oxldl  (Athens Research)

Journal: Aging Cell

Article Title: Telomerase Knockout in Myeloid Cells Predisposes Mice to Foam Cell Formation, Dyslipidemia, Lung Fibrosis, and Cardiac Dysfunction

doi: 10.1111/acel.70490

Figure Lengend Snippet: Tert KO induces lipid‐associated macrophages (LAMs). Starch‐induced i.p. macrophages from 2‐year‐old female mice were analyzed. (a) Upon adherence in primary culture, IF with antibodies against CD80 (M1‐macrophage) and CD206 (M2‐polarization) markers reveals a lower frequency of CD206 + macrophages in KO mice. (b) Data quantification from multiple fields of view in (a), indicating macrophage polarization shift toward the M1 phenotype. (c) Upon LPS (100 ng/mL, 4 h) treatment in primary culture, q‐RT‐PCR (normalized to 18S RNA) demonstrates higher expression of genes coding for inflammation markers IL1 and IL6 in KO macrophages. (d) Macrophages were induced to convert into foam cells by oxLDL (0.025 mg/mL) treatment for 24 h. Note increased uptake of red‐fluorescent C 12 ‐BODIPY (0.3 μM, 5 min) by mG+ KO cells (yellow arrows) compared to mG+ WT cells (green arrows) in primary culture. (e) q‐RT‐PCR (normalized to 18S RNA) demonstrates lower expression of genes coding for lipid efflux effectors APOE, LDLR, ABCA1, ABCG1, and higher expression of genes coding for lipid transporters CD36 and FABP5 in KO oxLDL‐treated macrophages. (f) OxLDL‐treated macrophages stained with Oil Red O: Note larger lipid droplets (arrows) in KO cells. For all data, mean+/− SEM (error bars). * p < 0.05, ** p < 0.01, *** p < 0.001 (two‐sided Student's t ‐test). Scale bar: 50 μm.

Article Snippet: Prior to Oil Red O staining (Sigma‐Aldrich, O0625) and BODIPY‐FL‐C 12 (Invitrogen, D3822) uptake analysis, oxLDL (Athensresearch, 12‐16‐120412‐OX) was added to the medium at 25 μg/mL for 24 h.

Techniques: Starch, Reverse Transcription Polymerase Chain Reaction, Expressing, Staining

Journal: iScience

Article Title: Adipose extracellular vesicles carrying miR-210-3p drive macrophage inflammation and nicotine-induced atherosclerosis

doi: 10.1016/j.isci.2026.115151

Figure Lengend Snippet: Inhibition of miR-210-3p in atherosclerotic plaques alleviates nicotine-induced atherosclerosis (A) Left: Representative en face images of aortic arch plaques from negative control (NC) and AAV9-anti-miR-210-3p-treated (miR-210-3p inhibition) mice. Right: schematic illustration of the experimental design. ApoE −/− mice were injected with either AAV9-NC inhibitors or AAV9–miR-210-3p inhibitors, followed by HFD+Ni treatment for 12 weeks before analysis (scale bars, 1mm). (B and C) H&E-stained sections of aortic sinuses from nicotine-treated ApoE −/− mice and corresponding quantification of lesion area ( n = 8; scale bars, 200 μm). (D and E) Oil red O-stained sections of aortic sinuses and quantification of oil red O-positive area ( n = 4; scale bars, 200 μm). (F–M) Immunohistochemical staining and corresponding quantification of SOD2 (F and G), IL-6 (H and I), TNF-α (J and K), and IL-1β (L and M) in aortic sinus sections from nicotine-treated ApoE −/− mice ( n = 8; scale bars, 200 μm). (N and O) Immunohistochemical staining and quantification of KLF7 expression in the aortic sinus ( n = 8; scale bars, 200 μm). (P and Q) Representative immunofluorescence images (P) of aortic-root atherosclerotic lesions stained for KLF7 (red), CD68(green; macrophage marker), and DAPI (blue; nuclei), with corresponding quantification of KLF7 fluorescence intensity (Q; n = 8; scale bars, 100 μm). (R) Alterations in body weight of ApoE −/− mice over a 12-week period in NC and miR-210-3p inhibition groups. (S–V) Serum lipid profiles, including TC, TG, LDL-C, and HDL-C, in NC and miR-210-3p inhibition groups ( n = 9). Values are shown as mean ± SEM. Statistical significance was determined using unpaired, two-tailed Student’s t tests. Sample sizes (n) indicate biological replicates per group; each dot represents one biological replicate (individual mouse). ∗p < 0.05 , ∗∗p < 0.01 , ∗∗∗p < 0.001 , ∗∗∗∗p < 0.0001.

