes reached approximately 60% confluence, they were treated with LPS (Beyotime, S1732, 1 μg/mL) alone, or in combination with the ABCA1 agonist CS-6253 (MCE, HY-P6306, 1 μM) for 24 h.

Techniques: Marker, MANN-WHITNEY, Control, Expressing, Electron Microscopy, Immunofluorescence, Fluorescence, Comparison

A UMAP plot showing human microglia (hMicro) subclusters. B Proportions of hMicro subclusters across sTBI stages, relative to total cortex (left) or hMicro (right). C Boxplots showing the proportions of hMicro subtypes across sTBI groups, with P-values from two-sided Mann–Whitney U test shown ( n = 4 for control, 4 for < 24 h, 9 for 24–49 h, 5 for 72–94 h). D Dot plots show the UMAP embedding from panel A for each sTBI stage, colored by pseudotime. E Density plot showing the pseudotime distributions across stages. F Left: Ligands significantly associated with sTBI stages, with a Sankey diagram in the center showing function and linking them to corresponding receptors. The heatmap (right) displays the q values of receptors, indicating the sTBI stage association across cell types ( q < 0.01). G , J Box plots showing the expression of CALM2 ( G ) and HMGB1 ( J ) in hMicro across sTBI stages ( n = 4 for control, 4 for < 24 h, 9 for 24–49 h, 5 for 72–94 h). P- values comparing each sTBI group with control derived from two-sided Wilcoxon rank-sum test with BH correction. H , K Scatter plots of donor-level correlations between CALM2 ( H ) or HMGB1 ( K ) in hMicro and ABCA1 in hOlig-ABCA1. Linear fits with 95% confidence intervals (shaded area) are shown. Spearman R and two-sided P -value are indicated. I Regulatory potential of CALM2 -associated ligands on ABCA1 co-expression genes. L Extracellular HMGB1 levels measured by ELISA in HMC3 cells following CALM2 knockdown (sh-CALM2) or overexpression (OE-CALM2), normalized to controls ( n = 4/group). M , N Relative ABCA1 mRNA expression measured by qPCR ( M : n = 3/group) and extracellular cholesterol levels ( N : n = 4/group) in differentiated MO3.13 cells under the indicated treatments. O Conceptual schematic summarizing inferred CALM2–HMGB1–ABCA1 relationships across microglia and oligodendrocytes in human and mouse sTBI, based on ligand–receptor analysis, co-expression patterns, and regulatory predictions. C , G , J Center line: median; box: interquartile range; whiskers: 1.5 × IQR. L – N Data are mean ± s.e.m. with two-tailed Student’s t test ( L ), one-way ANOVA with Tukey’s multiple comparison test ( M , N ). ( G , J , L – N ) Only significant P- values (< 0.05) are shown. Source data are provided as a Source Data file.

Journal: Nature Communications

Article Title: Single-nucleus analysis reveals human-specific oligodendrocyte polarization and conserved neuronal responses after severe traumatic brain injury

doi: 10.1038/s41467-026-73036-w

Figure Lengend Snippet: A UMAP plot showing human microglia (hMicro) subclusters. B Proportions of hMicro subclusters across sTBI stages, relative to total cortex (left) or hMicro (right). C Boxplots showing the proportions of hMicro subtypes across sTBI groups, with P-values from two-sided Mann–Whitney U test shown ( n = 4 for control, 4 for < 24 h, 9 for 24–49 h, 5 for 72–94 h). D Dot plots show the UMAP embedding from panel A for each sTBI stage, colored by pseudotime. E Density plot showing the pseudotime distributions across stages. F Left: Ligands significantly associated with sTBI stages, with a Sankey diagram in the center showing function and linking them to corresponding receptors. The heatmap (right) displays the q values of receptors, indicating the sTBI stage association across cell types ( q < 0.01). G , J Box plots showing the expression of CALM2 ( G ) and HMGB1 ( J ) in hMicro across sTBI stages ( n = 4 for control, 4 for < 24 h, 9 for 24–49 h, 5 for 72–94 h). P- values comparing each sTBI group with control derived from two-sided Wilcoxon rank-sum test with BH correction. H , K Scatter plots of donor-level correlations between CALM2 ( H ) or HMGB1 ( K ) in hMicro and ABCA1 in hOlig-ABCA1. Linear fits with 95% confidence intervals (shaded area) are shown. Spearman R and two-sided P -value are indicated. I Regulatory potential of CALM2 -associated ligands on ABCA1 co-expression genes. L Extracellular HMGB1 levels measured by ELISA in HMC3 cells following CALM2 knockdown (sh-CALM2) or overexpression (OE-CALM2), normalized to controls ( n = 4/group). M , N Relative ABCA1 mRNA expression measured by qPCR ( M : n = 3/group) and extracellular cholesterol levels ( N : n = 4/group) in differentiated MO3.13 cells under the indicated treatments. O Conceptual schematic summarizing inferred CALM2–HMGB1–ABCA1 relationships across microglia and oligodendrocytes in human and mouse sTBI, based on ligand–receptor analysis, co-expression patterns, and regulatory predictions. C , G , J Center line: median; box: interquartile range; whiskers: 1.5 × IQR. L – N Data are mean ± s.e.m. with two-tailed Student’s t test ( L ), one-way ANOVA with Tukey’s multiple comparison test ( M , N ). ( G , J , L – N ) Only significant P- values (< 0.05) are shown. Source data are provided as a Source Data file.

