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antibodies against apoa4 (Proteintech)

Name: antibodies against apoa4
Brand: Proteintech
Rating: 94 (19 reviews)

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Proteintech antibodies against apoa4

(A) Volcano plot of differentially expressed genes from RNA sequencing, showing upregulation of PCSK9 and downregulation of <t>APOA4</t> in the LD+TMAO group compared to the LD group. (B) qRT-qPCR analysis of APOA4 mRNA expression levels across groups (n = 3 per group). (C) qRT-qPCR analysis of PCSK9 mRNA levels across groups (n = 3 per group). (D) Western blot analysis of APOA4 and PCSK9 protein levels across groups (n = 3 per group). (E–F). Quantification results of the Western blot analysis using ImageJ. (G, H). Serum APOA4 and PCSK9 levels in patients with cholelithiasis and the control group detected by ELISA. ** p < 0.01, *** p < 0.001. LD, lithogenic diet; TMAO, trimethylamine-N-oxide; NC, negative control; APOA4, <t>apolipoprotein</t> <t>A4;</t> PCSK9, proprotein convertase subtilisin/kexin type 9; GSD, gallstone disease; ELISA, enzyme-linked immunosorbent assay.

Antibodies Against Apoa4, supplied by Proteintech, used in various techniques. Bioz Stars score: 94/100, based on 19 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/antibodies against apoa4/product/Proteintech
Average 94 stars, based on 19 article reviews

antibodies against apoa4 - by Bioz Stars, 2026-01

94/100 stars

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1) Product Images from "PCSK9 and APOA4 : The Dynamic Duo in TMAO-induced Cholesterol Metabolism and Cholelithiasis"

Article Title: PCSK9 and APOA4 : The Dynamic Duo in TMAO-induced Cholesterol Metabolism and Cholelithiasis

Journal: Journal of Clinical and Translational Hepatology

doi: 10.14218/JCTH.2024.00403

(A) Volcano plot of differentially expressed genes from RNA sequencing, showing upregulation of PCSK9 and downregulation of APOA4 in the LD+TMAO group compared to the LD group. (B) qRT-qPCR analysis of APOA4 mRNA expression levels across groups (n = 3 per group). (C) qRT-qPCR analysis of PCSK9 mRNA levels across groups (n = 3 per group). (D) Western blot analysis of APOA4 and PCSK9 protein levels across groups (n = 3 per group). (E–F). Quantification results of the Western blot analysis using ImageJ. (G, H). Serum APOA4 and PCSK9 levels in patients with cholelithiasis and the control group detected by ELISA. ** p < 0.01, *** p < 0.001. LD, lithogenic diet; TMAO, trimethylamine-N-oxide; NC, negative control; APOA4, apolipoprotein A4; PCSK9, proprotein convertase subtilisin/kexin type 9; GSD, gallstone disease; ELISA, enzyme-linked immunosorbent assay.

Figure Legend Snippet: (A) Volcano plot of differentially expressed genes from RNA sequencing, showing upregulation of PCSK9 and downregulation of APOA4 in the LD+TMAO group compared to the LD group. (B) qRT-qPCR analysis of APOA4 mRNA expression levels across groups (n = 3 per group). (C) qRT-qPCR analysis of PCSK9 mRNA levels across groups (n = 3 per group). (D) Western blot analysis of APOA4 and PCSK9 protein levels across groups (n = 3 per group). (E–F). Quantification results of the Western blot analysis using ImageJ. (G, H). Serum APOA4 and PCSK9 levels in patients with cholelithiasis and the control group detected by ELISA. ** p < 0.01, *** p < 0.001. LD, lithogenic diet; TMAO, trimethylamine-N-oxide; NC, negative control; APOA4, apolipoprotein A4; PCSK9, proprotein convertase subtilisin/kexin type 9; GSD, gallstone disease; ELISA, enzyme-linked immunosorbent assay.

Techniques Used: RNA Sequencing, Expressing, Western Blot, Control, Enzyme-linked Immunosorbent Assay, Negative Control

(A) Lithogenesis in mice from the LD and LD+DMB groups. (B) Weights of solid contents in the gallbladders of mice from each group. (C) Serum TMAO levels in the LD and LD+DMB groups detected by ELISA. (D) Immunofluorescence staining of APOA4 and PCSK9 in hepatic tissues from the LD and LD+DMB groups. (E, F) qRT-qPCR analysis of APOA4 and PCSK9 mRNA expression levels in hepatic tissues from the LD and LD+DMB groups. * p < 0.05, ** p < 0.01, **** p < 0.0001. LD, lithogenic diet; DMB, 3,3-dimethyl-1-butanol; TMAO, trimethylamine-N-oxide; ELISA, enzyme-linked immunosorbent assay; APOA4, apolipoprotein A4; PCSK9 proprotein convertase subtilisin/kexin type 9.

Figure Legend Snippet: (A) Lithogenesis in mice from the LD and LD+DMB groups. (B) Weights of solid contents in the gallbladders of mice from each group. (C) Serum TMAO levels in the LD and LD+DMB groups detected by ELISA. (D) Immunofluorescence staining of APOA4 and PCSK9 in hepatic tissues from the LD and LD+DMB groups. (E, F) qRT-qPCR analysis of APOA4 and PCSK9 mRNA expression levels in hepatic tissues from the LD and LD+DMB groups. * p < 0.05, ** p < 0.01, **** p < 0.0001. LD, lithogenic diet; DMB, 3,3-dimethyl-1-butanol; TMAO, trimethylamine-N-oxide; ELISA, enzyme-linked immunosorbent assay; APOA4, apolipoprotein A4; PCSK9 proprotein convertase subtilisin/kexin type 9.