Article Snippet: LDL-C assay kit , Nanjing Jiancheng Bioengineering , Cat# A113-1-1.

Techniques: Inhibition, Negative Control, Injection, Staining, Immunohistochemical staining, Expressing, Immunofluorescence, Marker, Fluorescence, Two Tailed Test

Journal: Frontiers in Nutrition

Article Title: Redistribution of branched-chain amino acid intake between active and inactive phases modulates hepatic metabolism in rats

doi: 10.3389/fnut.2026.1754879

Figure Lengend Snippet: Experimental design, growth, intake partitioning, skeletal-muscle S6 signaling, and endpoint plasma markers under phase-shifted BCAA regimens. (A) Simplified study design: rats were maintained on a 12-h light:12-h dark cycle and assigned for 12 weeks to Ctrl (AIN-93G throughout), D + N − (BCAA+20 during the light/inactive phase and BCAA−20 during the dark/active phase), or D − N + (BCAA−20 during the light/inactive phase and BCAA+20 during the dark/active phase), where BCAA+20 and BCAA−20 denote diets containing ~20% higher or lower total BCAA content than Ctrl, respectively; daily energy and nitrogen were intended to be matched while allowing minor day-to-day variation during implementation ( n = 6/group). (B,C) Individual body weight trajectories from week 0 (acclimation) to weeks 1–12 (experimental period) (B) and weekly body weight distributions shown as boxplots (weeks 1–12) with pairwise between-group comparisons annotated above brackets (C) . (D,E) Representative immunoblots of total ribosomal protein S6 and phosphorylated S6 (p-S6, Ser235/236) in skeletal muscle at the end of the study, with total protein staining (TPS; Ponceau S) used for normalization ( n = 4/group; region approximately ~32 kDa displayed) (D) , and densitometric quantification of S6/TPS, p-S6/TPS, and phosphorylation ratio (p-S6/S6 computed as (p-S6/TPS)/(S6/TPS)) with individual animals overlaid (E) . (F) Weekly feed intake partitioned by circadian phase (inactive/light phase: 07:00–19:00; active/dark phase: 19:00–07:00); within each week, upper brackets/ p -values compare whole-day (24 h) total intake between the groups, and lower brackets/ p -values compare inactive vs. active intake within each group (red p-values indicate p < 0.05 as displayed). (G) Endpoint fasting plasma HDL-C, LDL-C, triglycerides (TG), total cholesterol (TC), and malondialdehyde (MDA) across the groups (units as indicated on axes). Group colors follow Ctrl (red), D − N + (green), and D + N − (blue). Boxplots show median and interquartile range (IQR), whiskers extend to 1.5 × IQR, and points indicate individual values (with outliers beyond whiskers where shown). Pairwise statistics were computed using two-sided t-tests with Holm p -value adjustment.

Article Snippet: Specifically, serum lipids were quantified by measuring total cholesterol (TC) using the Total Cholesterol (TC) Colorimetric Assay kits from Elabscience (Wuhan, China) (catalog no. E-BC-K109-M), high-density lipoprotein cholesterol (HDL-C) using the HDL-C Colorimetric Assay kits from Elabscience (Wuhan, China) (catalog no. E-BC-K221-M), low-density lipoprotein cholesterol (LDL-C) using the LDL-C Colorimetric Assay kits from Elabscience (Wuhan, China) (catalog no. E-BC-K205-M), malondialdehyde (MDA) using the Malondialdehyde (MDA) Colorimetric Assay kits from Elabscience (Wuhan, China) (catalog no. E-BC-K025-M), and triglycerides (TGs) using the Triglyceride (TG) Colorimetric Assay kits from Elabscience (Wuhan, China) (catalog no. E-BC-K261-M).

Techniques: Clinical Proteomics, Western Blot, Staining, Phospho-proteomics