Techniques: MANN-WHITNEY, Control, Expressing, Derivative Assay, Enzyme-linked Immunosorbent Assay, Knockdown, Over Expression, Two Tailed Test, Comparison

The diagram depicts major cell populations analyzed, their relative changes across edema stages, and associated transcriptional programs. CALM2 and HMGB1 are highlighted in microglia. A human distinct oligodendrocyte subpopulation with elevated ABCA1 expression (OLIG-ABCA1) is enriched for lipid transport and cell adhesion genes (e.g., ITGB8, CDH19 ). Gene modules in deep-layer (L5/6) excitatory neurons associated with edema and schizophrenia-related GWAS enrichment are shown. Intercellular associations, including HMGB1–ABCA1 interaction, as represented in the schematic.

Journal: Nature Communications

Article Title: Single-nucleus analysis reveals human-specific oligodendrocyte polarization and conserved neuronal responses after severe traumatic brain injury

doi: 10.1038/s41467-026-73036-w

Figure Lengend Snippet: The diagram depicts major cell populations analyzed, their relative changes across edema stages, and associated transcriptional programs. CALM2 and HMGB1 are highlighted in microglia. A human distinct oligodendrocyte subpopulation with elevated ABCA1 expression (OLIG-ABCA1) is enriched for lipid transport and cell adhesion genes (e.g., ITGB8, CDH19 ). Gene modules in deep-layer (L5/6) excitatory neurons associated with edema and schizophrenia-related GWAS enrichment are shown. Intercellular associations, including HMGB1–ABCA1 interaction, as represented in the schematic.

Techniques: Expressing

Schematic of the anti-atherosclerotic mechanism of OPN-HMCN@MLT. ( A ) The study commenced with the synthesis of mesoporous carbon nanospheres (MCN) functionalized with an OPN-binding peptide and hyaluronic acid to construct the OPN-HMCN nanoplatform. The OPN-binding peptide was designed to recognize OPN enriched in the extracellular matrix and on the surface of foam cells, thereby enabling selective accumulation in OPN-rich pathological regions. Following OPN recognition, OPN-HMCN@MLT undergoes CD44-dependent endocytosis. Melatonin (MLT), a lipid autophagy–promoting agent, was subsequently encapsulated within the nanocarrier to form OPN-HMCN@MLT. Firstly, the released MLT can bind to and upregulate the expression of PPARα and PPARγ, which then promote the expression of downstream genes (ABCA1, ABCG1, ACOX-1, and CTP1A) and trigger the lipophagy. ( B ) Subsequently, its lipophagy-enhancing effects, including ABCA1/G1-mediated cholesterol efflux and CTP1A/ACOX-1-mediated mitochondrial fatty acid oxidation, were studied to confirm the reversal of foam cell formation. ( C ) These effects eventually promote foam cells to reverse into macrophages. Abbreviations: MCN, mesoporous carbon nanoparticle; OPN, osteopontin; MLT, melatonin; LDL, low-density lipoprotein; ox-LDL, oxidized low-density lipoprotein; PA, Photoacoustic.

Journal: Bioactive Materials

Article Title: A foam cell-targeted lipophagy restoration strategy stabilizes vulnerable atherosclerotic plaques

