rabbit anti-mouse abcg1 ab  (Novus Biologicals)

Journal: Cellular and molecular life sciences : CMLS

Article Title: Dysregulated cholesterol uptake and efflux of bone marrow-derived α-SMA + macrophages contribute to atherosclerotic plaque formation.

doi: 10.1007/s00018-025-05655-3

Figure Lengend Snippet: Fig. 4 α-SMA promotes the lipid uptake and inhibits lipid efflux in macrophages. A, B Flow cytometric analysis of binding and uptake of DiI-Ox-LDL in vector- or Acta2hi RAW264.7 cells A, and BMDMs from Acta2f/f or Acta2MKO mice B. The quantification results are shown on the right. n = 3. *P < 0.05, ***P < 0.001, ****P < 0.0001 by unpaired Student’s t-test. C, D SR-A, ABCA1, ABCG1 and α-SMA protein levels in vector- and Acta2hi RAW264.7 cells C, and BMDMs from Acta2Flox or Acta2MKO mice D. n = 3. *P < 0.05 by unpaired Student’s t-test. E–F Co-staining and quantification of SR-

Article Snippet: Primary antibodies used included mouse anti-mouse α-SMA (BM0002, Boster, USA), goat anti-mouse SR-A (af1797, R&D, USA), rabbit anti-mouse ABCA1 (PB0490, Boster, USA), human anti-mouse ABCG1 (bs-23382R, Bioss, China), rabbit anti-human CD36 (ab133625, Abcam, USA), mouse GAPDH (AF0006, Beyotime, China), rabbit anti-mouse p-Smad3 (AF1759, Beyotime, China), and rabbit anti-mammalian Smad3 (sc-101154, SANTA CRUZ, USA).

Techniques: Binding Assay, Plasmid Preparation, Staining

Journal: Cellular and molecular life sciences : CMLS

Article Title: Dysregulated cholesterol uptake and efflux of bone marrow-derived α-SMA + macrophages contribute to atherosclerotic plaque formation.

doi: 10.1007/s00018-025-05655-3

Figure Lengend Snippet: Fig. 5 AKT pathway is involved in α-SMA-induced lipid accumu- lation. A Abca1 mRNA levels in vector or Acta2hi RAW264.7 cells treated with 50 μg/ml Ox-LDL for 0, 6, 12, or 24 h. n = 3. *P < 0.05 by unpaired Student’s t-test. B Top 15 KEGG pathways of genes downregulated in Acta2hi RAW264.7 cells incubated with Ox-LDL for 6 h. C Protein levels of p-AKT, AKT, p-ERK, ERK, p-STAT3, STAT3, CD36, SR-A, ABCA1 and α-SMA treated with 50 μg/ml Ox- LDL for 6 h. n = 3. *P < 0.05 by one-way ANOVA. D–F Flow cyto-

Article Snippet: Primary antibodies used included mouse anti-mouse α-SMA (BM0002, Boster, USA), goat anti-mouse SR-A (af1797, R&D, USA), rabbit anti-mouse ABCA1 (PB0490, Boster, USA), human anti-mouse ABCG1 (bs-23382R, Bioss, China), rabbit anti-human CD36 (ab133625, Abcam, USA), mouse GAPDH (AF0006, Beyotime, China), rabbit anti-mouse p-Smad3 (AF1759, Beyotime, China), and rabbit anti-mammalian Smad3 (sc-101154, SANTA CRUZ, USA).

Techniques: Plasmid Preparation, Incubation

Journal: Cellular and molecular life sciences : CMLS

Article Title: Dysregulated cholesterol uptake and efflux of bone marrow-derived α-SMA + macrophages contribute to atherosclerotic plaque formation.

doi: 10.1007/s00018-025-05655-3

Figure Lengend Snippet: Fig. 6 Schematic diagram illustrating the role of bone marrow-derived α-SMA+ macrophages in atherosclerotic plaque formation. Macrophage- expressed α-SMA enhances SR-A expression via the AKT signaling pathway, leading to increased lipid binding and uptake. Concurrently, α-SMA suppresses ABCA1 expression, thereby reducing lipid efflux. This imbalance promotes lipid accumulation and contributes to atherosclerotic plaque formation

Article Snippet: Primary antibodies used included mouse anti-mouse α-SMA (BM0002, Boster, USA), goat anti-mouse SR-A (af1797, R&D, USA), rabbit anti-mouse ABCA1 (PB0490, Boster, USA), human anti-mouse ABCG1 (bs-23382R, Bioss, China), rabbit anti-human CD36 (ab133625, Abcam, USA), mouse GAPDH (AF0006, Beyotime, China), rabbit anti-mouse p-Smad3 (AF1759, Beyotime, China), and rabbit anti-mammalian Smad3 (sc-101154, SANTA CRUZ, USA).

