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fluvastatin (MedChemExpress)

Name: fluvastatin
Brand: MedChemExpress
Rating: 94 (19 reviews)

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MedChemExpress fluvastatin
Fluvastatin, supplied by MedChemExpress, 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/fluvastatin/product/MedChemExpress
Average 94 stars, based on 19 article reviews

fluvastatin - by Bioz Stars, 2026-03

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A. For phenotypic screening, we induced constitutive blebbing in A375 cells transduced with EGFP. B . Table of selected drugs identified in our phenotypic screen. C . Assay used to vertically confine cells down to ∼3 µm under non-adherent (BSA; 1%) conditions. D . Montage of vehicle (leader mobile; LM) and Fluvastatin (10 µM) treated (no leader; NL) cells. E . Percentage of leader mobile (LM), leader non-mobile (LNM), and no leader (NL) for vehicle ( n = 297) and Fluvastatin (10 µM; n = 270) treated cells (χ 2 < 0.0001). F. - G . Speed (median +/- 95% CI) and directionality (mean +/- SEM) for vehicle ( n = 297) and Fluvastatin (10 µM; n = 270) treated leader mobile (LM) cells. H . Assay used for 3D confinement under adherent (VCAM-1; 1 µg/mL) conditions. I . Percentage of vehicle ( n = 125) or Fluvastatin (10 µM; n = 170) treated cells adopting a hybrid, amoeboid, or mesenchymal phenotype in VCAM-1 (1 µg/mL) coated microchannels (χ 2 < 0.0001). J . Representative images of cells treated with vehicle (hybrid) and Fluvastatin (10 µM; mesenchymal) in VCAM-1 (1 µg/mL) coated microchannels. K . Percentage of vehicle ( n = 90) or Fluvastatin (10 µM; n = 153) treated cells adopting a hybrid, amoeboid, or mesenchymal phenotype in BSA (1%) coated microchannels (χ 2 < 0.0001). L . Representative image of a cell adopting an amoeboid phenotype in a BSA (1%) coated microchannel. LifeAct-mEmerald was used to mark F-actin. Significance levels: * - p ≤ 0.05, ** - p ≤ 0.01, *** - p ≤ 0.001, and **** - p ≤ 0.0001. See also Video S1-2 and source data 1.

Journal: bioRxiv

Article Title: Targeting Cholesterol-Dependent Piezo1 Activation Impairs Amoeboid Migration in Melanoma Cells

doi: 10.1101/2025.07.11.664494

Figure Lengend Snippet: A. For phenotypic screening, we induced constitutive blebbing in A375 cells transduced with EGFP. B . Table of selected drugs identified in our phenotypic screen. C . Assay used to vertically confine cells down to ∼3 µm under non-adherent (BSA; 1%) conditions. D . Montage of vehicle (leader mobile; LM) and Fluvastatin (10 µM) treated (no leader; NL) cells. E . Percentage of leader mobile (LM), leader non-mobile (LNM), and no leader (NL) for vehicle ( n = 297) and Fluvastatin (10 µM; n = 270) treated cells (χ 2 < 0.0001). F. - G . Speed (median +/- 95% CI) and directionality (mean +/- SEM) for vehicle ( n = 297) and Fluvastatin (10 µM; n = 270) treated leader mobile (LM) cells. H . Assay used for 3D confinement under adherent (VCAM-1; 1 µg/mL) conditions. I . Percentage of vehicle ( n = 125) or Fluvastatin (10 µM; n = 170) treated cells adopting a hybrid, amoeboid, or mesenchymal phenotype in VCAM-1 (1 µg/mL) coated microchannels (χ 2 < 0.0001). J . Representative images of cells treated with vehicle (hybrid) and Fluvastatin (10 µM; mesenchymal) in VCAM-1 (1 µg/mL) coated microchannels. K . Percentage of vehicle ( n = 90) or Fluvastatin (10 µM; n = 153) treated cells adopting a hybrid, amoeboid, or mesenchymal phenotype in BSA (1%) coated microchannels (χ 2 < 0.0001). L . Representative image of a cell adopting an amoeboid phenotype in a BSA (1%) coated microchannel. LifeAct-mEmerald was used to mark F-actin. Significance levels: * - p ≤ 0.05, ** - p ≤ 0.01, *** - p ≤ 0.001, and **** - p ≤ 0.0001. See also Video S1-2 and source data 1.