doi: 10.1016/j.bioactmat.2026.02.041

Figure Lengend Snippet: Schematic of the anti-atherosclerotic mechanism of OPN-HMCN@MLT. ( A ) The study commenced with the synthesis of mesoporous carbon nanospheres (MCN) functionalized with an OPN-binding peptide and hyaluronic acid to construct the OPN-HMCN nanoplatform. The OPN-binding peptide was designed to recognize OPN enriched in the extracellular matrix and on the surface of foam cells, thereby enabling selective accumulation in OPN-rich pathological regions. Following OPN recognition, OPN-HMCN@MLT undergoes CD44-dependent endocytosis. Melatonin (MLT), a lipid autophagy–promoting agent, was subsequently encapsulated within the nanocarrier to form OPN-HMCN@MLT. Firstly, the released MLT can bind to and upregulate the expression of PPARα and PPARγ, which then promote the expression of downstream genes (ABCA1, ABCG1, ACOX-1, and CTP1A) and trigger the lipophagy. ( B ) Subsequently, its lipophagy-enhancing effects, including ABCA1/G1-mediated cholesterol efflux and CTP1A/ACOX-1-mediated mitochondrial fatty acid oxidation, were studied to confirm the reversal of foam cell formation. ( C ) These effects eventually promote foam cells to reverse into macrophages. Abbreviations: MCN, mesoporous carbon nanoparticle; OPN, osteopontin; MLT, melatonin; LDL, low-density lipoprotein; ox-LDL, oxidized low-density lipoprotein; PA, Photoacoustic.

Article Snippet: To block nonspecific binding, membranes were incubated with 5% skim milk for 1 h. Thereafter, membranes were incubated overnight at 4 °C with primary antibodies against ABCA1, ABCG1, ACOX1, CPT1A, LC3 (ab192890, 1:2000, abcam), LAMP1 (84658-5-RR, 1:8000, Proteintech), PPARα (66826-1-Ig, 1:3000, Proteintech), PPARγ (66936-1-Ig, 1:10000, Proteintech), P62 (18420-1-AP, 1:10000, Proteintech), MCAD (55210-1-AP, 1:3000, Proteintech), LCAD (17526-1-AP, 1:10000, Proteintech), tubulin (80762-1-RR, 1:10000, Proteintech), GAPDH (60004-1-Ig, 1:50000, Proteintech), and β-actin (66009-1-Ig, 1:20000, Proteintech).

Techniques: Binding Assay, Construct, Expressing

Virtual screening identifies a candidate ABCA1-targeting small molecule that reduces lipid droplet accumulation. A Schematic overview of the structure-guided virtual screening and validation workflow. B Representative immunofluorescence images showing lipid droplets (BODIPY, green) in primary microglia following myelin debris stimulation and treatment with candidate compounds. C Quantification of lipid droplet number per cell and integrated BODIPY fluorescence intensity (n = 3). D Flow cytometric analysis of BODIPY fluorescence in primary microglia under the indicated conditions. E Quantification of BODIPY mean fluorescence intensity by flow cytometry (n = 3). F Cell viability analysis of candidate compounds assessed by CCK-8 assay. G Chemical structure of Z231. H Docking visualization of Z231 bound to ABCA1. I Surface plasmon resonance (SPR) sensorgrams showing ABCA1–Z231 binding. J Microscale thermophoresis (MST) analysis of ABCA1–Z231 interaction. K Representative immunofluorescence images showing lipid droplet accumulation in spinal cord sections from ABCA1-CKO mice following spinal cord injury and treatment with Z231 or vehicle control. Lipid droplets were visualized by BODIPY staining (green), with IBA1 (red) labeling microglia/macrophages and DAPI (blue) labeling nuclei. Scale bars=500μm (overview) and 50μm (magnified images). Data are presented as mean ± SEM. ns indicates no significance, *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001 by onr-way ANOVA with Tukey’s test for multiple comparisons ( C and E )

Journal: Journal of Neuroinflammation

Article Title: ABCA1-mediated lipid efflux restrains oxidative stress and neuroinflammation after spinal cord injury

doi: 10.1186/s12974-026-03859-3

Figure Lengend Snippet: Virtual screening identifies a candidate ABCA1-targeting small molecule that reduces lipid droplet accumulation. A Schematic overview of the structure-guided virtual screening and validation workflow. B Representative immunofluorescence images showing lipid droplets (BODIPY, green) in primary microglia following myelin debris stimulation and treatment with candidate compounds. C Quantification of lipid droplet number per cell and integrated BODIPY fluorescence intensity (n = 3). D Flow cytometric analysis of BODIPY fluorescence in primary microglia under the indicated conditions. E Quantification of BODIPY mean fluorescence intensity by flow cytometry (n = 3). F Cell viability analysis of candidate compounds assessed by CCK-8 assay. G Chemical structure of Z231. H Docking visualization of Z231 bound to ABCA1. I Surface plasmon resonance (SPR) sensorgrams showing ABCA1–Z231 binding. J Microscale thermophoresis (MST) analysis of ABCA1–Z231 interaction. K Representative immunofluorescence images showing lipid droplet accumulation in spinal cord sections from ABCA1-CKO mice following spinal cord injury and treatment with Z231 or vehicle control. Lipid droplets were visualized by BODIPY staining (green), with IBA1 (red) labeling microglia/macrophages and DAPI (blue) labeling nuclei. Scale bars=500μm (overview) and 50μm (magnified images). Data are presented as mean ± SEM. ns indicates no significance, *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001 by onr-way ANOVA with Tukey’s test for multiple comparisons ( C and E )

Article Snippet: For ABCA1 deletion, mice received intraperitoneal injections of tamoxifen (20 mg mL -1 ; HY-13757 A, MCE) for 7 consecutive days.