Techniques Used: Enzyme-linked Immunosorbent Assay, Immunofluorescence, Staining, Expressing

(A–E) APOA4 , PCSK9 , HMGCR, ABCG5 , and ABCG8 mRNA expression levels in TMAO-treated and control AML12 cells (n = 3 per group). (F) Immunofluorescence staining for APOA4, PCSK9, HMGCR, ABCG5, and ABCG8 in cells from each group. ** p < 0.01, *** p < 0.001. TMAO, trimethylamine-N-oxide; APOA4, apolipoprotein A4; PCSK9, proprotein convertase subtilisin/kexin type 9; ABCG5, ATP-binding cassette sub-family G member 5; ABCG8, ATP-binding cassette sub-family G member 8; HMGCR, 3-hydroxy-3-methylglutaryl-CoA reductase.

Figure Legend Snippet: (A–E) APOA4 , PCSK9 , HMGCR, ABCG5 , and ABCG8 mRNA expression levels in TMAO-treated and control AML12 cells (n = 3 per group). (F) Immunofluorescence staining for APOA4, PCSK9, HMGCR, ABCG5, and ABCG8 in cells from each group. ** p < 0.01, *** p < 0.001. TMAO, trimethylamine-N-oxide; APOA4, apolipoprotein A4; PCSK9, proprotein convertase subtilisin/kexin type 9; ABCG5, ATP-binding cassette sub-family G member 5; ABCG8, ATP-binding cassette sub-family G member 8; HMGCR, 3-hydroxy-3-methylglutaryl-CoA reductase.

Techniques Used: Expressing, Control, Immunofluorescence, Staining, Binding Assay

(A) WB analysis of PCSK9, HMGCR, ABCG5, and ABCG8 in NC, TMAO-treated, and APOA4-overexpressed cells. (B–E) Changes in PCSK9 , HMGCR , ABCG5 , and ABCG8 mRNA levels after APOA4 overexpression (n = 3 per group). (F) Immunofluorescence staining for intracellular PCSK9, HMGCR, ABCG5, and ABCG8 after APOA4 overexpression. (G) WB analysis of APOA4, HMGCR, ABCG5, and ABCG8 in NC, TMAO-treated, and PCSK9-knockdown cells. (H–K) Changes in mRNA levels of PCSK9 , HMGCR , ABCG5 , and ABCG8 after PCSK9 knockdown (n = 3 per group). (L) Immunofluorescence staining for PCSK9, HMGCR, ABCG5, and ABCG8 in cells after PCSK9 knockdown. * p < 0.05, ** p < 0.01. +, positive expression; -, negative expression; TMAO, trimethylamine-N-oxide; APOA4, apolipoprotein A4; PCSK9, proprotein convertase subtilisin/kexin type 9; ABCG5, ATP-binding cassette sub-family G member 5; ABCG8, ATP-binding cassette sub-family G member 8; HMGCR, 3-hydroxy-3-methylglutaryl-CoA reductase; GAPDH, glyceraldehyde-3-phosphate dehydrogenase.

Figure Legend Snippet: (A) WB analysis of PCSK9, HMGCR, ABCG5, and ABCG8 in NC, TMAO-treated, and APOA4-overexpressed cells. (B–E) Changes in PCSK9 , HMGCR , ABCG5 , and ABCG8 mRNA levels after APOA4 overexpression (n = 3 per group). (F) Immunofluorescence staining for intracellular PCSK9, HMGCR, ABCG5, and ABCG8 after APOA4 overexpression. (G) WB analysis of APOA4, HMGCR, ABCG5, and ABCG8 in NC, TMAO-treated, and PCSK9-knockdown cells. (H–K) Changes in mRNA levels of PCSK9 , HMGCR , ABCG5 , and ABCG8 after PCSK9 knockdown (n = 3 per group). (L) Immunofluorescence staining for PCSK9, HMGCR, ABCG5, and ABCG8 in cells after PCSK9 knockdown. * p < 0.05, ** p < 0.01. +, positive expression; -, negative expression; TMAO, trimethylamine-N-oxide; APOA4, apolipoprotein A4; PCSK9, proprotein convertase subtilisin/kexin type 9; ABCG5, ATP-binding cassette sub-family G member 5; ABCG8, ATP-binding cassette sub-family G member 8; HMGCR, 3-hydroxy-3-methylglutaryl-CoA reductase; GAPDH, glyceraldehyde-3-phosphate dehydrogenase.

Techniques Used: Over Expression, Immunofluorescence, Staining, Knockdown, Expressing, Binding Assay

Gut microbiota produce trimethylamine, which enters the liver via the portal circulation and is primarily oxidized by FMO3 to produce TMAO. TMAO upregulates hepatic PCSK9 gene expression while downregulating APOA4 expression. PCSK9 overexpression inhibits APOA4 expression, while low APOA4 expression further promotes PCSK9 expression, forming a feedback loop that dysregulates cholesterol metabolism. This upregulates cholesterol synthesis by HMGCR and cholesterol efflux by ABCG5/8. Consequently, biliary concentrations of cholesterol and bile acids increase and decrease, respectively, thereby promoting cholesterol gallstone formation. TMAO, trimethylamine-N-oxide; APOA4, apolipoprotein A4; PCSK9, proprotein convertase subtilisin/kexin type 9; ABCG5, ATP-binding cassette sub-family G member 5; ABCG8, ATP-binding cassette sub-family G member 8; FMO3, flavin containing monooxygenase 3; TMA, Trimethylamine.