Article Snippet: Latrunculin (3973), Fluvastatin (3309), Pitavastatin (4942), Pravastatin (2318), Piezo1/2 inhibitor (4912), and Piezo1/2 activator (5586) were purchased from Tocris Bioscience (Bristol, UK).

Techniques: Transduction

A. Relative transmigration of Fluvastatin (10 µM) treated cells through 12, 8, or 5 µm pores towards fetal bovine serum (FBS; 10%) (mean +/- SEM). B . Relative transmigration of Fluvastatin (10 µM) +/- mevalonic acid (MVA; 100 µM), Pravastatin (10 µM) +/- mevalonic acid (MVA; 100 µM), and mevalonic acid (MVA; 100 µM) through 5 µm pores towards fetal bovine serum (FBS; 10%) (mean +/- SEM). C . Cell proliferation for vehicle, Fluvastatin (10 µM) +/- mevalonic acid (MVA; 100 µM), Pravastatin (10 µM) +/- mevalonic acid (MVA; 100 µM), mevalonic acid (MVA; 100 µM), and cholesterol (1 mM) over 5 days (mean +/- SEM). D . Fold change in cholesterol over 12 hr for Fluvastatin (10 µM) +/- mevalonic acid (MVA; 100 µM), Pravastatin (10 µM) +/- mevalonic acid (MVA; 100 µM), and mevalonic acid (MVA; 100 µM) treated cells cultured in the absence of serum lipids (mean +/- SEM). E . Relative transmigration of Fluvastatin (10 µM) treated cells supplemented with 0.01, 0.1, or 1.0 mM of cholesterol through 5 µm pores towards fetal bovine serum (FBS; 10%) (mean +/- SEM). F . Relative transmigration of cells supplemented with 0.01, 0.1, or 1.0 mM of cholesterol through 5 µm pores towards fetal bovine serum (FBS; 10%) (mean +/- SEM). G . Relative transmigration of Pitavastatin (10 µM) treated cells through 8 and 5 µm pores towards fetal bovine serum (FBS; 10%) (mean +/- SEM). H . Relative transmigration of Fluvastatin (10 µM) treated Yale University mouse melanoma (YUMM) 3.3 cells through 8 and 5 µm pores towards fetal bovine serum (FBS; 10%) (mean +/- SEM). I . Relative transmigration of Fluvastatin (10 µM) treated human foreskin fibroblast (HFF) 1 cells through 8 and 5 µm pores towards fetal bovine serum (FBS; 10%) (mean +/- SEM). J . Proliferation of vehicle and Fluvastatin (10 µM) treated human foreskin fibroblast (HFF) 1 cells over 5 days (mean +/- SEM). Significance levels: * - p ≤ 0.05, ** - p ≤ 0.01, *** - p ≤ 0.001, and **** - p ≤ 0.0001.

Journal: bioRxiv

Article Title: Targeting Cholesterol-Dependent Piezo1 Activation Impairs Amoeboid Migration in Melanoma Cells