Techniques: Biomarker Discovery, Immunofluorescence, Fluorescence, Flow Cytometry, CCK-8 Assay, SPR Assay, Binding Assay, Microscale Thermophoresis, Control, Staining, Labeling

Z231 activates ABCA1 to reverse lipid-laden ILLM phenotypes and promote spinal cord repair after injury. A After spinal cord injury, lesion-associated microglia/macrophages accumulate lipid droplets, forming ILLMs with elevated ROS and pro-inflammatory signaling. Z231 enhances ABCA1-dependent lipid efflux, reducing lipid burden, attenuating oxidative stress and inflammation, and partially improving functional recovery. This schematic summarizes the molecular and cellular mechanism linking ABCA1 activity to metabolic and inflammatory regulation in ILLMs

Journal: Journal of Neuroinflammation

Article Title: ABCA1-mediated lipid efflux restrains oxidative stress and neuroinflammation after spinal cord injury

doi: 10.1186/s12974-026-03859-3

Figure Lengend Snippet: Z231 activates ABCA1 to reverse lipid-laden ILLM phenotypes and promote spinal cord repair after injury. A After spinal cord injury, lesion-associated microglia/macrophages accumulate lipid droplets, forming ILLMs with elevated ROS and pro-inflammatory signaling. Z231 enhances ABCA1-dependent lipid efflux, reducing lipid burden, attenuating oxidative stress and inflammation, and partially improving functional recovery. This schematic summarizes the molecular and cellular mechanism linking ABCA1 activity to metabolic and inflammatory regulation in ILLMs

Article Snippet: For ABCA1 deletion, mice received intraperitoneal injections of tamoxifen (20 mg mL -1 ; HY-13757 A, MCE) for 7 consecutive days.

Techniques: Functional Assay, Activity Assay

Single-cell and immune-enriched transcriptomics reveal lipid efflux–associated microglia/macrophage states after SCI. A UMAP visualization of snRNA-seq profiling showing 14 major cell classes across SHAM and SCI time points (total 187,212 nuclei). B Stacked bar plot showing relative proportions of major cell classes across time, highlighting dynamic remodeling of the myeloid compartment after SCI. C Heatmap of gene-set scores for cholesterol handling–related programs across major cell classes. D KEGG pathway enrichment analyses of microglial DEGs for each post-injury comparison versus SHAM. E KEGG pathway enrichment analyses of macrophage DEGs for each post-injury comparison versus SHAM. F , G Differential expression of genes within the ABC transporter pathway in microglia ( F ) and macrophages ( G ) at each post-injury comparison versus SHAM. H UMAP visualization of CD45⁺ cell-enriched scRNA-seq dataset (total 59,095 cells) showing 10 immune cell classes across SHAM, 7 dpi, 14 dpi, and 30 dpi. I Stacked bar plot showing immune cell-type composition across the four CD45⁺ scRNA-seq time points. J PHATE embedding of myeloid subclustering identifying microglial subclusters (MG1–MG3) and macrophage subclusters (MP1–MP5). K Temporal composition changes of MG and MP subclusters across SHAM and post-injury time points. L Violin plots showing Cholesterol Efflux gene-set scores across myeloid subclusters and time points. M PHATE-based gene expression density maps for ABCA1 and ABCG1 within microglial and macrophage manifolds. N PHATE-based feature plot showing the expression distribution of Lgals3 within microglia and macrophage populations

Journal: Journal of Neuroinflammation

Article Title: ABCA1-mediated lipid efflux restrains oxidative stress and neuroinflammation after spinal cord injury