Figure Legend Snippet: Gut microbiota produce trimethylamine, which enters the liver via the portal circulation and is primarily oxidized by FMO3 to produce TMAO. TMAO upregulates hepatic PCSK9 gene expression while downregulating APOA4 expression. PCSK9 overexpression inhibits APOA4 expression, while low APOA4 expression further promotes PCSK9 expression, forming a feedback loop that dysregulates cholesterol metabolism. This upregulates cholesterol synthesis by HMGCR and cholesterol efflux by ABCG5/8. Consequently, biliary concentrations of cholesterol and bile acids increase and decrease, respectively, thereby promoting cholesterol gallstone formation. TMAO, trimethylamine-N-oxide; APOA4, apolipoprotein A4; PCSK9, proprotein convertase subtilisin/kexin type 9; ABCG5, ATP-binding cassette sub-family G member 5; ABCG8, ATP-binding cassette sub-family G member 8; FMO3, flavin containing monooxygenase 3; TMA, Trimethylamine.

Techniques Used: Gene Expression, Expressing, Over Expression, Binding Assay

Image Search Results

CD300LG directly binds TRLs and ApoA4. A-B) Representative images (A) and quantification (B) from high-content fluorescence microscopy of Dil-labeled chylomicrons (Dil-CMs) binding to TIME cells transfected with human CD300LG or empty vector. C) Quantification of Dil-labeled VLDL, LDL, and HDL (human) binding to human CD300LG or empty vector- transfected TIME cells by high-content imaging. D) Dose-dependent competition of DiI-CM binding to CD300LG by recombinant human CD300LG-Fc quantified by high-content imaging. E) Dil-CMs directly bind recombinant human CD300LG-Fc, but not control-Fc, immobilized on ELISA plates. Total fluorescence intensity was measured across entire wells. F) Binding of Dil-CMs following a pre-incubation of TIME cells overexpressing CD300LG with the indicated concentrations of unlabeled VLDL, LDL, or HDL. Binding was quantified by high-content imaging and normalized to cells incubated with Dil-CMs alone. G) Binding of hCD300LG-Fc or control Fc to purified apolipoproteins immobilized to ELISA plates. Error bars denote S.D. *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001 by two-way ANOVA. All data are representative of a minimum of two independent experiments.

Journal: bioRxiv

Article Title: CD300LG is a receptor for triglyceride-rich lipoproteins that facilitates postprandial lipid clearance

doi: 10.1101/2025.08.08.669356

Figure Lengend Snippet: CD300LG directly binds TRLs and ApoA4. A-B) Representative images (A) and quantification (B) from high-content fluorescence microscopy of Dil-labeled chylomicrons (Dil-CMs) binding to TIME cells transfected with human CD300LG or empty vector. C) Quantification of Dil-labeled VLDL, LDL, and HDL (human) binding to human CD300LG or empty vector- transfected TIME cells by high-content imaging. D) Dose-dependent competition of DiI-CM binding to CD300LG by recombinant human CD300LG-Fc quantified by high-content imaging. E) Dil-CMs directly bind recombinant human CD300LG-Fc, but not control-Fc, immobilized on ELISA plates. Total fluorescence intensity was measured across entire wells. F) Binding of Dil-CMs following a pre-incubation of TIME cells overexpressing CD300LG with the indicated concentrations of unlabeled VLDL, LDL, or HDL. Binding was quantified by high-content imaging and normalized to cells incubated with Dil-CMs alone. G) Binding of hCD300LG-Fc or control Fc to purified apolipoproteins immobilized to ELISA plates. Error bars denote S.D. *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001 by two-way ANOVA. All data are representative of a minimum of two independent experiments.

Article Snippet: A total of 25 pmol of each of the recombinant human apolipoproteins ApoC2 (LSBio, LS-G20488), ApoC3 (LSBio, LS-G20489), ApoA4 (Sino Biological, 16082-H08H), and ApoA5 (Prospec-Tany, Cyt-025) were attached to a 96-well polystyrene plate similar to as described for CD300LG-Fc.

Techniques: Fluorescence, Microscopy, Labeling, Binding Assay, Transfection, Plasmid Preparation, Imaging, Recombinant, Control, Enzyme-linked Immunosorbent Assay, Incubation, Purification

The c-terminus of ApoA4 contributes to CD300LG binding to TRLs. A) Sequence alignment of the conserved EQXQ motif in the C-terminal region of ApoA4 across species. B) Helical wheel diagram of the c-terminus of ApoA4 showing the one- sided charge distribution of glutamate residues created by the repeating EQXQ motif. C) Helical wheel diagram showing the redistribution of the charged glutamate residues within the “scrambled” control peptides. D-E) Direct binding of peptides corresponding to the human (D) or mouse (E) ApoA4 C-terminus (hA4-Cterm, mA4-Cterm) or scrambled controls (hA4-Scr, mA4- Scr) to recombinant human CD300LG-Fc. F) hA4-Cterm peptide inhibits the binding between human CD300LG-Fc and Dil-CMs. CD300LG-Fc coated plates were pre-incubated with peptides for 2 hours prior to the addition of CMs. G) hA4-Cterm peptide dose-dependently inhibits the binding of Dil-CM to CD300LG expressing TIME cells. TIME cells were pre-incubated with peptides for 30 minutes on ice prior to the addition of Dil-CMs. H) Oral fat tolerance test (OFTT) for WT mice treated with saline or 40 µg of mA4-Cterm or mA4-Scr 15 minutes before an oral gavage of olive oil (N = 9-11). AUC is quantified on the right. *p<0.05, **p<0.01, ****p<0.0001 by one-way or two-way ANOVA as appropriate. All data are representative of a minimum of two independent experiments. Data points in panels D and E represent the average of 2 independent experiments.