doi: 10.1101/2025.07.11.664494

Figure Lengend Snippet: A. Relative transmigration of Fluvastatin (10 µM) treated cells through 12, 8, or 5 µm pores towards fetal bovine serum (FBS; 10%) (mean +/- SEM). B . Relative transmigration of Fluvastatin (10 µM) +/- mevalonic acid (MVA; 100 µM), Pravastatin (10 µM) +/- mevalonic acid (MVA; 100 µM), and mevalonic acid (MVA; 100 µM) through 5 µm pores towards fetal bovine serum (FBS; 10%) (mean +/- SEM). C . Cell proliferation for vehicle, Fluvastatin (10 µM) +/- mevalonic acid (MVA; 100 µM), Pravastatin (10 µM) +/- mevalonic acid (MVA; 100 µM), mevalonic acid (MVA; 100 µM), and cholesterol (1 mM) over 5 days (mean +/- SEM). D . Fold change in cholesterol over 12 hr for Fluvastatin (10 µM) +/- mevalonic acid (MVA; 100 µM), Pravastatin (10 µM) +/- mevalonic acid (MVA; 100 µM), and mevalonic acid (MVA; 100 µM) treated cells cultured in the absence of serum lipids (mean +/- SEM). E . Relative transmigration of Fluvastatin (10 µM) treated cells supplemented with 0.01, 0.1, or 1.0 mM of cholesterol through 5 µm pores towards fetal bovine serum (FBS; 10%) (mean +/- SEM). F . Relative transmigration of cells supplemented with 0.01, 0.1, or 1.0 mM of cholesterol through 5 µm pores towards fetal bovine serum (FBS; 10%) (mean +/- SEM). G . Relative transmigration of Pitavastatin (10 µM) treated cells through 8 and 5 µm pores towards fetal bovine serum (FBS; 10%) (mean +/- SEM). H . Relative transmigration of Fluvastatin (10 µM) treated Yale University mouse melanoma (YUMM) 3.3 cells through 8 and 5 µm pores towards fetal bovine serum (FBS; 10%) (mean +/- SEM). I . Relative transmigration of Fluvastatin (10 µM) treated human foreskin fibroblast (HFF) 1 cells through 8 and 5 µm pores towards fetal bovine serum (FBS; 10%) (mean +/- SEM). J . Proliferation of vehicle and Fluvastatin (10 µM) treated human foreskin fibroblast (HFF) 1 cells over 5 days (mean +/- SEM). Significance levels: * - p ≤ 0.05, ** - p ≤ 0.01, *** - p ≤ 0.001, and **** - p ≤ 0.0001.

Techniques: Transmigration Assay, Cell Culture

A. Relative transmigration of cells treated with an HMGCR siRNA through 5 µm pores towards fetal bovine serum (FBS; 10%) (mean +/- SEM). B . Fold change in mRNA after HMGCR RNAi, as measured by RT-qPCR (mean +/- SEM). C . Fold change in cholesterol after RNAi of HMGCR on days 1, 2, and 3 for cells cultured in the presence of serum lipids. D . Fold change in cholesterol after RNAi of HMGCR on days 1, 2, and 3 for cells cultured in the absence of serum lipids. E . Relative transmigration of cells treated with an HMGCR siRNA through 5 µm pores towards lipid-free serum (10%) (mean +/- SEM). F . Fold change in LDL uptake for cells treated with a non- targeting or HMGCR siRNA for 3 days (mean +/- SEM). G . Fold change in LDL uptake for cells treated with vehicle or Fluvastatin (10 µM) for 12 hr (mean +/- SEM). H . Percentage of leader mobile (LM), leader non-mobile (LNM), and no leader (NL) for vehicle ( n = 156), Fluvastatin (10 µM; n = 161) (χ 2 < 0.0001), Fluvastatin (10 µM) + cholesterol (1 mM; n = 47) (χ 2 < 0.0001), and cholesterol (1 mM; n = 144) (χ 2 = 0.03938) treated A375 cells transduced with EGFP. Significance levels: * - p ≤ 0.05, ** - p ≤ 0.01, *** - p ≤ 0.001, and **** - p ≤ 0.0001. See also source data 1.

Journal: bioRxiv

Article Title: Targeting Cholesterol-Dependent Piezo1 Activation Impairs Amoeboid Migration in Melanoma Cells

