fabp4 inhibitor bms-309403  (ApexBio)

Journal: Cell Death & Disease

Article Title: Pre-emptive pharmacological inhibition of fatty acid–binding protein 4 attenuates kidney fibrosis by reprogramming tubular lipid metabolism

doi: 10.1038/s41419-021-03850-1

Figure Lengend Snippet: a Fluorescence microscopy revealed that FABP4 was mainly expressed in kidney tubular epithelial, and increased in UUO-treated mice. Quantitative image to depict fluorescence intensity (Right panel). Scale bars: 50 μm. b Western blot showed that FABP4 was increased in UUO mice. Schematic representation of quantitative data of indicated proteins. Representative images from three independent experiments are shown above. n = 6 mice. c Protein expression of FABP4 was detected in HK-2 cells treated with 10 ng/mL TGF-β for 48 h. Schematic representation of quantitative data of indicated proteins. Representative images from three independent experiments are shown above. d In the study of Ju CKD tubules, CKD was associated with significantly increased mRNA value of Fabp4 compared with biopsy samples from health control. e A negative correlation between tubular FABP4 and eGFR was observed in public Ju CKD dataset. Data were presented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P <0.001, ns means no statistical significance.

Article Snippet: FABP4 inhibitor BMS309403 (R&D systems, 5258/10).

Techniques: Fluorescence, Microscopy, Western Blot, Expressing, Control

Journal: Cell Death & Disease

Article Title: Pre-emptive pharmacological inhibition of fatty acid–binding protein 4 attenuates kidney fibrosis by reprogramming tubular lipid metabolism

doi: 10.1038/s41419-021-03850-1

Figure Lengend Snippet: a One day before UUO surgery treatment with FABP4 inhibitor BMS309403, and then sacrificed on day 7. b BMS309403 has no significant change in the ratio of body weight to kidney weight (BW/KW). c Cell viability of HK-2 cells was detected by CCK8, which was treated by various doses of BMS309403 for 48 h. d Oil red O staining in frozen section from mice tubulointerstititum. e Oil red O staining in HK-2 cells co-treated with or without BMS309403 for 48 h. f Content of lipid in peripheral blood of mice. g Content of lipid in kidney tissue of mice. Data were presented as mean ± SEM. * P < 0.05, *** P < 0.001, ns means no statistical significance. Scale bars: 50 μm.

Article Snippet: FABP4 inhibitor BMS309403 (R&D systems, 5258/10).

Techniques: Staining

Journal: Cell Death & Disease

Article Title: Pre-emptive pharmacological inhibition of fatty acid–binding protein 4 attenuates kidney fibrosis by reprogramming tubular lipid metabolism

doi: 10.1038/s41419-021-03850-1

Figure Lengend Snippet: a Western blot of HK-2 cell lysates for FABP4, fibronectin, collagen-I, and α-SMA expression. GAPDH sets as loading control. b RT-qPCR for fibronectin, collagen-I, and α-SMA transcripts normalized to Gapdh in HK-2 cells. c Western blot and band intensity quantitation for TGF-β, p-Smad2, and p-Smad3 in HK-2 cells. Blots were stripped and reprobed for GAPDH. d RT-qPCR for TGF-β, CTGF, FGF2, PDGFB transcripts normalized to Gapdh in total RNA extracts of HK-2 cells from DMSO- or BMS309403-treated normal and TGF-β-treated cells. These data were calculated from three independent experiments. *** P < 0.001.

Article Snippet: FABP4 inhibitor BMS309403 (R&D systems, 5258/10).