Journal: bioRxiv

Article Title: CD300LG is a receptor for triglyceride-rich lipoproteins that facilitates postprandial lipid clearance

doi: 10.1101/2025.08.08.669356

Figure Lengend Snippet: The c-terminus of ApoA4 contributes to CD300LG binding to TRLs. A) Sequence alignment of the conserved EQXQ motif in the C-terminal region of ApoA4 across species. B) Helical wheel diagram of the c-terminus of ApoA4 showing the one- sided charge distribution of glutamate residues created by the repeating EQXQ motif. C) Helical wheel diagram showing the redistribution of the charged glutamate residues within the “scrambled” control peptides. D-E) Direct binding of peptides corresponding to the human (D) or mouse (E) ApoA4 C-terminus (hA4-Cterm, mA4-Cterm) or scrambled controls (hA4-Scr, mA4- Scr) to recombinant human CD300LG-Fc. F) hA4-Cterm peptide inhibits the binding between human CD300LG-Fc and Dil-CMs. CD300LG-Fc coated plates were pre-incubated with peptides for 2 hours prior to the addition of CMs. G) hA4-Cterm peptide dose-dependently inhibits the binding of Dil-CM to CD300LG expressing TIME cells. TIME cells were pre-incubated with peptides for 30 minutes on ice prior to the addition of Dil-CMs. H) Oral fat tolerance test (OFTT) for WT mice treated with saline or 40 µg of mA4-Cterm or mA4-Scr 15 minutes before an oral gavage of olive oil (N = 9-11). AUC is quantified on the right. *p<0.05, **p<0.01, ****p<0.0001 by one-way or two-way ANOVA as appropriate. All data are representative of a minimum of two independent experiments. Data points in panels D and E represent the average of 2 independent experiments.

Techniques: Binding Assay, Sequencing, Control, Recombinant, Incubation, Expressing, Saline

Fig. 1 BMP4 increased enterocyte marker expression and inhibited intestinal stemness in human duodenum and mouse SI organoids. A–D Human duodenum organoids were cultured in the presence of BMP4 (500 ng/ml) or control PBS for 4 d. Total RNA was extracted, and KRT20, APOA4, FABP1, and VILLIN mRNA expression was assessed by qPCR (A). Data are normalized to GAPDH; n = 3 biological repeats. Representative image of organoids from control PBS and BMP4 treatment groups is shown in B with quantiﬁcation of the organoid area shown in (C) (98 organoids per PBS group and 105 organoids per BMP4 group were measured). qPCR analysis of OLFM4 expression (D). E–H Mouse SI organoids were cultured in the presence of BMP4 (500 ng/ml) or control PBS for 4 d. qPCR analysis of selected enterocyte markers in mouse SI organoids differentiated in the absence or presence of BMP4 (E). Data are normalized to GAPDH; n = 3 biological repeats. Representative image of organoids from control PBS and BMP4 treatment is shown in (F). Quantiﬁcation of the organoid area is shown in (G) (21 organoids per PBS group and 25 organoids per BMP4 group were measured). OLFM4, Ki67, and CCND1 mRNA expression were assessed by qPCR (H). Data are normalized to GAPDH; n = 3 biological repeats. ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.005.

Journal: Cell death & disease

Article Title: miR-181a-5p mediates the effects of BMP4 on intestinal cell proliferation and differentiation.

doi: 10.1038/s41419-025-07730-w

Figure Lengend Snippet: Fig. 1 BMP4 increased enterocyte marker expression and inhibited intestinal stemness in human duodenum and mouse SI organoids. A–D Human duodenum organoids were cultured in the presence of BMP4 (500 ng/ml) or control PBS for 4 d. Total RNA was extracted, and KRT20, APOA4, FABP1, and VILLIN mRNA expression was assessed by qPCR (A). Data are normalized to GAPDH; n = 3 biological repeats. Representative image of organoids from control PBS and BMP4 treatment groups is shown in B with quantiﬁcation of the organoid area shown in (C) (98 organoids per PBS group and 105 organoids per BMP4 group were measured). qPCR analysis of OLFM4 expression (D). E–H Mouse SI organoids were cultured in the presence of BMP4 (500 ng/ml) or control PBS for 4 d. qPCR analysis of selected enterocyte markers in mouse SI organoids differentiated in the absence or presence of BMP4 (E). Data are normalized to GAPDH; n = 3 biological repeats. Representative image of organoids from control PBS and BMP4 treatment is shown in (F). Quantiﬁcation of the organoid area is shown in (G) (21 organoids per PBS group and 25 organoids per BMP4 group were measured). OLFM4, Ki67, and CCND1 mRNA expression were assessed by qPCR (H). Data are normalized to GAPDH; n = 3 biological repeats. ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.005.