doi: 10.1186/s12974-026-03859-3

Figure Lengend Snippet: Single-cell and immune-enriched transcriptomics reveal lipid efflux–associated microglia/macrophage states after SCI. A UMAP visualization of snRNA-seq profiling showing 14 major cell classes across SHAM and SCI time points (total 187,212 nuclei). B Stacked bar plot showing relative proportions of major cell classes across time, highlighting dynamic remodeling of the myeloid compartment after SCI. C Heatmap of gene-set scores for cholesterol handling–related programs across major cell classes. D KEGG pathway enrichment analyses of microglial DEGs for each post-injury comparison versus SHAM. E KEGG pathway enrichment analyses of macrophage DEGs for each post-injury comparison versus SHAM. F , G Differential expression of genes within the ABC transporter pathway in microglia ( F ) and macrophages ( G ) at each post-injury comparison versus SHAM. H UMAP visualization of CD45⁺ cell-enriched scRNA-seq dataset (total 59,095 cells) showing 10 immune cell classes across SHAM, 7 dpi, 14 dpi, and 30 dpi. I Stacked bar plot showing immune cell-type composition across the four CD45⁺ scRNA-seq time points. J PHATE embedding of myeloid subclustering identifying microglial subclusters (MG1–MG3) and macrophage subclusters (MP1–MP5). K Temporal composition changes of MG and MP subclusters across SHAM and post-injury time points. L Violin plots showing Cholesterol Efflux gene-set scores across myeloid subclusters and time points. M PHATE-based gene expression density maps for ABCA1 and ABCG1 within microglial and macrophage manifolds. N PHATE-based feature plot showing the expression distribution of Lgals3 within microglia and macrophage populations

Article Snippet: For ABCA1 deletion, mice received intraperitoneal injections of tamoxifen (20 mg mL -1 ; HY-13757 A, MCE) for 7 consecutive days.

Techniques: Single Cell, Transcriptomics, Comparison, Quantitative Proteomics, Gene Expression, Expressing

ABCA1 deletion exacerbates lipid droplet burden and impairs functional recovery. A Representative immunofluorescence images showing lipid droplets (BODIPY, green) in IBA1⁺ microglia/macrophages (IBA1, red) in ABCA1 f/f and ABCA1-CKO mice at the indicated time points after SCI. DAPI labels nuclei (blue). B Quantification of BODIPY+ area and integrated fluorescence intensity ( n = 6). C Representative images of degraded myelin basic protein (dMBP, green) within IBA1⁺ microglia/macrophages in ABCA1 f/f and ABCA1-CKO mice at the indicated time points. D Quantification of dMBP+ area and integrated fluorescence intensity ( n = 6). E Basso Mouse Scale (BMS) scores assessing locomotor recovery over time after SCI ( n = 6). F Representative hindlimb electromyography (EMG) traces recorded at 30 and 42 dpi. G Quantification of EMG amplitude and latency, expressed as percentages relative to SHAM -ABCA1 ff ( n =6). H Representative CatWalk footprint patterns at 30 and 42 dpi. I , K Principal component analysis (PCA) of gait parameters derived from CatWalk analysis. J , L Quantification of representative gait parameters associated with PC1, including base of support and stride length, expressed as percentages relative to SHAM -ABCA1 ff ( n =6). M Schematic of hindlimb landmark labeling and motion capture setup for kinematic analysis. N Representative joint trajectory plots at 30 and 42 dpi. O , P Quantification of kinematic parameters, including paw drag percentage, limb swing amplitude, and mean step height, expressed as percentages relative to SHAM -ABCA1 ff ( n =6). Data are presented as mean ± SEM. ns indicates no significance, *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001 by two-way ANOVA with Tukey’s test for multiple comparisons ( C , D ), one-way ANOVA with Tukey’s test ( G , J , L , O and P )

Journal: Journal of Neuroinflammation

Article Title: ABCA1-mediated lipid efflux restrains oxidative stress and neuroinflammation after spinal cord injury

doi: 10.1186/s12974-026-03859-3

Figure Lengend Snippet: ABCA1 deletion exacerbates lipid droplet burden and impairs functional recovery. A Representative immunofluorescence images showing lipid droplets (BODIPY, green) in IBA1⁺ microglia/macrophages (IBA1, red) in ABCA1 f/f and ABCA1-CKO mice at the indicated time points after SCI. DAPI labels nuclei (blue). B Quantification of BODIPY+ area and integrated fluorescence intensity ( n = 6). C Representative images of degraded myelin basic protein (dMBP, green) within IBA1⁺ microglia/macrophages in ABCA1 f/f and ABCA1-CKO mice at the indicated time points. D Quantification of dMBP+ area and integrated fluorescence intensity ( n = 6). E Basso Mouse Scale (BMS) scores assessing locomotor recovery over time after SCI ( n = 6). F Representative hindlimb electromyography (EMG) traces recorded at 30 and 42 dpi. G Quantification of EMG amplitude and latency, expressed as percentages relative to SHAM -ABCA1 ff ( n =6). H Representative CatWalk footprint patterns at 30 and 42 dpi. I , K Principal component analysis (PCA) of gait parameters derived from CatWalk analysis. J , L Quantification of representative gait parameters associated with PC1, including base of support and stride length, expressed as percentages relative to SHAM -ABCA1 ff ( n =6). M Schematic of hindlimb landmark labeling and motion capture setup for kinematic analysis. N Representative joint trajectory plots at 30 and 42 dpi. O , P Quantification of kinematic parameters, including paw drag percentage, limb swing amplitude, and mean step height, expressed as percentages relative to SHAM -ABCA1 ff ( n =6). Data are presented as mean ± SEM. ns indicates no significance, *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001 by two-way ANOVA with Tukey’s test for multiple comparisons ( C , D ), one-way ANOVA with Tukey’s test ( G , J , L , O and P )

Article Snippet: For ABCA1 deletion, mice received intraperitoneal injections of tamoxifen (20 mg mL -1 ; HY-13757 A, MCE) for 7 consecutive days.

