Journal: Frontiers in Immunology

Article Title: miR-223 alleviates DSS-induced colitis by prompting macrophage M2 polarization through PPAR-γ/FOXO1 signaling

doi: 10.3389/fimmu.2025.1598781

Figure Lengend Snippet: Relieving colitis by miR-223 through the promotion of macrophage M2 polarization via the modulation of PPAR-γ/FOXO1 signaling. (A) Representative images of western blots indicating the protein expression levels of PPAR-γ and FOXO1. The data represent the findings from three independent experiments. (B, C) Changes in the expression of PPAR-γ and FOXO1. (D, E) Changes in the mRNA levels of PPAR-γ and FOXO1. All the data are expressed as the means ± SDs (n=6 each group). *p<0.05, **p<0.01, ***p<0.001. (F, G) Correlations of colonic miR-223 expression with PPAR-γ and FOXO1 expression in the colon. Pearson analyses were used to correlate miR-223 with colonic PPAR-γ and FOXO1 expression. PPAR-γ, peroxisome proliferator-activated receptor gamma; FOXO1, Forkhead box transcription factor O1.

Article Snippet: After being blocked with bovine serum albumin blocking buffer (3% in PBS), the slides were incubated with the following primary antibodies: anti-PPAR-γ antibody (1:3000) (Cat.# GB11163, Servicebio, Wuhai, China), anti-FOXO1 antibody (1:10000) (Cat.# GB11286-1, Servicebio), anti-CD206 (1:5000) (Cat.# GB113497 , Servicebio), anti-CD86 (1:5000) (Cat.# GB115630 , Servicebio) or anti-F4/80 (1:2000) (Cat.# GB113373 , Servicebio) overnight at 4°C.

Techniques: Western Blot, Expressing

Journal: Frontiers in Immunology

Article Title: miR-223 alleviates DSS-induced colitis by prompting macrophage M2 polarization through PPAR-γ/FOXO1 signaling

doi: 10.3389/fimmu.2025.1598781

Figure Lengend Snippet: Immunofluorescence analysis of PPAR-γ and M2 macrophage marker CD206 in colonic tissue. Representative micrographs depict protein expression levels of PPAR-γ (red) and its co-localization (yellow) with CD206 (green) in colon sections. Nuclei were counterstained with DAPI (blue). Scale bar: 100 µm.

Article Snippet: After being blocked with bovine serum albumin blocking buffer (3% in PBS), the slides were incubated with the following primary antibodies: anti-PPAR-γ antibody (1:3000) (Cat.# GB11163, Servicebio, Wuhai, China), anti-FOXO1 antibody (1:10000) (Cat.# GB11286-1, Servicebio), anti-CD206 (1:5000) (Cat.# GB113497 , Servicebio), anti-CD86 (1:5000) (Cat.# GB115630 , Servicebio) or anti-F4/80 (1:2000) (Cat.# GB113373 , Servicebio) overnight at 4°C.

Techniques: Immunofluorescence, Marker, Expressing

Journal: Frontiers in Immunology

Article Title: miR-223 alleviates DSS-induced colitis by prompting macrophage M2 polarization through PPAR-γ/FOXO1 signaling

doi: 10.3389/fimmu.2025.1598781

Figure Lengend Snippet: Schematic representation of the potential mechanisms underlying the targeted therapy of miR-223 supplement for DSS-induced colitis. miR-223 ameliorates DSS-induced colitis through promoting macrophage M2 polarization via modulation of PPAR-γ and FOXO1 signaling. DSS, dextran sodium sulfate.

Article Snippet: After being blocked with bovine serum albumin blocking buffer (3% in PBS), the slides were incubated with the following primary antibodies: anti-PPAR-γ antibody (1:3000) (Cat.# GB11163, Servicebio, Wuhai, China), anti-FOXO1 antibody (1:10000) (Cat.# GB11286-1, Servicebio), anti-CD206 (1:5000) (Cat.# GB113497 , Servicebio), anti-CD86 (1:5000) (Cat.# GB115630 , Servicebio) or anti-F4/80 (1:2000) (Cat.# GB113373 , Servicebio) overnight at 4°C.