doi: 10.1101/2025.07.11.664494

Figure Lengend Snippet: A. Relative transmigration of cells treated with an HMGCR siRNA through 5 µm pores towards fetal bovine serum (FBS; 10%) (mean +/- SEM). B . Fold change in mRNA after HMGCR RNAi, as measured by RT-qPCR (mean +/- SEM). C . Fold change in cholesterol after RNAi of HMGCR on days 1, 2, and 3 for cells cultured in the presence of serum lipids. D . Fold change in cholesterol after RNAi of HMGCR on days 1, 2, and 3 for cells cultured in the absence of serum lipids. E . Relative transmigration of cells treated with an HMGCR siRNA through 5 µm pores towards lipid-free serum (10%) (mean +/- SEM). F . Fold change in LDL uptake for cells treated with a non- targeting or HMGCR siRNA for 3 days (mean +/- SEM). G . Fold change in LDL uptake for cells treated with vehicle or Fluvastatin (10 µM) for 12 hr (mean +/- SEM). H . Percentage of leader mobile (LM), leader non-mobile (LNM), and no leader (NL) for vehicle ( n = 156), Fluvastatin (10 µM; n = 161) (χ 2 < 0.0001), Fluvastatin (10 µM) + cholesterol (1 mM; n = 47) (χ 2 < 0.0001), and cholesterol (1 mM; n = 144) (χ 2 = 0.03938) treated A375 cells transduced with EGFP. Significance levels: * - p ≤ 0.05, ** - p ≤ 0.01, *** - p ≤ 0.001, and **** - p ≤ 0.0001. See also source data 1.

Techniques: Transmigration Assay, Quantitative RT-PCR, Cell Culture, Transduction

A. Pseudocolored montage of cholesterol (1 mM) supplemented cells transfected with GCaMP. B . Quantification of spontaneous Ca 2+ transients in cells treated with vehicle, 0.1, or 1 mM of cholesterol, as measured by the fold change in GCaMP fluorescence (mean +/- SEM). A Dunnett’s multiple comparison test was used to determine statistical significance. C . Quantification of spontaneous Ca 2+ transients in cholesterol (1 mM) supplemented cells treated with a Piezo1/2 inhibitor (10 µM), as measured by the fold change in GCaMP fluorescence (mean +/- SEM). D . Quantification of spontaneous Ca 2+ transients in cholesterol (1 mM) supplemented cells treated with a non-targeting or Piezo1 siRNA, as measured by the fold change in GCaMP fluorescence (mean +/- SEM). E . Fold change in mRNA after Piezo1 RNAi, as measured by RT-qPCR (mean +/- SEM). F . Fold change in Piezo1 mRNA after Fluvastatin treatment (10 µM; 12 hr), as measured by RT-qPCR (mean +/- SEM). G . Relative transmigration of cells treated with a Piezo1 siRNA through 5 µm pores towards fetal bovine serum (FBS; 10%) (mean +/- SEM). H . Assay used to variably (≥ 3 µm) confine cells under non-adherent (BSA; 1%) conditions. I. - K . Intracellular Ca 2+ levels in vehicle, Fluvastatin (10 µM), and Fluvastatin (10 µM) + cholesterol (1 mM) treated variably confined (≥ 3 µm) cells under non-adherent conditions (BSA; 1%). We measured intracellular Ca 2+ levels by taking the ratio of a red fluorescent Ca 2+ indicator to a green fluorescent dye. Spearman rank correlation coefficients were used to determine statistical significance. Significance levels: * - p ≤ 0.05, ** - p ≤ 0.01, *** - p ≤ 0.001, and **** - p ≤ 0.0001. See also Figure S1.

Journal: bioRxiv

Article Title: Targeting Cholesterol-Dependent Piezo1 Activation Impairs Amoeboid Migration in Melanoma Cells

doi: 10.1101/2025.07.11.664494

Figure Lengend Snippet: A. Pseudocolored montage of cholesterol (1 mM) supplemented cells transfected with GCaMP. B . Quantification of spontaneous Ca 2+ transients in cells treated with vehicle, 0.1, or 1 mM of cholesterol, as measured by the fold change in GCaMP fluorescence (mean +/- SEM). A Dunnett’s multiple comparison test was used to determine statistical significance. C . Quantification of spontaneous Ca 2+ transients in cholesterol (1 mM) supplemented cells treated with a Piezo1/2 inhibitor (10 µM), as measured by the fold change in GCaMP fluorescence (mean +/- SEM). D . Quantification of spontaneous Ca 2+ transients in cholesterol (1 mM) supplemented cells treated with a non-targeting or Piezo1 siRNA, as measured by the fold change in GCaMP fluorescence (mean +/- SEM). E . Fold change in mRNA after Piezo1 RNAi, as measured by RT-qPCR (mean +/- SEM). F . Fold change in Piezo1 mRNA after Fluvastatin treatment (10 µM; 12 hr), as measured by RT-qPCR (mean +/- SEM). G . Relative transmigration of cells treated with a Piezo1 siRNA through 5 µm pores towards fetal bovine serum (FBS; 10%) (mean +/- SEM). H . Assay used to variably (≥ 3 µm) confine cells under non-adherent (BSA; 1%) conditions. I. - K . Intracellular Ca 2+ levels in vehicle, Fluvastatin (10 µM), and Fluvastatin (10 µM) + cholesterol (1 mM) treated variably confined (≥ 3 µm) cells under non-adherent conditions (BSA; 1%). We measured intracellular Ca 2+ levels by taking the ratio of a red fluorescent Ca 2+ indicator to a green fluorescent dye. Spearman rank correlation coefficients were used to determine statistical significance. Significance levels: * - p ≤ 0.05, ** - p ≤ 0.01, *** - p ≤ 0.001, and **** - p ≤ 0.0001. See also Figure S1.