Techniques: Derivative Assay, Expressing, Binding Assay

Journal: JCI Insight

Article Title: Dicarbonyl-modified lipoproteins contribute to proteinuric kidney injury

doi: 10.1172/jci.insight.161878

Figure Lengend Snippet: ( A ) Proximal tubular cells (megalin-positive, green) of NEP25 proteinuric kidneys absorbed apoAI (red, top panel). Uptake of apoAI (red) also occurred independently of megalin, illustrated in NEP25/megalin KO (middle panel) and NEP25/megalin mosaic KO mice (bottom panel). ( B ) IHC staining showed greater expression of lipoprotein transporters ABCA1 and SRBI, but not ABCG1, in NEP25 mice versus WT. Scale bar: 50 μm.

Article Snippet: Sections with primary Abs were incubated overnight at 4°C by adding rabbit anti-mouse ABCA1 Ab (1:200; Novus Biologicals), rabbit anti-mouse SRBI Ab (1:200; Novus Biologicals), and rabbit anti-mouse ABCG1 Ab (1:200; Novus Biologicals).

Techniques: Immunohistochemistry, Expressing

Journal: Communications Biology

Article Title: Macrophage Jak2 deficiency accelerates atherosclerosis through defects in cholesterol efflux

doi: 10.1038/s42003-022-03078-5

Figure Lengend Snippet: a – c mRNA level of ABCA1, ABCG1 , and SCARB1 in BMDM under basal conditions, after loading with oxLDL or after loading with oxLDL and treating with TO901317 with ApoA1 to induce efflux ( n = 10–19/group). d , e Cholesterol efflux from BMDM of M-Jak2 KO and WT mice treated with the LXR agonist, TO901317 in response to ApoB-depleted plasma ( n = 8/group) and to purified ApoA1 ( n = 8/group). f – i Representative en face images of Oil-red-O-stained lesser curvature of the aortic arch from M-Jak2 KO and WT mice treated with TO901317 or vehicle while on HCD for 3 weeks starting at 6 weeks of age. Scale bar, 1 mm ( j ) and their quantification ( n = 4–9/group). Statistical analysis: a – e two-way ANOVA with Tukey’s multiple comparisons and ( j ) multiple t tests with Holm–Sidak correction were performed. Data are presented as the mean ± SEM, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. See also Supplementary Fig. .

Article Snippet: Membranes were probed overnight at 4 °C with a primary antibody: total JAK2 (CST#3230; 1:1000), total ABCA1 (NB400-105; 1:500), total SRB1 (NB400-104; 1:1000), total ABCG1 (NB400-132; 1:500), and β-actin (CST#4967; 1:1000).

Techniques: Purification, Staining

Journal: PloS one

Article Title: Bone marrow deficiency of MCPIP1 results in severe multi-organ inflammation but diminishes atherogenesis in hyperlipidemic mice.

doi: 10.1371/journal.pone.0080089

Figure Lengend Snippet: Figure 9. MCPIP1 deficiency increased macrophage cholesterol efflux. A. Bone marrow-derived macrophages were loaded with ac-LDL and cholesterol efflux to DMEM, apoAI and HDL was measured. Data were presented as mean 6 SEM. N = 3 in each group. B. Bone marrow-derived macrophages were cultured in DMEM for 48 h with or without ac-LDL. Cell lysates were used for western blotting analysis for ABCA1 and ABCG1. Representative western blotting result was shown. C. Quantitative analysis of the western blots. Data were presented as mean 6 SEM. N = 4 in each group. Open column: WT macrophages; Black column, MCPIP12/2 macrophages. doi:10.1371/journal.pone.0080089.g009

Article Snippet: Rabbit antimouse ABCA1 and anti-mouse ABCG1 antibodies were from Novus Biologicals (Littleton, CO).

Techniques: Derivative Assay, Cell Culture, Western Blot