Techniques: Western Blot, Expressing, Control, Quantitative RT-PCR, Quantitation Assay

Journal: Cell Death & Disease

Article Title: Pre-emptive pharmacological inhibition of fatty acid–binding protein 4 attenuates kidney fibrosis by reprogramming tubular lipid metabolism

doi: 10.1038/s41419-021-03850-1

Figure Lengend Snippet: a The changes in PGC1α and PPARγ expression levels were confirmed in HK-2 cells by immunoblotting studies. b RT-qPCR for Ppargc1a, Pparg, Cpt1a, Cpt2, Acox1, and Acox2 transcripts normalized to Gapdh in HK-2 cells. c Western blot of whole-cell lysates for Bcl-2, cleaved caspase-3 expression in HK-2 cells. GAPDH sets as loading control. d Western blot of whole-cell lysates for Grp78 (Bip), CHOP expression in HK-2 cells. GAPDH sets as loading control. e , f ER stress related genes were analyzed by RT-qPCR in HK-2 cells from DMSO- or BMS309403-treated normal and TGF-β-treated cells. The transcript normalized to Gapdh. These data were calculated from three independent experiments. * P < 0.05, ** P < 0.01, *** P < 0.001, ns means no statistical significance.

Article Snippet: FABP4 inhibitor BMS309403 (R&D systems, 5258/10).

Techniques: Expressing, Western Blot, Quantitative RT-PCR, Control

Journal: Cell Death & Disease

Article Title: Pre-emptive pharmacological inhibition of fatty acid–binding protein 4 attenuates kidney fibrosis by reprogramming tubular lipid metabolism

doi: 10.1038/s41419-021-03850-1

Figure Lengend Snippet: a Staining with HE, PAS, and MTS of kidney sections from obstructed (UUO) or sham-operated kidneys (control). Animals received BMS309403 (40 mg/kg for 8 days) or vehicle as indicated. n = 6 per group. b Western blot of whole-kidney lysates for FABP4, fibronectin, collagen-I, and α-SMA expression. GAPDH sets as loading control. c Fibronectin, collagen-I, and α-SMA mRNA expression by RT-qPCR. Schematic representation of quantitative data of indicated proteins. The transcripts normalized to Gapdh. Representative images from three independent experiments are shown above. ** P < 0.01, *** P < 0.001, ns means no statistical significance. Scale bars: 25 μm.

Article Snippet: FABP4 inhibitor BMS309403 (R&D systems, 5258/10).

Techniques: Staining, Control, Western Blot, Expressing, Quantitative RT-PCR

Journal: Cell Death & Disease

Article Title: Pre-emptive pharmacological inhibition of fatty acid–binding protein 4 attenuates kidney fibrosis by reprogramming tubular lipid metabolism

doi: 10.1038/s41419-021-03850-1

Figure Lengend Snippet: a TGF-β, p-Smad2, and p-Smad3 expression was verified in kidney samples by Western blot. Blots were stripped and reprobed for GAPDH. b RT-qPCR for TGF-β, CTGF, PDGFB, and FGF2 transcripts normalized to Gapdh in kidney tissue. c The changes in PGC1α and PPARγ expression levels were confirmed in mouse kidneys by immunoblotting studies. d Ppargc1a, Pparg, Cpt1a, Cpt2, Acox1, and Acox2 mRNA expression were analyzed by RT-qPCR in total RNA extracts of kidneys from saline- or BMS309403-treated normal and UUO mice. The transcript normalized to Gapdh. Representative images from three independent experiments are shown above. * P < 0.05, ** P < 0.01, *** P < 0.001, ns means no statistical significance.

Article Snippet: FABP4 inhibitor BMS309403 (R&D systems, 5258/10).

Techniques: Expressing, Western Blot, Quantitative RT-PCR, Saline

Journal: Cell Death & Disease

Article Title: Pre-emptive pharmacological inhibition of fatty acid–binding protein 4 attenuates kidney fibrosis by reprogramming tubular lipid metabolism

doi: 10.1038/s41419-021-03850-1

Figure Lengend Snippet: BMS309403 reduces lipotoxicity to improve kidney fibrosis mainly by reducing lipid accumulation and increasing FAO pathway, and also reduce the secretion of a series of profibrotic cytokines by kidney TECs to relieve kidney fibrosis.

Article Snippet: FABP4 inhibitor BMS309403 (R&D systems, 5258/10).