Techniques:

Journal: Heliyon

Article Title: Pharmacological investigation of taxifolin for its therapeutic potential in depression

doi: 10.1016/j.heliyon.2024.e30467

Figure Lengend Snippet: The best conformational pose, binding energy (kcal/mol), number of hydrogen bonds, bonding residues forming other hydrophobic interactions, of taxifolin and fluoxetine with target proteins such as peroxisome proliferator-activated receptor gamma (PPAR-γ), cyclooxygenase-2 (COX-2), Toll like receptor-4 (TLR4), c-Jun N-terminal kinase (JNK), brain-derived neurotrophic factor (BDNF), monoamine oxidase A (MAO-A), heme oxygenase-1 (HO-1), cyclooxygenase-1 (COX-1), sodium channels (NA+),Glutamate receptor (GRM2), phosphoinositide 3-kinase (PI3k), tumor necrosis factor-alpha (TNF-α), prostaglandins (PGE2), mitogen activated protein kinases (MAPK), Beta- 2 adrenergic receptor (ADRB2), Neurokinin receptor (NK-1), Procaspase activating compound (PAC-1), nuclear factor kappa B (NF-κB), nitric oxidase synthesis (iNOS), interleukin-4 (IL-4), high mobility group box 1 (HMGB1), Protein -c –fos, Beta catenin (β-Catenin), serotonin receptors (SERT), nuclear factor erythroid 2-related factor 2 (Nrf2), vasoactive intestinal peptide (VIP), Gamma-aminobutyric acid (GABA A), peptidoglycan (PG), interleukin-2 (IL-2), Dopamine receptor (D2).

Article Snippet: The ELISA kit COX-2 (CAT# PRS-30205Ra) and the ELISA kit PPAR gamma (CAT# E-EL-R0724) were supplied by Elabscience.

Techniques: Binding Assay

Journal: Heliyon

Article Title: Pharmacological investigation of taxifolin for its therapeutic potential in depression

doi: 10.1016/j.heliyon.2024.e30467

Figure Lengend Snippet: Effects of Taxifolin and Fluoxetine against (A) Peroxisomes proliferation-activated receptor-γ (PPAR-γ) and (B) Cyclooxygenase-2 (COX-2) concentration in rat's cortex tissues using enzyme linked immunosorbent assay technique (ELISA). Values expressed as mean ± SEM (n = 6). One-way ANOVA with post hoc Tukey’ s test. ### P < 0.001 vs. saline group, *P < 0.05, **P < 0.01, ***P < 0.001 vs. LPS group.

Article Snippet: The ELISA kit COX-2 (CAT# PRS-30205Ra) and the ELISA kit PPAR gamma (CAT# E-EL-R0724) were supplied by Elabscience.

Techniques: Concentration Assay, Enzyme-linked Immunosorbent Assay, Saline

Journal: Heliyon

Article Title: Pharmacological investigation of taxifolin for its therapeutic potential in depression

doi: 10.1016/j.heliyon.2024.e30467

Figure Lengend Snippet: Effects of Taxifolin and Fluoxetine against Peroxisomes proliferation-activated receptor-γ (PPAR-γ) by RT-PCR. Values expressed as mean ± SEM (n = 6). One-way ANOVA with post hoc Tukey’ s test. ### P < 0.001 vs saline group, **P < 0.01, ***P < 0.001 vs. LPS group.

Article Snippet: The ELISA kit COX-2 (CAT# PRS-30205Ra) and the ELISA kit PPAR gamma (CAT# E-EL-R0724) were supplied by Elabscience.

Techniques: Reverse Transcription Polymerase Chain Reaction, Saline

Journal: bioRxiv

Article Title: PPARG directs trophoblast cell fate and establishment of the uterine-placental interface

doi: 10.1101/2025.10.08.681177

Figure Lengend Snippet: A ) Two significantly enriched PPARG binding motifs were observed within PPARG ChIP-seq peaks. B ) Number of peaks observed within specific locations of the genome. C ) Pie chart showing the distribution of PPARG peaks in genomic regions for all genes and protein-coding genes. D ) Venn diagram showing the integration of PPARG responsive genes identified by RNA-seq of EVT cells ( see ) and PPARG gene targets identified by PPARG ChIP-seq from EVT cells. E ) Gene ontology ( GO ) analysis of the PPARG ChIP-seq dataset performed on EVT cells. F ) GO analysis of an integrated dataset generated from PPARG responsive genes identified by RNA-seq of EVT cells ( see ) and PPARG gene targets identified by PPARG ChIP-seq from EVT cells. G ) PPARG ChIP-Seq peaks at selected gene loci that exhibit sensitivity to PPARG inhibition. Visualization was performed using the University of California at Santa Cruz Genome browser. Red peaks represent PPARG bound regions, whereas black peaks represent the input DNA.

Article Snippet: Membranes were subsequently blocked with 5% milk for 1 h at room temperature, followed by incubation with antibodies to PPARG (1:500, 2435S, Cell Signaling Technology or GAPDH (1:5,000, AM4300, Invitrogen) in 5% milk overnight at 4°C.