Techniques: Transfection, Fluorescence, Comparison, Quantitative RT-PCR, Transmigration Assay

A. Assay used to vertically confine cells down to ∼3 µm under non-adherent (BSA; 1%) conditions. B . Percentage of leader mobile (LM), leader non-mobile (LNM), and no leader (NL) for vehicle ( n = 297), Fluvastatin (10 µM; n = 270) (χ 2 < 0.0001), Fluvastatin (10 µM) + Piezo1/2 activator (1 µM; n = 246) (χ 2 = 0.4346), and Piezo1/2 activator (1 µM; n = 225) (χ 2 = 0.1825) treated cells. C. - D . Speed (median +/- 95% CI) and directionality (mean +/- SEM) for vehicle ( n = 297), Fluvastatin (10 µM; n = 270), Fluvastatin (10 µM) + Piezo1/2 activator (1 µM; n = 246), and Piezo1/2 activator (1 µM; n = 225) treated leader mobile (LM) cells. E . Assay used for 3D confinement under adherent (VCAM-1; 1 µg/mL) conditions. F . Percentage of vehicle ( n = 125), Fluvastatin (10 µM; n = 170) (χ 2 < 0.0001), Fluvastatin (10 µM) + Piezo1/2 activator (1 µM; n = 147) (χ 2 = 0.0052), and Piezo1/2 activator (1 µM; n = 101) (χ 2 < 0.0001) treated cells adopting a hybrid, amoeboid, or mesenchymal phenotype in VCAM-1 (1 µg/mL) coated microchannels. G . Model depicting the role of plasma membrane cholesterol in transmitting tension to Piezo1, promoting the transition to amoeboid ( i . e ., bleb-based) migration in confined environments. H . Table of cholesterol biosynthesis enzyme levels (transcripts per million; TPM) for primary and metastatic tumors, hazard ratios, and prognosis for skin cutaneous melanoma (SKCM). Significance levels: * - p ≤ 0.05, ** - p ≤ 0.01, *** - p ≤ 0.001, and **** - p ≤ 0.0001. See also source data 1.

Journal: bioRxiv

Article Title: Targeting Cholesterol-Dependent Piezo1 Activation Impairs Amoeboid Migration in Melanoma Cells

doi: 10.1101/2025.07.11.664494

Figure Lengend Snippet: A. Assay used to vertically confine cells down to ∼3 µm under non-adherent (BSA; 1%) conditions. B . Percentage of leader mobile (LM), leader non-mobile (LNM), and no leader (NL) for vehicle ( n = 297), Fluvastatin (10 µM; n = 270) (χ 2 < 0.0001), Fluvastatin (10 µM) + Piezo1/2 activator (1 µM; n = 246) (χ 2 = 0.4346), and Piezo1/2 activator (1 µM; n = 225) (χ 2 = 0.1825) treated cells. C. - D . Speed (median +/- 95% CI) and directionality (mean +/- SEM) for vehicle ( n = 297), Fluvastatin (10 µM; n = 270), Fluvastatin (10 µM) + Piezo1/2 activator (1 µM; n = 246), and Piezo1/2 activator (1 µM; n = 225) treated leader mobile (LM) cells. E . Assay used for 3D confinement under adherent (VCAM-1; 1 µg/mL) conditions. F . Percentage of vehicle ( n = 125), Fluvastatin (10 µM; n = 170) (χ 2 < 0.0001), Fluvastatin (10 µM) + Piezo1/2 activator (1 µM; n = 147) (χ 2 = 0.0052), and Piezo1/2 activator (1 µM; n = 101) (χ 2 < 0.0001) treated cells adopting a hybrid, amoeboid, or mesenchymal phenotype in VCAM-1 (1 µg/mL) coated microchannels. G . Model depicting the role of plasma membrane cholesterol in transmitting tension to Piezo1, promoting the transition to amoeboid ( i . e ., bleb-based) migration in confined environments. H . Table of cholesterol biosynthesis enzyme levels (transcripts per million; TPM) for primary and metastatic tumors, hazard ratios, and prognosis for skin cutaneous melanoma (SKCM). Significance levels: * - p ≤ 0.05, ** - p ≤ 0.01, *** - p ≤ 0.001, and **** - p ≤ 0.0001. See also source data 1.