Article Snippet: Antibodies to Cyclin D1 (ab134175) and KRT20 (ab854) from Abcam (Cambridge, UK), OLFM4 (#39141), APOA4 (#5700), FABP1 (#13368), HK1 (#2024), Na-K ATPase (#3010) (all from Cell Signaling, Danvers, MA) and HK2 (GeneTex, Irvine, CA; GTX124375), VILLIN (sc-7672, Santa Cruz Biotechnology, Dallas, TX), and β-actin (A1978, Sigma) were used, and following blotting with a horseradish peroxidase-conjugated secondary antibody, protein expression was visualized using an enhanced chemiluminescence (ECL) detection system.

Techniques: Marker, Expressing, Cell Culture, Control

Fig. 3 Inhibition of miR-181a-5p increased enterocyte marker expression in mouse SI organoids. Mouse SI organoids were cultured in the presence of LNA miR-181a-5p inhibitor or control oligos (0.75 μM) for 5 d. A qPCR analysis of selected enterocyte markers; n = 3 biological repeats. B Mouse organoid lysates were extracted, and IAP activity determined; n = 3 biological repeats. C Treatment with LNA miR-181a-5p inhibitor increased enterocyte marker protein expression. The images are representative of three independent experiments. VILLIN, APOA4, and FABP1 signals from three separate experiments were quantitated by densitometer and expressed as fold change with respect to β-actin. D LNA miR-181a-5p inhibitor decreased endogenous miR-181a-5p expression; n = 3 biological repeats. E–G Microscopy analysis of enterocytes in mouse SI organoids. The relative ﬂuorescence intensities of KRT20 (control oligos n = 14 organoids; miR-181a-5p inhibitor n = 11 organoids), Na,K-ATPase (control oligos n = 14 organoids; miR-181a-5p inhibitor n = 12 organoids), and VILLIN (control oligos n = 10 organoids; miR-181a-5p inhibitor n = 10 organoids) staining were quantiﬁed using ImageJ. H–J C57BL/6 mice were injected IP with control oligos (n = 5 mice) or miR-181a-5p inhibitor (n = 5 mice). Seven d after injection, mouse SI were harvested and analyzed. Western blot analysis (H). Image signals from ﬁve mice were quantitated by densitometer and expressed as fold change with respect to β-actin. Representative Fast Red staining of the small intestine revealed an increase in IAP activity (J). ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.005.

Journal: Cell death & disease

Article Title: miR-181a-5p mediates the effects of BMP4 on intestinal cell proliferation and differentiation.

doi: 10.1038/s41419-025-07730-w

Figure Lengend Snippet: Fig. 3 Inhibition of miR-181a-5p increased enterocyte marker expression in mouse SI organoids. Mouse SI organoids were cultured in the presence of LNA miR-181a-5p inhibitor or control oligos (0.75 μM) for 5 d. A qPCR analysis of selected enterocyte markers; n = 3 biological repeats. B Mouse organoid lysates were extracted, and IAP activity determined; n = 3 biological repeats. C Treatment with LNA miR-181a-5p inhibitor increased enterocyte marker protein expression. The images are representative of three independent experiments. VILLIN, APOA4, and FABP1 signals from three separate experiments were quantitated by densitometer and expressed as fold change with respect to β-actin. D LNA miR-181a-5p inhibitor decreased endogenous miR-181a-5p expression; n = 3 biological repeats. E–G Microscopy analysis of enterocytes in mouse SI organoids. The relative ﬂuorescence intensities of KRT20 (control oligos n = 14 organoids; miR-181a-5p inhibitor n = 11 organoids), Na,K-ATPase (control oligos n = 14 organoids; miR-181a-5p inhibitor n = 12 organoids), and VILLIN (control oligos n = 10 organoids; miR-181a-5p inhibitor n = 10 organoids) staining were quantiﬁed using ImageJ. H–J C57BL/6 mice were injected IP with control oligos (n = 5 mice) or miR-181a-5p inhibitor (n = 5 mice). Seven d after injection, mouse SI were harvested and analyzed. Western blot analysis (H). Image signals from ﬁve mice were quantitated by densitometer and expressed as fold change with respect to β-actin. Representative Fast Red staining of the small intestine revealed an increase in IAP activity (J). ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.005.

Techniques: Inhibition, Marker, Expressing, Cell Culture, Control, Activity Assay, Microscopy, Staining, Injection, Western Blot

Fig. 5 Inhibition of miR-181a-5p increased enterocyte marker expression in human duodenum organoids. Human duodenum organoids were cultured in the presence of LNA miR-181a-5p inhibitor or control oligos (1 μM) for 7 d. A qPCR analysis of enterocyte markers IAP, APOA4, FABP1, VILLIN, and Na,K-ATPase expression; n = 3 biological repeats. B Treatment with LNA miR-181a-5p inhibitor decreased endogenous miR- 181a-5p expression; n = 3 biological repeats. C–E IF staining of organoids for KRT20 (C), Na,K-ATPase (D), and VILLIN (E). The relative ﬂuorescence intensity of KRT20 (control oligos n = 10 organoids; miR-181a-5p inhibitor n = 10 organoids), Na,K-ATPase (control oligos n = 14 organoids; miR-181a-5p inhibitor n = 11 organoids), and VILLIN (control oligos n = 17 organoids; miR-181a-5p inhibitor n = 9 organoids) staining was quantiﬁed using ImageJ ﬂuorescence analyzer. ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.005.