Techniques: Functional Assay, Immunofluorescence, Fluorescence, Derivative Assay, Labeling

Z231 activates ABCA1 to reverse lipid-induced microglial stress and inflammation. A Representative immunofluorescence images showing lipid droplets (BODIPY) and cellular ROS (CellROX) in primary microglia under the indicated conditions. B Quantification of CellROX fluorescence intensity ( n = 3). C , D Flow cytometric analysis and quantification of CellROX fluorescence ( n = 3). E Representative images of mitochondrial ROS detected by MitoSOX staining. F Quantification of MitoSOX fluorescence intensity ( n = 3). G , H Flow cytometric analysis and quantification of MitoSOX fluorescence ( n = 3). I Heatmap summarizing expression of inflammatory cytokines and chemokines. J qPCR analysis of pro- and anti-inflammatory cytokines ( n = 4). K Seahorse XF mitochondrial stress test showing oxygen consumption rate (OCR). L Quantification of mitochondrial respiration parameters ( n = 3). Data are presented as mean ± SEM. ns indicates no significance, *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001 by one-way ANOVA with Tukey’s test ( B , D , F , H , G and L )

Journal: Journal of Neuroinflammation

Article Title: ABCA1-mediated lipid efflux restrains oxidative stress and neuroinflammation after spinal cord injury

doi: 10.1186/s12974-026-03859-3

Figure Lengend Snippet: Z231 activates ABCA1 to reverse lipid-induced microglial stress and inflammation. A Representative immunofluorescence images showing lipid droplets (BODIPY) and cellular ROS (CellROX) in primary microglia under the indicated conditions. B Quantification of CellROX fluorescence intensity ( n = 3). C , D Flow cytometric analysis and quantification of CellROX fluorescence ( n = 3). E Representative images of mitochondrial ROS detected by MitoSOX staining. F Quantification of MitoSOX fluorescence intensity ( n = 3). G , H Flow cytometric analysis and quantification of MitoSOX fluorescence ( n = 3). I Heatmap summarizing expression of inflammatory cytokines and chemokines. J qPCR analysis of pro- and anti-inflammatory cytokines ( n = 4). K Seahorse XF mitochondrial stress test showing oxygen consumption rate (OCR). L Quantification of mitochondrial respiration parameters ( n = 3). Data are presented as mean ± SEM. ns indicates no significance, *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001 by one-way ANOVA with Tukey’s test ( B , D , F , H , G and L )

Article Snippet: For ABCA1 deletion, mice received intraperitoneal injections of tamoxifen (20 mg mL -1 ; HY-13757 A, MCE) for 7 consecutive days.

Techniques: Immunofluorescence, Fluorescence, Staining, Expressing

Molecular dynamic support stable binding of Z231 to ABCA1 and reveal a compact, stabilized conformational ensemble. A Ligand RMSD of Z231 during a 100-ns MD simulation, indicating rapid equilibration followed by stable positioning within the binding pocket. B Backbone RMSD comparison between apo ABCA1 and the ABCA1–Z231 complex across 100 ns, showing reduced conformational drift in the ligand-bound state. C RMSF profiles for apo ABCA1 and ABCA1–Z231, reporting residue-level flexibility changes upon ligand binding. D Radius of gyration (Rg) for apo ABCA1 and ABCA1–Z231, reflecting global compactness dynamics over time. E SASA of apo ABCA1 and ABCA1–Z231, with reduced SASA in the complex consistent with partial solvent shielding and a tighter conformation. F Number of protein–ligand hydrogen bonds across the simulation, indicating persistent polar interactions. G Per-residue binding free-energy decomposition (MM/GBSA) highlighting the top contributing residues within the Z231-binding pocket. H Free-energy landscape of the ABCA1–Z231 trajectory projected onto RMSD and Rg, illustrating the dominant low-energy conformational basin populated during simulation