Techniques: Binding Assay, ChIP-sequencing, RNA Sequencing, Generated, Inhibition

Journal: Journal of translational medicine

Article Title: Identification of matrix stiffness-related molecular subtypes in HCC via integrating multi-omics analysis and machine learning algorithms.

doi: 10.1186/s12967-025-06733-7

Figure Lengend Snippet: Fig. 8 The expression pattern and tissue localization of PPARG in tumor samples. (A) PPARG expression levels in tumor and normal samples of the TCGA dataset. (B) PPARG was correlated with pathological grades in the TCGA dataset. (C) Survival analysis of OS time between high and low-PPARG groups. (D) Survival analysis of DSS time between high and low-PPARG groups. (E) Correlation analyses between PPARG expression and tumor phenotypes. (F, H, J) PPARG expression in different cell types of spatial transcriptomics. F: LIHC1, H: LIHC2, J: LIHC3. (G, I, K) The comparisons of PPARG expression levels between malignant and normal samples. (L) The visualizations of the relationship between PPARG expression and various components of TME

Article Snippet: The PPARG shRNA plasmid (#sc-29456) and the full-length PPARG overexpression plasmid (PLVX3flag-PPARG) were obtained from Santa Cruz Biotechnology, Inc. and Tsingke Biotech Co. (Beijing, China), respectively.

Techniques: Expressing

Journal: Journal of translational medicine

Article Title: Identification of matrix stiffness-related molecular subtypes in HCC via integrating multi-omics analysis and machine learning algorithms.

doi: 10.1186/s12967-025-06733-7

Figure Lengend Snippet: Fig. 9 PPARG-mediated matrix stiffness induced cell proliferation, lipogenesis, and cancer stem features of HCC cells. (A) 16 kPa stiffness level promoted the proliferation ability of HepG2 cells, confirmed by colony formation assay. (B) 16 kPa stiffness level promoted lipogenesis of HepG2 cells, confirmed by BODIPY 493/503 staining assay. (C) 16 kPa stiffness level elevated cancer stemness in tumor sphere formation assay. Figure 9A-C all proved that the knockdown of PPARG abrogated the high stiffness-mediated tumor-promotion effects. (D) Western blot assay demonstrated that 16 kPa stiffness level greatly increased the expression of PPARG, fatty acid metabolism-related genes (ACC1, FASN), and cancer stemness-related genes (CD44, EPCAM, and ALDH1A1) in HepG2 cells. While silencing PPARG repressed the stiffness-induced upregulation of these genes. The magnification is ×200, with scale bars representing 50 μm. Data are based on three independent experiments (n = 3). *P < 0.01, determined using one-way ANOVA

Article Snippet: The PPARG shRNA plasmid (#sc-29456) and the full-length PPARG overexpression plasmid (PLVX3flag-PPARG) were obtained from Santa Cruz Biotechnology, Inc. and Tsingke Biotech Co. (Beijing, China), respectively.

Techniques: Colony Assay, Staining, Tube Formation Assay, Knockdown, Western Blot, Expressing

Journal: Journal of translational medicine

Article Title: Identification of matrix stiffness-related molecular subtypes in HCC via integrating multi-omics analysis and machine learning algorithms.

doi: 10.1186/s12967-025-06733-7

Figure Lengend Snippet: Fig. 10 Targeting PPARG repressed tumorigenicity and HCC growth in vivo. (A-C) PPARG depletion effectively suppressed HCC tumor growth compared with the shControl group. (D-E) Immunohistochemical analysis of subcutaneous tumor tissues from the PPARG depletion group compared to specimens from the shControl group. Magnification is × 400, the scale bar represents 20 μm, n = 6. (D, F) Sirius Red staining and Masson staining visualized the col lagen deposit in the stroma of the subcutaneous tumor. Magnification is × 400, the scale bar represents 20 μm, n = 6

Article Snippet: The PPARG shRNA plasmid (#sc-29456) and the full-length PPARG overexpression plasmid (PLVX3flag-PPARG) were obtained from Santa Cruz Biotechnology, Inc. and Tsingke Biotech Co. (Beijing, China), respectively.

Techniques: In Vivo, Immunohistochemical staining, Staining

Journal: Journal of translational medicine

Article Title: Identification of matrix stiffness-related molecular subtypes in HCC via integrating multi-omics analysis and machine learning algorithms.

doi: 10.1186/s12967-025-06733-7

Figure Lengend Snippet: Fig. 11 MAPK cascades were identified as the downstream signaling of PPARG under a matrix stiffness microenvironment. (A) The binding proteins of PPARG in the BioGRID database. (B) The binding proteins of PPARG in the ComPPI database. (C, D) HepG2 cells with PPARG knockdown were cultured on 0.5 kPa and 16 kPa gels. Western blot assay was used to detect the expression of PPARG, p-ERK1/2, and p-JNK1/2 under a matrix stiffness microenviron ment. *P < 0.05

Article Snippet: The PPARG shRNA plasmid (#sc-29456) and the full-length PPARG overexpression plasmid (PLVX3flag-PPARG) were obtained from Santa Cruz Biotechnology, Inc. and Tsingke Biotech Co. (Beijing, China), respectively.