Techniques:

Journal: EMBO Molecular Medicine

Article Title: Saturated fatty acids induce lipotoxicity in lymphatic endothelial cells contributing to secondary lymphedema development

doi: 10.1038/s44321-025-00286-4

Figure Lengend Snippet: ( A ) Circulating levels of fatty acid-binding protein 4 (FABP4) measured by ELISA in plasma samples from patients with lymphedema ( n = 51) and non-lymphedema controls ( n = 18). ( B ) Quantification of cell death (trypan blue assay) in HDLECs treated with SA (50 µM) or palmitic acid (PA, 250 µM) with or without the FABP4 inhibitor BMS-309403 (BMS, 5 µM) pre-treatment ( n = 4 independent experiments). ( C ) Representative western blot of ER stress markers (sXBP1 and CHOP) in HDLECs treated with SA at increasing concentrations (10–50 µM) with or without BMS pre-treatment. ( D ) Representative immunofluorescence images of HDLECs treated with SA and BMS showing FABP4 (red) and the endoplasmic reticulum marker calreticulin (green). DAPI stains the nucleus (blue). Scale bars: 50 µm. ( E ) Colocalization quantification between FABP4 and calreticulin using Pearson’s correlation coefficient, showing no significant differences between treatment groups ( n = 3 independent experiments). ( F ) Quantification of cell death in HDLECs transfected with siFABP4 or scrambled siRNA (Sc-siRNA), with or without SA treatment, showing reduced cell death following FABP4 knockdown ( n = 6 independent experiments). ( G ) Western blot confirming FABP4 knockdown in HDLECs transfected with FABP4-targeting siRNA (siFABP4), with no effect on FABP5 expression ( n = 2). Data are presented as mean ± SEM. Statistical analysis: two-tailed unpaired t test for ( A ); one-way ANOVA with Tukey’s post hoc test for ( B , E , F ). Significance: ** P < 0.01, *** P < 0.001, **** P < 0.0001. Exact P values for the statistical comparisons are shown in Appendix Table . FABP4 fatty acid binding protein 1, sXBP-1 spliced X-box binding protein 1, CHOP C/EBP homologous protein, DAPI 4′,6-diamidino-2-phenylindole. .

Article Snippet: To determine the effects of pharmacological inhibition of FABP4, either the FABP4 inhibitor BMS-309403 (15 mg·kg − 1·day − 1; HY-101903A, MedChemExpress, NJ, USA) or vehicle (phosphate-buffered saline, PBS) was administered chronically by daily oral gavage for 4 weeks starting on the day of the lymphatic surgery.

Techniques: Binding Assay, Enzyme-linked Immunosorbent Assay, Clinical Proteomics, Western Blot, Immunofluorescence, Marker, Transfection, Knockdown, Expressing, Two Tailed Test

Journal: EMBO Molecular Medicine

Article Title: Saturated fatty acids induce lipotoxicity in lymphatic endothelial cells contributing to secondary lymphedema development

doi: 10.1038/s44321-025-00286-4

Figure Lengend Snippet: ( A , B ) Oil Red O staining of tail tissue from sham and lymphedema (LE) mice maintained on a high saturated fat diet (HSFD) or treated with the FABP4 inhibitor BMS-309403 (HSFD + BMS) or switched to a control diet (HSFD → CD) after lymphatic injury. ( A ) Representative images showing lipid accumulation (red) in lymphedematous tails. Scale bars: 100 μm. ( B ) Quantification of Oil Red O positive area reveals increased lipid deposition in lymphedema tissue under HSFD, which is significantly reduced by BMS treatment or dietary transition ( n = 4 mice). ( C – E ) Immunofluorescence staining for FABP4 (red) in tail tissue from CD, HSFD-, HSFD + BMS-, or HSFD → CD-fed lymphedema mice. DAPI (blue) marks nuclei. ( C ) Representative images showing increased FABP4 positive adipocytes in HSFD-fed mice. Scale bars: 50 μm. ( D ) Quantification of FABP4 positive adipocyte number. ( E ) Quantification of FABP4 positive adipocyte area ( n = 4 mice). ( F ) Circulating FABP4 levels measured in mice with lymphedema, showing increased plasma FABP4 in HSFD-fed mice and partial reduction with BMS treatment ( n = 7 mice). Data are presented as mean ± SEM. Statistical analysis: one-way ANOVA with Tukey’s post hoc test. Significance: * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. Exact P values for the statistical comparisons are shown in Appendix Table . HSFD high saturated fat diet, CD control diet, FABP4 fatty acid-binding protein 4, BMS BMS-309403, DAPI 4′,6-diamidino-2-phenylindole. .