Journal: Cell death & disease

Article Title: miR-181a-5p mediates the effects of BMP4 on intestinal cell proliferation and differentiation.

doi: 10.1038/s41419-025-07730-w

Figure Lengend Snippet: Fig. 5 Inhibition of miR-181a-5p increased enterocyte marker expression in human duodenum organoids. Human duodenum organoids were cultured in the presence of LNA miR-181a-5p inhibitor or control oligos (1 μM) for 7 d. A qPCR analysis of enterocyte markers IAP, APOA4, FABP1, VILLIN, and Na,K-ATPase expression; n = 3 biological repeats. B Treatment with LNA miR-181a-5p inhibitor decreased endogenous miR- 181a-5p expression; n = 3 biological repeats. C–E IF staining of organoids for KRT20 (C), Na,K-ATPase (D), and VILLIN (E). The relative ﬂuorescence intensity of KRT20 (control oligos n = 10 organoids; miR-181a-5p inhibitor n = 10 organoids), Na,K-ATPase (control oligos n = 14 organoids; miR-181a-5p inhibitor n = 11 organoids), and VILLIN (control oligos n = 17 organoids; miR-181a-5p inhibitor n = 9 organoids) staining was quantiﬁed using ImageJ ﬂuorescence analyzer. ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.005.

Techniques: Inhibition, Marker, Expressing, Cell Culture, Control, Staining

Journal: Journal of Clinical and Translational Hepatology

Article Title: PCSK9 and APOA4 : The Dynamic Duo in TMAO-induced Cholesterol Metabolism and Cholelithiasis

doi: 10.14218/JCTH.2024.00403

Figure Lengend Snippet: (A) Volcano plot of differentially expressed genes from RNA sequencing, showing upregulation of PCSK9 and downregulation of APOA4 in the LD+TMAO group compared to the LD group. (B) qRT-qPCR analysis of APOA4 mRNA expression levels across groups (n = 3 per group). (C) qRT-qPCR analysis of PCSK9 mRNA levels across groups (n = 3 per group). (D) Western blot analysis of APOA4 and PCSK9 protein levels across groups (n = 3 per group). (E–F). Quantification results of the Western blot analysis using ImageJ. (G, H). Serum APOA4 and PCSK9 levels in patients with cholelithiasis and the control group detected by ELISA. ** p < 0.01, *** p < 0.001. LD, lithogenic diet; TMAO, trimethylamine-N-oxide; NC, negative control; APOA4, apolipoprotein A4; PCSK9, proprotein convertase subtilisin/kexin type 9; GSD, gallstone disease; ELISA, enzyme-linked immunosorbent assay.

Article Snippet: Paraffin-embedded tissue sections were incubated overnight at 4°C with antibodies against APOA4 (Proteintech, China), 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) (CUSABIO, China), ATP-binding cassette sub-family G member 5 (ABCG5) (Abmart, China), PCSK9, and ATP-binding cassette sub-family G member 8 (ABCG8) (Abclonal, China).

Techniques: RNA Sequencing, Expressing, Western Blot, Control, Enzyme-linked Immunosorbent Assay, Negative Control

Journal: Journal of Clinical and Translational Hepatology

Article Title: PCSK9 and APOA4 : The Dynamic Duo in TMAO-induced Cholesterol Metabolism and Cholelithiasis

doi: 10.14218/JCTH.2024.00403

Figure Lengend Snippet: (A) Lithogenesis in mice from the LD and LD+DMB groups. (B) Weights of solid contents in the gallbladders of mice from each group. (C) Serum TMAO levels in the LD and LD+DMB groups detected by ELISA. (D) Immunofluorescence staining of APOA4 and PCSK9 in hepatic tissues from the LD and LD+DMB groups. (E, F) qRT-qPCR analysis of APOA4 and PCSK9 mRNA expression levels in hepatic tissues from the LD and LD+DMB groups. * p < 0.05, ** p < 0.01, **** p < 0.0001. LD, lithogenic diet; DMB, 3,3-dimethyl-1-butanol; TMAO, trimethylamine-N-oxide; ELISA, enzyme-linked immunosorbent assay; APOA4, apolipoprotein A4; PCSK9 proprotein convertase subtilisin/kexin type 9.

Techniques: Enzyme-linked Immunosorbent Assay, Immunofluorescence, Staining, Expressing

Journal: Journal of Clinical and Translational Hepatology

Article Title: PCSK9 and APOA4 : The Dynamic Duo in TMAO-induced Cholesterol Metabolism and Cholelithiasis

doi: 10.14218/JCTH.2024.00403

Figure Lengend Snippet: (A–E) APOA4 , PCSK9 , HMGCR, ABCG5 , and ABCG8 mRNA expression levels in TMAO-treated and control AML12 cells (n = 3 per group). (F) Immunofluorescence staining for APOA4, PCSK9, HMGCR, ABCG5, and ABCG8 in cells from each group. ** p < 0.01, *** p < 0.001. TMAO, trimethylamine-N-oxide; APOA4, apolipoprotein A4; PCSK9, proprotein convertase subtilisin/kexin type 9; ABCG5, ATP-binding cassette sub-family G member 5; ABCG8, ATP-binding cassette sub-family G member 8; HMGCR, 3-hydroxy-3-methylglutaryl-CoA reductase.