Journal: Journal of Neuroinflammation

Article Title: ABCA1-mediated lipid efflux restrains oxidative stress and neuroinflammation after spinal cord injury

doi: 10.1186/s12974-026-03859-3

Figure Lengend Snippet: Molecular dynamic support stable binding of Z231 to ABCA1 and reveal a compact, stabilized conformational ensemble. A Ligand RMSD of Z231 during a 100-ns MD simulation, indicating rapid equilibration followed by stable positioning within the binding pocket. B Backbone RMSD comparison between apo ABCA1 and the ABCA1–Z231 complex across 100 ns, showing reduced conformational drift in the ligand-bound state. C RMSF profiles for apo ABCA1 and ABCA1–Z231, reporting residue-level flexibility changes upon ligand binding. D Radius of gyration (Rg) for apo ABCA1 and ABCA1–Z231, reflecting global compactness dynamics over time. E SASA of apo ABCA1 and ABCA1–Z231, with reduced SASA in the complex consistent with partial solvent shielding and a tighter conformation. F Number of protein–ligand hydrogen bonds across the simulation, indicating persistent polar interactions. G Per-residue binding free-energy decomposition (MM/GBSA) highlighting the top contributing residues within the Z231-binding pocket. H Free-energy landscape of the ABCA1–Z231 trajectory projected onto RMSD and Rg, illustrating the dominant low-energy conformational basin populated during simulation

Article Snippet: For ABCA1 deletion, mice received intraperitoneal injections of tamoxifen (20 mg mL -1 ; HY-13757 A, MCE) for 7 consecutive days.

Techniques: Binding Assay, Comparison, Residue, Ligand Binding Assay, Solvent

Developmental expression of lipoprotein receptors in brain endothelial cells. (A) Expression of all genes coding for proteins with apolipoprotein binding activity in endothelial cells from the brain during embryonic development and adulthood. (B) Expression of Abca1 and Scarb1 in different cell types in the adult mouse brain. AC: astrocytes, EC: endothelial cells, MG: microglia, Myel: myeloid cells, Neu: neurons, Olig: oligodendrocytes, OPC: oligodendrocyte progenitor cells.

Journal: Frontiers in Cell and Developmental Biology

Article Title: Altered brain vascularization and transcriptional changes in embryos lacking ABCA1 support a role of cholesterol in brain angiogenesis

doi: 10.3389/fcell.2026.1783696

Figure Lengend Snippet: Developmental expression of lipoprotein receptors in brain endothelial cells. (A) Expression of all genes coding for proteins with apolipoprotein binding activity in endothelial cells from the brain during embryonic development and adulthood. (B) Expression of Abca1 and Scarb1 in different cell types in the adult mouse brain. AC: astrocytes, EC: endothelial cells, MG: microglia, Myel: myeloid cells, Neu: neurons, Olig: oligodendrocytes, OPC: oligodendrocyte progenitor cells.

Article Snippet: ABCA1 KO mice in the DBA background were originally generated by Dr. Omar Francone (Homology Medicines, Inc., Bedford, MA, US) ( ) and are currently maintained at Dr. Dolores Busso’s lab. Wild-type C57Bl6/J mice for pharmacological studies were purchased from the Chilean Public Health Institute.

Techniques: Expressing, Binding Assay, Activity Assay

Alterations in the brain vasculature of fetuses lacking ABCA1. (A) Representative coronal sections of fetal brains obtained from ABCA1 +/+ and ABCA1 −/− fetuses at E14.5, E18.5 and P120 and stained for PECAM1 to reveal blood vessels. Bars: 200 μm in E14.5; 500 μm in E18.5; 100 μm in P120. (B–D) Morphometric analyses in blood vessels at indicated developmental stages. N: E14.5 N = 6 ABCA1 +/+ and 4 ABCA1 −/− ; E18.5 N = 6 per group; P120 N = 6 per group. Exact p-values are shown; t-test with Welch correction.

Journal: Frontiers in Cell and Developmental Biology

Article Title: Altered brain vascularization and transcriptional changes in embryos lacking ABCA1 support a role of cholesterol in brain angiogenesis

doi: 10.3389/fcell.2026.1783696

Figure Lengend Snippet: Alterations in the brain vasculature of fetuses lacking ABCA1. (A) Representative coronal sections of fetal brains obtained from ABCA1 +/+ and ABCA1 −/− fetuses at E14.5, E18.5 and P120 and stained for PECAM1 to reveal blood vessels. Bars: 200 μm in E14.5; 500 μm in E18.5; 100 μm in P120. (B–D) Morphometric analyses in blood vessels at indicated developmental stages. N: E14.5 N = 6 ABCA1 +/+ and 4 ABCA1 −/− ; E18.5 N = 6 per group; P120 N = 6 per group. Exact p-values are shown; t-test with Welch correction.