Article Snippet: To determine the effects of pharmacological inhibition of FABP4, either the FABP4 inhibitor BMS-309403 (15 mg·kg − 1·day − 1; HY-101903A, MedChemExpress, NJ, USA) or vehicle (phosphate-buffered saline, PBS) was administered chronically by daily oral gavage for 4 weeks starting on the day of the lymphatic surgery.

Techniques: Staining, Control, Immunofluorescence, Clinical Proteomics, Binding Assay

Journal: EMBO Molecular Medicine

Article Title: Saturated fatty acids induce lipotoxicity in lymphatic endothelial cells contributing to secondary lymphedema development

doi: 10.1038/s44321-025-00286-4

Figure Lengend Snippet: ( A ) Tail volume measurements over time in mice with lymphedema (LE), showing that prolonged swelling induced by HSFD is significantly reduced with treatment using the FABP4 inhibitor BMS-309403 (HSFD + BMS) compared to HSFD + PBS controls ( n = 3–7 mice). ( B ) Scatter plots showing the changes in tail volume 28 days post-lymphatic surgery ( n = 3–7 mice). ( C ) Representative immunofluorescence staining of LYVE-1-positive cells (green) and markers of ER stress (sXBP-1, CHOP) and apoptosis (TUNEL) (red) in tail tissues from lymphedema mice across diets, 28 days post-surgery. DAPI stains the nucleus (blue). Scale bars: 25 μm. Scatter plots showing ( D , G ) sXBP-1 + LYVE-1+ colocalization and perilymphatic sXBP-1 intensities, ( E , H ) CHOP + LYVE-1+ colocalization and perilymphatic CHOP intensities, and ( F , I ) TUNEL + LYVE-1+ colocalization and perilymphatic TUNEL intensities comparing the groups ( n = 3–7 mice). Data are presented as mean ± SEM. Statistical analysis: two-way ANOVA with Šídák’s post hoc test for ( A ); one-way ANOVA with Tukey’s post hoc test for ( B , D – I ). Significance: * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. Exact P values for the statistical comparisons are shown in Appendix Table . LYVE-1 lymphatic vessel endothelial hyaluronan receptor-1, sXBP-1 spliced X-box binding protein 1, CHOP C/EBP homologous protein, TUNEL terminal deoxynucleotidyl transferase dUTP nick end labeling, DAPI 4′,6-diamidino-2-phenylindole. .

Article Snippet: To determine the effects of pharmacological inhibition of FABP4, either the FABP4 inhibitor BMS-309403 (15 mg·kg − 1·day − 1; HY-101903A, MedChemExpress, NJ, USA) or vehicle (phosphate-buffered saline, PBS) was administered chronically by daily oral gavage for 4 weeks starting on the day of the lymphatic surgery.