Techniques: Clinical Proteomics, Membrane, Migration

Percentage of leader mobile (LM), leader non-mobile (LNM), and no leader (NL) for vehicle ( n = 334), Fluvastatin (10 µM; n = 340) (χ 2 < 0.0001), Fluvastatin (10 µM) + MYPT1 RNAi ( n = 530) (χ 2 < 0.0001), and MYPT1 RNAi ( n = 320) (χ 2 < 0.0001) cells. B . Fold change in mRNA after MYPT1 RNAi, as measured by RT-qPCR (mean +/- SEM). C . Western blots against phosphorylated regulatory light chain (pRLC; S19) and regulatory light chain (RLC) from lysates of vehicle, Fluvastatin (10 µM; 3 hr), and Fluvastatin (10 µM; 3 hr) + cholesterol (1 mM; 3 hr) treated cells (mean +/- SEM). A Dunnett’s multiple comparison test was used to determine statistical significance. D . Normalized emission ratio for Eevee-ROCK from starved cells pre- treated (2 hr) with vehicle or Fluvastatin (10 µM). Fetal bovine serum (FBS; 10%) was added after 5 min (mean +/- SEM). Significance levels: * - p ≤ 0.05, ** - p ≤ 0.01, *** - p ≤ 0.001, and **** - p ≤ 0.0001. See also source data 1.

Journal: bioRxiv

Article Title: Targeting Cholesterol-Dependent Piezo1 Activation Impairs Amoeboid Migration in Melanoma Cells

doi: 10.1101/2025.07.11.664494

Figure Lengend Snippet: Percentage of leader mobile (LM), leader non-mobile (LNM), and no leader (NL) for vehicle ( n = 334), Fluvastatin (10 µM; n = 340) (χ 2 < 0.0001), Fluvastatin (10 µM) + MYPT1 RNAi ( n = 530) (χ 2 < 0.0001), and MYPT1 RNAi ( n = 320) (χ 2 < 0.0001) cells. B . Fold change in mRNA after MYPT1 RNAi, as measured by RT-qPCR (mean +/- SEM). C . Western blots against phosphorylated regulatory light chain (pRLC; S19) and regulatory light chain (RLC) from lysates of vehicle, Fluvastatin (10 µM; 3 hr), and Fluvastatin (10 µM; 3 hr) + cholesterol (1 mM; 3 hr) treated cells (mean +/- SEM). A Dunnett’s multiple comparison test was used to determine statistical significance. D . Normalized emission ratio for Eevee-ROCK from starved cells pre- treated (2 hr) with vehicle or Fluvastatin (10 µM). Fetal bovine serum (FBS; 10%) was added after 5 min (mean +/- SEM). Significance levels: * - p ≤ 0.05, ** - p ≤ 0.01, *** - p ≤ 0.001, and **** - p ≤ 0.0001. See also source data 1.