Techniques: Staining

Transcriptomic changes associated with ABCA1 deficiency. (A) Fetal brains from heterozygous intercrosses were collected at E18.5 and vascular fragments were isolated for transcriptomic profiling. (B) Volcano plot showing differentially expressed genes. Genes involved in cholesterol synthesis (blue dots) or angiogenesis (red dots) are highlighted. (C) Enriched biological processes in the list of differentially expressed genes. (D) Levels of differentially expressed genes involved in cholesterol synthesis and angiogenesis.

Journal: Frontiers in Cell and Developmental Biology

Article Title: Altered brain vascularization and transcriptional changes in embryos lacking ABCA1 support a role of cholesterol in brain angiogenesis

doi: 10.3389/fcell.2026.1783696

Figure Lengend Snippet: Transcriptomic changes associated with ABCA1 deficiency. (A) Fetal brains from heterozygous intercrosses were collected at E18.5 and vascular fragments were isolated for transcriptomic profiling. (B) Volcano plot showing differentially expressed genes. Genes involved in cholesterol synthesis (blue dots) or angiogenesis (red dots) are highlighted. (C) Enriched biological processes in the list of differentially expressed genes. (D) Levels of differentially expressed genes involved in cholesterol synthesis and angiogenesis.

Techniques: Isolation

ABCA1 deficiency extends the timing of angiogenesis in the brain. (A) Detection of filopodia in brains from ABCA1 +/+ and ABCA1 −/− fetuses at E14.5 and E18.5. A vessel with several filopodia is shown at higher magnification in the inset. Bars: 100 μm in E14.5; 200 μm in E18.5. (B) Quantitative analyses of filopodia. N: E14.5 N = 6 ABCA1 +/+ and 4 ABCA1 −/− ; E18.5 N = 6 per group. Exact p-values are shown; t-test with Welch correction (E14.5) or generalized linear model with Wald´s test (E18.5).

Journal: Frontiers in Cell and Developmental Biology

Article Title: Altered brain vascularization and transcriptional changes in embryos lacking ABCA1 support a role of cholesterol in brain angiogenesis

doi: 10.3389/fcell.2026.1783696

Figure Lengend Snippet: ABCA1 deficiency extends the timing of angiogenesis in the brain. (A) Detection of filopodia in brains from ABCA1 +/+ and ABCA1 −/− fetuses at E14.5 and E18.5. A vessel with several filopodia is shown at higher magnification in the inset. Bars: 100 μm in E14.5; 200 μm in E18.5. (B) Quantitative analyses of filopodia. N: E14.5 N = 6 ABCA1 +/+ and 4 ABCA1 −/− ; E18.5 N = 6 per group. Exact p-values are shown; t-test with Welch correction (E14.5) or generalized linear model with Wald´s test (E18.5).

Techniques:

Evaluation of the blood-brain barrier in animals lacking ABCA1. (A) Expression levels of differentially expressed genes in vascular fragments from ABCA1 +/+ and ABCA1 −/− fetal brains. (B) Representative images of E18.5 fetal brains stained for CLDN5 and PECAM1. Bar: 100 μm. (C) Quantification of fluorescence intensity for CLDN5 in E18.5 fetal brains. Groups were compared with t-test with Welch correction. N = 6 per group. (D) Representative stainings of adult brains to reveal AQP4, PECAM1, and intracardially infused sulfo-NHS-biotin. Bar: 100 μm. (E) Quantification of AQP4 positive vessels in ABCA1 +/+ and ABCA1 −/− fetal brains. Groups were compared with t-test with Welch correction. N = 6 per group.

Journal: Frontiers in Cell and Developmental Biology

Article Title: Altered brain vascularization and transcriptional changes in embryos lacking ABCA1 support a role of cholesterol in brain angiogenesis

doi: 10.3389/fcell.2026.1783696

Figure Lengend Snippet: Evaluation of the blood-brain barrier in animals lacking ABCA1. (A) Expression levels of differentially expressed genes in vascular fragments from ABCA1 +/+ and ABCA1 −/− fetal brains. (B) Representative images of E18.5 fetal brains stained for CLDN5 and PECAM1. Bar: 100 μm. (C) Quantification of fluorescence intensity for CLDN5 in E18.5 fetal brains. Groups were compared with t-test with Welch correction. N = 6 per group. (D) Representative stainings of adult brains to reveal AQP4, PECAM1, and intracardially infused sulfo-NHS-biotin. Bar: 100 μm. (E) Quantification of AQP4 positive vessels in ABCA1 +/+ and ABCA1 −/− fetal brains. Groups were compared with t-test with Welch correction. N = 6 per group.

Techniques: Expressing, Staining, Fluorescence

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