Techniques: Immunofluorescence, Staining, TUNEL Assay, Binding Assay

Journal: EMBO Molecular Medicine

Article Title: Saturated fatty acids induce lipotoxicity in lymphatic endothelial cells contributing to secondary lymphedema development

doi: 10.1038/s44321-025-00286-4

Figure Lengend Snippet: Representative immunohistochemistry images showing ( A ) F4/80 positive macrophages and ( B ) CD4 positive T cells in the perilymphatic region of tail tissue from mice with lymphedema fed a high saturated fat diet (HSFD), treated with the FABP4 inhibitor BMS-309403 (HSFD + BMS), or switched to a control diet after lymphatic injury (HSFD → CD). Scale bars: 50 μm. Quantification of immune cell infiltration for ( C ) F4/80 positive macrophages and ( D ) CD4 positive T cells ( n = 5 mice). HSFD-fed mice exhibited significantly higher perilymphatic immune cell infiltration, which was attenuated by FABP4 inhibition or dietary transition. Data are presented as mean ± SEM. Statistical analysis: one-way ANOVA with Tukey’s post hoc test. Significance: * P < 0.05, ** P < 0.01, *** P < 0.001. Exact P values for the statistical comparisons are shown in Appendix Table . HSFD high saturated fat diet, CD control diet, FABP4 fatty acid-binding protein 4. .

Article Snippet: To determine the effects of pharmacological inhibition of FABP4, either the FABP4 inhibitor BMS-309403 (15 mg·kg − 1·day − 1; HY-101903A, MedChemExpress, NJ, USA) or vehicle (phosphate-buffered saline, PBS) was administered chronically by daily oral gavage for 4 weeks starting on the day of the lymphatic surgery.

Techniques: Immunohistochemistry, Control, Inhibition, Binding Assay

Journal: Translational Lung Cancer Research

Article Title: Impaired natural killer cell maturation in lung adenocarcinoma driven by FABP4 and SPON2 downregulation through disrupted lipid metabolism

doi: 10.21037/tlcr-24-1027

Figure Lengend Snippet: Pseudotime ordering and pathway analysis of NK1 cluster. (A) Pseudotime ordering of NK1 reveals a trajectory. (B) Significant shift toward the NK1 phenotype in T group and N group. (C) Differentially expressed genes (rows) along pseudotime (columns) are clustered hierarchically into two modules. Color key from blue to red indicates relative expression from low to high. (D) Expression dynamics of 103 genes in module 2 in pseudotime, shown as pink lines. The red line indicates the average gene expression patterns in module 2. (E) GO analyses of module 2. (F) Superimposition of expression of specific genes ( FABP4 and SPON2 ) on the reprogramming trajectories. FABP4 , fatty acid-binding protein 4; GO, Gene Ontology; N, non-malignant lung; NK, natural killer; SPON2 , spondin2; T, tumor.

Article Snippet: NK92 cells were treated with an FABP4 inhibitor BMS-309403 (20 μmol/L; APExBIO, Houston, TX, USA) for 48 h at 37 °C.

Techniques: Expressing, Gene Expression, Binding Assay

Journal: Translational Lung Cancer Research

Article Title: Impaired natural killer cell maturation in lung adenocarcinoma driven by FABP4 and SPON2 downregulation through disrupted lipid metabolism

doi: 10.21037/tlcr-24-1027

Figure Lengend Snippet: FABP4 and SPON2 expression in lung adenocarcinoma. (A,B) FABP4 and SPON2 expression in NK cells in a pair of representative samples determined using multiplex IF (400×). Scale bar represents 50 μm. (C) Graph bars showing the relative fluorescence intensity of FABP4 and SPON2 expression, measured from 10 NK cells randomly selected per visual field (400×) for each patient. (D) FABP4 and SPON2 expression in patients with lung adenocarcinoma in TCGA. (E,F) FABP4 and SPON2 expression in patient samples determined using IHC (40×). Scale bar represents 20 μm. **, P<0.01; ***, P<0.001. FABP4 , fatty acid-binding protein 4; IHC, immunohistochemistry; ns, not significant; SPON2 , spondin2; TCGA, The Cancer Genome Atlas.

Article Snippet: NK92 cells were treated with an FABP4 inhibitor BMS-309403 (20 μmol/L; APExBIO, Houston, TX, USA) for 48 h at 37 °C.