Techniques: Quantitative RT-PCR, Western Blot, Comparison

(A) Ingenuity Pathway Analysis (IPA) of RNAseq for activated (red bars) and inhibited (blue bars) pathways on bone marrow derived macrophages (BMDMs) pre-treated with hippuric acid (10µM) for 1hr and then stimulated with LPS (100ng/ml) plus IFNγ (100ng/ml) for 8hr. Differentially expressed genes passing FDR <5% were used. n=3. (B) RNAseq analysis of BMDMs treated as in (A) for heatmap showing differential gene expression of indicated RNA transcripts of lipid metabolism using the LIPID MAPS proteome database (LMPD). Differentially expressed genes passing FDR <5% and fold change >1.5 were used. n=3. (C) Lipidomics analysis of BMDMs treated as in (A) for volcano plot showing changes in individual lipid species. Lipidomics was performed using LC-MS/MS. n=4. (D) Lipidomics analysis of BMDMs treated as in (A) for changes in lipid classes shown as bar graphs. n=4. (E) Colorimetric assay for cholesterol quantitation in BMDMs obtained from wild type or MyD88 KO mice and pre-treated with hippuric acid (10µM) for 1hr and then stimulated with LPS (100ng/ml) plus IFNγ (100ng/ml) for 8hr. n=4. (F) ELISA showing measurements of IL-12p40 and IL-6 production by BMDMs obtained from wild type or MyD88 KO mice and pre-treated with hippuric acid (10µM) or fluvastatin (10µM) for 1hr and then stimulated with LPS (100ng/ml) plus IFNγ (100ng/ml) for 8hr. n=4. In (C), significant change was defined as |FC| > 2; q < 0.1 (Benjamini-Hochberg FDR-adjusted P value). In (D), P values were determined by two-tailed Student’s t-tests . In (E-F), P values were determined by two-way ANOVA with post hoc multiple comparisons. Data are presented as means ± SD.

Journal: bioRxiv

Article Title: Aromatic Microbial Metabolite Hippuric Acid Potentiates Pro-Inflammatory Responses in Macrophages through TLR-MyD88 Signaling and Lipid Remodeling

doi: 10.1101/2025.05.19.654724

Figure Lengend Snippet: (A) Ingenuity Pathway Analysis (IPA) of RNAseq for activated (red bars) and inhibited (blue bars) pathways on bone marrow derived macrophages (BMDMs) pre-treated with hippuric acid (10µM) for 1hr and then stimulated with LPS (100ng/ml) plus IFNγ (100ng/ml) for 8hr. Differentially expressed genes passing FDR <5% were used. n=3. (B) RNAseq analysis of BMDMs treated as in (A) for heatmap showing differential gene expression of indicated RNA transcripts of lipid metabolism using the LIPID MAPS proteome database (LMPD). Differentially expressed genes passing FDR <5% and fold change >1.5 were used. n=3. (C) Lipidomics analysis of BMDMs treated as in (A) for volcano plot showing changes in individual lipid species. Lipidomics was performed using LC-MS/MS. n=4. (D) Lipidomics analysis of BMDMs treated as in (A) for changes in lipid classes shown as bar graphs. n=4. (E) Colorimetric assay for cholesterol quantitation in BMDMs obtained from wild type or MyD88 KO mice and pre-treated with hippuric acid (10µM) for 1hr and then stimulated with LPS (100ng/ml) plus IFNγ (100ng/ml) for 8hr. n=4. (F) ELISA showing measurements of IL-12p40 and IL-6 production by BMDMs obtained from wild type or MyD88 KO mice and pre-treated with hippuric acid (10µM) or fluvastatin (10µM) for 1hr and then stimulated with LPS (100ng/ml) plus IFNγ (100ng/ml) for 8hr. n=4. In (C), significant change was defined as |FC| > 2; q < 0.1 (Benjamini-Hochberg FDR-adjusted P value). In (D), P values were determined by two-tailed Student’s t-tests . In (E-F), P values were determined by two-way ANOVA with post hoc multiple comparisons. Data are presented as means ± SD.

Article Snippet: BMDMs were treated with Fluvastatin (100uM; Cayman chemical, 10010334) and Simvastatin (10uM; Cayman chemical, 10010344) for 8 hours following HA (100uM) treatment for 1 hour.

Techniques: Derivative Assay, Gene Expression, Liquid Chromatography with Mass Spectroscopy, Colorimetric Assay, Quantitation Assay, Enzyme-linked Immunosorbent Assay, Two Tailed Test

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