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

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

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.

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: Staining

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.

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: Isolation

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).

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:

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.

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, Staining, Fluorescence