Techniques: Expressing, Multiplex Assay, Fluorescence, Binding Assay, Immunohistochemistry

Journal: Translational Lung Cancer Research

Article Title: Impaired natural killer cell maturation in lung adenocarcinoma driven by FABP4 and SPON2 downregulation through disrupted lipid metabolism

doi: 10.21037/tlcr-24-1027

Figure Lengend Snippet: Function analysis of FABP4-deficient NK92 cells. (A) Violin plot showing FABP4 , SPON2 , Tbx21 , and EOMES expression in tumors and adjacent tissues in TCGA data. (B) NK92 cells transfected with shFABP4 lentivirus (200×). (C) FABP4 , Tbx21 , and EOMES expression in NK92 cells transfected with shFABP4 analyzed using fluorescence quantitative polymerase chain reaction. (D) Flow cytometry analysis showing the percentage of degranulated NK cells (CD56 + CD107a + ) among total NK cells (CD56 + ). (E) Volcano plot displaying differential expression of lipids in NK cells across various groups. (F,G) Bar and bubble charts illustrating the enriched signaling pathways for these differentially expressed lipids. **, P<0.01; ***, P<0.001. EOMES , eomesodermin; FABP4 , fatty acid-binding protein 4; ns, not significant; SPON2 , spondin2; Tbx21 , T-box 21; TCGA, The Cancer Genome Atlas.

Article Snippet: NK92 cells were treated with an FABP4 inhibitor BMS-309403 (20 μmol/L; APExBIO, Houston, TX, USA) for 48 h at 37 °C.

Techniques: Expressing, Transfection, Fluorescence, Real-time Polymerase Chain Reaction, Flow Cytometry, Quantitative Proteomics, Protein-Protein interactions, Binding Assay

Journal: Cellular and Molecular Life Sciences

Article Title: Integrated multi-omic analysis identifies fatty acid binding protein 4 as a biomarker and therapeutic target of ischemia–reperfusion injury in steatotic liver transplantation

doi: 10.1007/s00018-023-05110-1

Figure Lengend Snippet: Proteomic profile revealing the change during liver transplantation. A Heatmap of the differentially expressed proteins. Red rectangles mean that proteins are upregulated, and green ones mean that they are downregulated. B Principal component analysis of the duplicate samples, in which the degree of aggregation among samples represents statistical consistency. C Volcano plot of the differentially expressed proteins between NC SHAM and HF SHAM groups. Gray dots represent genes that are not differentially expressed; red dots and blue dots represent genes that are upregulated and downregulated significantly. D Volcano plot of the differentially expressed proteins between NC LT and HF LT groups. E Venn diagram demonstrating shared and discrete proteins in each of these four groups. F Expression patterns of these differentially expressed proteins based on membership and expression. G Protein–protein interaction network of differentially expressed proteins with FABP4

Article Snippet: The other two groups of mouse LT were performed after confirmation of the injury target screened by proteomic analysis: (v) normal control donor liver transplantation group treated with fatty acid binding protein 4 (FABP4) inhibitor (BMS-309403, MedChemExpress) group (NC BMS group), and (vi) high-fat donor liver transplantation treated with FABP4 inhibitor group (HF BMS group).

Techniques: Transplantation Assay, Expressing

Journal: Cellular and Molecular Life Sciences

Article Title: Integrated multi-omic analysis identifies fatty acid binding protein 4 as a biomarker and therapeutic target of ischemia–reperfusion injury in steatotic liver transplantation

doi: 10.1007/s00018-023-05110-1

Figure Lengend Snippet: Relationship with FABP4 expression and liver transplantation recipients’ overall survival. A FABP4 is a high expression of donors’ liver tissue microarray IHC staining. B FABP4 low expression of IHC staining. C Comparison of overall survival rate between FABP4 high- and low-expression groups. D Comparison of the incidence of early allograft dysfunction. E Comparison of the risk of liver steatosis

Article Snippet: The other two groups of mouse LT were performed after confirmation of the injury target screened by proteomic analysis: (v) normal control donor liver transplantation group treated with fatty acid binding protein 4 (FABP4) inhibitor (BMS-309403, MedChemExpress) group (NC BMS group), and (vi) high-fat donor liver transplantation treated with FABP4 inhibitor group (HF BMS group).