Techniques: Binding Assay, Knockdown, Cell Culture, Western Blot, Expressing

Journal: PLoS ONE

Article Title: Transcriptional Regulation of Flotillins by the Extracellularly Regulated Kinases and Retinoid X Receptor Complexes

doi: 10.1371/journal.pone.0045514

Figure Lengend Snippet: Oligonucleotides and plasmids.

Article Snippet: pSV Sport PPARγ , PPARγ expression plasmid , Addgene 8886, .

Techniques: Luciferase, Plasmid Preparation, Expressing, Control, Dominant Negative Mutation

Journal: PLoS ONE

Article Title: Transcriptional Regulation of Flotillins by the Extracellularly Regulated Kinases and Retinoid X Receptor Complexes

doi: 10.1371/journal.pone.0045514

Figure Lengend Snippet: Flotillin promoter constructs F1-1330 (A, C) or F2-2130 (B, D) were cotransfected into Hela cells together with expression plasmids for RAR, RXR, PPARγ or with empty PSV control plasmid. One day post-transfection, the cells were stimulated with trans-RA (1 µM) for 24 h in serum-free medium. Relative luciferase activity of the unstimulated control sample was set as 1. F1-1330 (E) and F2-2130 (F) transfected Hela cells were stimulated with troglitazone for 24 h in serum-free medium. Values are mean ± standard deviation of at least 3 experiments measured in duplicates. ***p<0.001; **p<0.01; *p<0.05 vs. respective control.

Article Snippet: pSV Sport PPARγ , PPARγ expression plasmid , Addgene 8886, .

Techniques: Construct, Expressing, Control, Plasmid Preparation, Transfection, Luciferase, Activity Assay, Standard Deviation

Journal: PLoS ONE

Article Title: Transcriptional Regulation of Flotillins by the Extracellularly Regulated Kinases and Retinoid X Receptor Complexes

doi: 10.1371/journal.pone.0045514

Figure Lengend Snippet: Hela cells were transiently transfected with expression constructs for RAR, RXR, or a combination of both. Empty PSV vector served as a control. One day post-transfection, the cells were stimulated with trans-RA (1 µM) in serum-free medium for 24 h. Cell lysates were analyzed for flotillin-1 (A), flotillin-2 (B), RAR and RXR (C) by Western blotting. D and E show a densitometric quantification of flotillin expression. F: Cells were transfected with RAR or PPARγ expression construct or empty PSV. RNA was isolated, transcribed into cDNA and flotillin mRNA was measured by qPCR. Values are mean ± standard deviation of at least 3 experiments. ###, p<0.001; #, p<0.05; vs control *, p<0.05 vs. unstimulated sample.

Article Snippet: pSV Sport PPARγ , PPARγ expression plasmid , Addgene 8886, .

Techniques: Transfection, Expressing, Construct, Plasmid Preparation, Control, Western Blot, Isolation, Standard Deviation

Journal: British journal of pharmacology

Article Title: Inactivation of SERCA2 Cys 674 accelerates aortic aneurysms by suppressing PPARγ.

doi: 10.1111/bph.15411

Figure Lengend Snippet: FIGURE 1 Inactivation of SERCA2 C674 suppresses PPARγ by activation of calcineurin/ NFAT/NF-κB pathways. (a) The main signalling pathways from the Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis in duplicate aorta samples of WT and SKI mice in LDLR−/−background. (b) The mRNA levels of PPARγ2 in aortas of WT and SKI mice in LDLR−/−

Article Snippet: The PPARγ2 plasmids (ORIGENE, Cat# MR208132) or its control CMV-GFP plasmids (ORIGENE, Cat# PS100040) were transfected into SKI SMCs according to Effectene® Transfection Reagent Handbook (Qiagen, Cat#301305).

Techniques: Activation Assay

Journal: British journal of pharmacology

Article Title: Inactivation of SERCA2 Cys 674 accelerates aortic aneurysms by suppressing PPARγ.

doi: 10.1111/bph.15411

Figure Lengend Snippet: FIGURE 3 The down-regulation of PPARγ2 accounts for the phenotypic modulation of SKI SMCs. (a) Representative western blots from SKI aortic SMCs transfected with PPARγ2 plasmids and quantification of band intensities in graph. Data shown are means ± SEM; n = 5. *P < .05, significantly different as indicated; unpaired Student's t test.. (b) Cell proliferation. (c) Cell migration. (d) Macrophage adhesion to aortic SMCs. In (b–d), data shown are means ± SEM; n = 6. *P < .05, significantly different as indicated; unpaired Student's t test

Article Snippet: The PPARγ2 plasmids (ORIGENE, Cat# MR208132) or its control CMV-GFP plasmids (ORIGENE, Cat# PS100040) were transfected into SKI SMCs according to Effectene® Transfection Reagent Handbook (Qiagen, Cat#301305).

Techniques: Western Blot, Transfection, Migration