Techniques: Expressing, Control, Immunofluorescence, Staining, Binding Assay

Journal: Journal of Clinical and Translational Hepatology

Article Title: PCSK9 and APOA4 : The Dynamic Duo in TMAO-induced Cholesterol Metabolism and Cholelithiasis

doi: 10.14218/JCTH.2024.00403

Figure Lengend Snippet: (A) WB analysis of PCSK9, HMGCR, ABCG5, and ABCG8 in NC, TMAO-treated, and APOA4-overexpressed cells. (B–E) Changes in PCSK9 , HMGCR , ABCG5 , and ABCG8 mRNA levels after APOA4 overexpression (n = 3 per group). (F) Immunofluorescence staining for intracellular PCSK9, HMGCR, ABCG5, and ABCG8 after APOA4 overexpression. (G) WB analysis of APOA4, HMGCR, ABCG5, and ABCG8 in NC, TMAO-treated, and PCSK9-knockdown cells. (H–K) Changes in mRNA levels of PCSK9 , HMGCR , ABCG5 , and ABCG8 after PCSK9 knockdown (n = 3 per group). (L) Immunofluorescence staining for PCSK9, HMGCR, ABCG5, and ABCG8 in cells after PCSK9 knockdown. * p < 0.05, ** p < 0.01. +, positive expression; -, negative expression; TMAO, trimethylamine-N-oxide; APOA4, apolipoprotein A4; PCSK9, proprotein convertase subtilisin/kexin type 9; ABCG5, ATP-binding cassette sub-family G member 5; ABCG8, ATP-binding cassette sub-family G member 8; HMGCR, 3-hydroxy-3-methylglutaryl-CoA reductase; GAPDH, glyceraldehyde-3-phosphate dehydrogenase.

Techniques: Over Expression, Immunofluorescence, Staining, Knockdown, Expressing, Binding Assay

Journal: Journal of Clinical and Translational Hepatology

Article Title: PCSK9 and APOA4 : The Dynamic Duo in TMAO-induced Cholesterol Metabolism and Cholelithiasis

doi: 10.14218/JCTH.2024.00403

Figure Lengend Snippet: Gut microbiota produce trimethylamine, which enters the liver via the portal circulation and is primarily oxidized by FMO3 to produce TMAO. TMAO upregulates hepatic PCSK9 gene expression while downregulating APOA4 expression. PCSK9 overexpression inhibits APOA4 expression, while low APOA4 expression further promotes PCSK9 expression, forming a feedback loop that dysregulates cholesterol metabolism. This upregulates cholesterol synthesis by HMGCR and cholesterol efflux by ABCG5/8. Consequently, biliary concentrations of cholesterol and bile acids increase and decrease, respectively, thereby promoting cholesterol gallstone formation. TMAO, trimethylamine-N-oxide; APOA4, apolipoprotein A4; PCSK9, proprotein convertase subtilisin/kexin type 9; ABCG5, ATP-binding cassette sub-family G member 5; ABCG8, ATP-binding cassette sub-family G member 8; FMO3, flavin containing monooxygenase 3; TMA, Trimethylamine.

Techniques: Gene Expression, Expressing, Over Expression, Binding Assay

Journal: Biomolecules and Biomedicine

Article Title: Therapeutic potential of simvastatin in ALS: Enhanced axonal integrity and motor neuron survival through Apoa4 and Alb modulation

doi: 10.17305/bb.2024.11218

Figure Lengend Snippet: PCR primers and conditions

Article Snippet: Primary antibodies: C4a (1:3000, 22233-1-AP, Proteintech, Wuhan, China); C5 (1:600, A8104, Abclonal, Wuhan, China); C3 (1:10,000, 21337-1-AP, Proteintech); PI3K (1:1000, ab302958, Abcam, UK); p-PI3K p85 alpha (Tyr607) (1:1000, AF3241, Affinity, Jiangsu, China); Alb (1:10,000, 16475-1-AP, Proteintech); p-AKT (Ser473) (1:10,000, 66444-1-Ig, Proteintech); AKT (1:5000, 60203-2-Ig, Proteintech); PPARγ (1:5000, 16643-1-AP, Proteintech); APOA4 (1:8000, 17996-1-AP, Proteintech); C1qB (1:1000, A5339, Abclonal, Wuhan, China); CRP (1:2000, 66250-1-Ig, Proteintech); and GAPDH (1:10,000, 60004-1-Ig, Proteintech).

Techniques:

Alb and Apoa4 expression levels in spinal cord tissues detected by qRT-PCR. (A) Venn diagram showing the intersection of two genes obtained from the WT vs SOD1 G93A + PBS group and SOD1 G93A + PBS vs SOD1 G93A + simvastatin group; (B and C) The expression levels of Apoa4 (B) and Alb (C) decreased in the SOD1 G93A + PBS group compared with the WT group but increased in the SOD1 G93A + simvastatin group compared with the SOD1 G93A + PBS group. * P < 0.05, ** P < 0.01, vs WT group; ## P < 0.01, vs SOD1 G93A + PBS group. SOD1: Superoxide dismutase 1; WT: Wilt-type; qRT-PCR: Quantitative real-time polymerase chain reaction.