Techniques: Expressing, Transplantation Assay, Microarray, Immunohistochemistry, Comparison

Journal: Cellular and Molecular Life Sciences

Article Title: Integrated multi-omic analysis identifies fatty acid binding protein 4 as a biomarker and therapeutic target of ischemia–reperfusion injury in steatotic liver transplantation

doi: 10.1007/s00018-023-05110-1

Figure Lengend Snippet: Influence of FABP4 inhibitor on mouse high fatty liver transplantation model. A H&E staining of mouse liver transplantation model after using FABP4 inhibitor. B TUNEL staining. C – F Liver function detection of ALT, AST, LDH, and TB. G – I Oxidative stress injury assay of GSH, MDA, and SOD. J – N Relative expression of FABP4, Bax, cleaved Caspase-3, and cleaved PARP. ns, not significant; * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.001

Article Snippet: The other two groups of mouse LT were performed after confirmation of the injury target screened by proteomic analysis: (v) normal control donor liver transplantation group treated with fatty acid binding protein 4 (FABP4) inhibitor (BMS-309403, MedChemExpress) group (NC BMS group), and (vi) high-fat donor liver transplantation treated with FABP4 inhibitor group (HF BMS group).

Techniques: Transplantation Assay, Staining, TUNEL Assay, Expressing

Journal: Cellular and Molecular Life Sciences

Article Title: Integrated multi-omic analysis identifies fatty acid binding protein 4 as a biomarker and therapeutic target of ischemia–reperfusion injury in steatotic liver transplantation

doi: 10.1007/s00018-023-05110-1

Figure Lengend Snippet: Transcriptomic profiles revealing the influence of FABP4 inhibitor. A Violin diagram of expression patterns of all genes. B Principal component analysis of the duplicate samples. C Heatmap of the differentially expressed genes. D Volcano plot of the differentially expressed genes between HF LT and HF BMS groups. E Gene ontology pathway enrichment for differentially expressed proteins. The circle sizes represent the number of genes enriched in pathways, and the circle’s color means significance. F KEGG pathway enrichment for differentially expressed proteins

Article Snippet: The other two groups of mouse LT were performed after confirmation of the injury target screened by proteomic analysis: (v) normal control donor liver transplantation group treated with fatty acid binding protein 4 (FABP4) inhibitor (BMS-309403, MedChemExpress) group (NC BMS group), and (vi) high-fat donor liver transplantation treated with FABP4 inhibitor group (HF BMS group).

Techniques: Expressing

Journal: Cellular and Molecular Life Sciences

Article Title: Integrated multi-omic analysis identifies fatty acid binding protein 4 as a biomarker and therapeutic target of ischemia–reperfusion injury in steatotic liver transplantation

doi: 10.1007/s00018-023-05110-1

Figure Lengend Snippet: Metabolomic profiles revealing the influence of FABP4 inhibitor. A Total ion chromatogram of spectral overlap comparison, with response intensity and retention time overlapping. B Principal component analysis of the duplicate samples. C Volcano plot of the differentially expressed metabolites between HF LT and HF BMS groups. D Heatmap of the differentially expressed metabolites. E Correlation analysis between metabolites and visualized in the form of correlation heatmaps. F Revealing the co-regulatory relationships between various metabolites by chord diagrams

Article Snippet: The other two groups of mouse LT were performed after confirmation of the injury target screened by proteomic analysis: (v) normal control donor liver transplantation group treated with fatty acid binding protein 4 (FABP4) inhibitor (BMS-309403, MedChemExpress) group (NC BMS group), and (vi) high-fat donor liver transplantation treated with FABP4 inhibitor group (HF BMS group).

Techniques: Comparison

Journal: Cellular and Molecular Life Sciences

Article Title: Integrated multi-omic analysis identifies fatty acid binding protein 4 as a biomarker and therapeutic target of ischemia–reperfusion injury in steatotic liver transplantation

doi: 10.1007/s00018-023-05110-1

Figure Lengend Snippet: Influence of FABP4 inhibitor on cAMP signaling pathway. A – E Relative expression of HHIP, ADRB2, RAC2, and PKA. F , G The content of Prostaglandin i2 and N-oleoylethanolamine validated by ELISA. H – K The mRNA expression of Hhip, Adrb2, Rac2, and Adcy7 of HF LT and HF BMS groups. ns, not significant; * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.001

Article Snippet: The other two groups of mouse LT were performed after confirmation of the injury target screened by proteomic analysis: (v) normal control donor liver transplantation group treated with fatty acid binding protein 4 (FABP4) inhibitor (BMS-309403, MedChemExpress) group (NC BMS group), and (vi) high-fat donor liver transplantation treated with FABP4 inhibitor group (HF BMS group).

Techniques: Expressing, Enzyme-linked Immunosorbent Assay

Journal: Cellular and Molecular Life Sciences

Article Title: Integrated multi-omic analysis identifies fatty acid binding protein 4 as a biomarker and therapeutic target of ischemia–reperfusion injury in steatotic liver transplantation

doi: 10.1007/s00018-023-05110-1

Figure Lengend Snippet: Influence of FABP4 inhibitor on high fatty liver mitochondrion. A – C Transmission electron microscopy image of mouse liver in each group. A The mitochondrial structure was clear, and no autophagosomes were presented in the HF SHAM group. B Autophagosomes and autolysosomes were found in the HF LT group with mitochondrial swelling. C The mitochondrial structure of the HF BMS group was clear, and damaged parts of mitochondria were lytic. D – F Multiplex immunofluorescence staining of rhodamine reagent for detecting mitochondrial membrane potential. Green fluorescence represents mitochondrial membranous potential, red fluorescence represents apoptotic hepatocytes, and blue fluorescence represents nuclear staining. G – I Relative expression of DRP1 and MFN-1. ns, not significant; * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.001. AP, autophagosomes; ASS, autolysosome; LD, lipid droplets; M, mitochondria; RER, rough endoplasmic reticulum

Article Snippet: The other two groups of mouse LT were performed after confirmation of the injury target screened by proteomic analysis: (v) normal control donor liver transplantation group treated with fatty acid binding protein 4 (FABP4) inhibitor (BMS-309403, MedChemExpress) group (NC BMS group), and (vi) high-fat donor liver transplantation treated with FABP4 inhibitor group (HF BMS group).

Techniques: Transmission Assay, Electron Microscopy, Multiplex Assay, Immunofluorescence, Staining, Membrane, Fluorescence, Expressing

Journal: Cellular and Molecular Life Sciences

Article Title: Integrated multi-omic analysis identifies fatty acid binding protein 4 as a biomarker and therapeutic target of ischemia–reperfusion injury in steatotic liver transplantation

doi: 10.1007/s00018-023-05110-1

Figure Lengend Snippet: Influence of FABP4 siRNA on in vitro hypoxia / reoxygenation model. A – D Flow cytometry was performed to detect the hypoxic injury-induced apoptosis of AML12 cells. E – H Liver function detection of ALT, AST, LDH, and TB using the supernatant of each group. I – P Relative expression of FABP4, PKA, RAC2, HHIP, ADRB, DRP1, and MFN-1. ns, not significant; * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.001

Article Snippet: The other two groups of mouse LT were performed after confirmation of the injury target screened by proteomic analysis: (v) normal control donor liver transplantation group treated with fatty acid binding protein 4 (FABP4) inhibitor (BMS-309403, MedChemExpress) group (NC BMS group), and (vi) high-fat donor liver transplantation treated with FABP4 inhibitor group (HF BMS group).

Techniques: In Vitro, Flow Cytometry, Expressing