Journal: Biomolecules and Biomedicine

Article Title: Therapeutic potential of simvastatin in ALS: Enhanced axonal integrity and motor neuron survival through Apoa4 and Alb modulation

doi: 10.17305/bb.2024.11218

Figure Lengend Snippet: Alb and Apoa4 expression levels in spinal cord tissues detected by qRT-PCR. (A) Venn diagram showing the intersection of two genes obtained from the WT vs SOD1 G93A + PBS group and SOD1 G93A + PBS vs SOD1 G93A + simvastatin group; (B and C) The expression levels of Apoa4 (B) and Alb (C) decreased in the SOD1 G93A + PBS group compared with the WT group but increased in the SOD1 G93A + simvastatin group compared with the SOD1 G93A + PBS group. * P < 0.05, ** P < 0.01, vs WT group; ## P < 0.01, vs SOD1 G93A + PBS group. SOD1: Superoxide dismutase 1; WT: Wilt-type; qRT-PCR: Quantitative real-time polymerase chain reaction.

Techniques: Expressing, Quantitative RT-PCR, Real-time Polymerase Chain Reaction

PPI network and enrichment analysis. (A) PPI network constructed for Alb; (B) GO analysis revealed that Alb participated in lipid localization, vesicle lumen, and peptidase regulator activity; (C) KEGG pathway annotation revealed that Alb was mainly enriched in complement and coagulation cascades and cholesterol metabolism; (D) PPI network constructed for Apoa4; (E) GO analysis revealed that Apoa4 participated in the regulation of plasma lipoprotein particle levels, protein–lipid complexes, and protein–lipid complex binding; (F) KEGG pathway annotation revealed that Apoa4 was mainly enriched in cholesterol metabolism, PPAR signaling pathway, fat digestion and absorption, and complement and coagulation cascades. GO: Gene Ontology; KEGG: Kyoto Encyclopedia of Genes and Genomes; PPI: Protein–protein interaction; PPAR: Peroxisome proliferator-activated receptor.

Journal: Biomolecules and Biomedicine

Article Title: Therapeutic potential of simvastatin in ALS: Enhanced axonal integrity and motor neuron survival through Apoa4 and Alb modulation

doi: 10.17305/bb.2024.11218

Figure Lengend Snippet: PPI network and enrichment analysis. (A) PPI network constructed for Alb; (B) GO analysis revealed that Alb participated in lipid localization, vesicle lumen, and peptidase regulator activity; (C) KEGG pathway annotation revealed that Alb was mainly enriched in complement and coagulation cascades and cholesterol metabolism; (D) PPI network constructed for Apoa4; (E) GO analysis revealed that Apoa4 participated in the regulation of plasma lipoprotein particle levels, protein–lipid complexes, and protein–lipid complex binding; (F) KEGG pathway annotation revealed that Apoa4 was mainly enriched in cholesterol metabolism, PPAR signaling pathway, fat digestion and absorption, and complement and coagulation cascades. GO: Gene Ontology; KEGG: Kyoto Encyclopedia of Genes and Genomes; PPI: Protein–protein interaction; PPAR: Peroxisome proliferator-activated receptor.

Techniques: Construct, Activity Assay, Coagulation, Clinical Proteomics, Binding Assay

Expression of mRNA and proteins. qRT-PCR results presented the expression levels of PI3K (A), AKT (B), C5 (C), PPARγ (D), C4a (E), C3 (F), C1qB (G), and CRP (H) mRNA in different groups; the expression levels of PI3K, p-PI3K, p-AKT, AKT, PPARγ, Apoa4 (I), and C4a, C5, C3, Alb, C1qB, and CRP (J) in different groups were detected. The levels of p-PI3K, p-AKT, PPARγ, Apoa4, C5, and Alb decreased, while C4a, C3, C1qB, and CRP increased in the SOD1G93A + PBS group compared with the WT group; * P < 0.05, ** P < 0.01, vs WT group; # P < 0.05, ## P < 0.01, vs SOD1 G93A + PBS group. qRT-PCR: Quantitative real-time polymerase chain reaction; SOD1: Superoxide dismutase 1; WT: Wilt-type; PPAR: Peroxisome proliferator-activated receptor.

Journal: Biomolecules and Biomedicine

Article Title: Therapeutic potential of simvastatin in ALS: Enhanced axonal integrity and motor neuron survival through Apoa4 and Alb modulation

doi: 10.17305/bb.2024.11218

Figure Lengend Snippet: Expression of mRNA and proteins. qRT-PCR results presented the expression levels of PI3K (A), AKT (B), C5 (C), PPARγ (D), C4a (E), C3 (F), C1qB (G), and CRP (H) mRNA in different groups; the expression levels of PI3K, p-PI3K, p-AKT, AKT, PPARγ, Apoa4 (I), and C4a, C5, C3, Alb, C1qB, and CRP (J) in different groups were detected. The levels of p-PI3K, p-AKT, PPARγ, Apoa4, C5, and Alb decreased, while C4a, C3, C1qB, and CRP increased in the SOD1G93A + PBS group compared with the WT group; * P < 0.05, ** P < 0.01, vs WT group; # P < 0.05, ## P < 0.01, vs SOD1 G93A + PBS group. qRT-PCR: Quantitative real-time polymerase chain reaction; SOD1: Superoxide dismutase 1; WT: Wilt-type; PPAR: Peroxisome proliferator-activated receptor.

Techniques: Expressing, Quantitative RT-PCR, Real-time Polymerase Chain Reaction

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