Journal: Redox Biology

Article Title: PPARγ contributes to cardioprotection against heat stroke through ABCC5-dependent lipid metabolism

doi: 10.1016/j.redox.2026.104113

Figure Lengend Snippet: RNA-seq identifies ABCC5 as a potential key downstream effector of PPARγ in HS. (A) Volcano plot illustrating differentially expressed genes between the WT + HS and PPARγ-OE + HS groups. (B) GO enrichment analysis of differentially expressed genes between the WT + HS and PPARγ-OE + HS groups. (C) KEGG pathway enrichment analysis of DEGs between the WT + HS and PPARγ-OE + HS groups. (D) Heatmap displaying expression changes of ABC transporter family members across the indicated groups. (E) Measurement of cellular free fatty acids and triglycerides in cells under the indicated treatments. (F) RT-qPCR analysis of PPARγ mRNA expression in PPARγ NC + HS and PPARγ OE + HS cells. (G) RT-qPCR analysis of selected ABC transporter genes (ABCC5, ABCB1A, ABCC6, TAP2, ABCA6, ABCB4, ABCC10, ABCA2, ABCG4, ABCA1, ABCA8A, ABCA9, ABCB2, ABCB7, and ABCA3) under the specified conditions. Error bars represent mean ± SD (n = 3). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, and ∗∗∗∗ P < 0.0001 versus the PPARγ-NC + HS group (E–G). Statistical comparisons were performed using Student's t-test (F–G) or one-way ANOVA (E).

Article Snippet: For immunofluorescence, tissues and cells were fixed in 4% paraformaldehyde, permeabilized with 0.5% Triton X-100, and blocked with 5% normal goat serum in PBS for 1 h. Sections and cells were then incubated overnight at 4 °C with primary antibodies against PPARγ (Proteintech, 66936-1-1g) and ABCC5 (Bioss, bs-1437R), followed by incubation with appropriate secondary antibodies for 1 h. Images were acquired using a fluorescence microscope (Invitrogen EVOS M5000, Thermo Fisher Scientific, Waltham, MA, USA), and fluorescence intensity was quantified with ImageJ Pro Plus software.

Techniques: RNA Sequencing, Expressing, Quantitative RT-PCR

Journal: Redox Biology

Article Title: PPARγ contributes to cardioprotection against heat stroke through ABCC5-dependent lipid metabolism

doi: 10.1016/j.redox.2026.104113

Figure Lengend Snippet: Time-dependent changes in ABCC5 expression in vivo. (A) Representative immunofluorescence images of ABCC5 (green) and DAPI (blue) in cardiac tissues from sham mice and from mice subjected to HS at the indicated time points after injury. (B) Representative immunohistochemical staining of ABCC5 in cardiac tissues from sham and HS-injured mice. (C) RT-qPCR analysis of Leptin mRNA in cardiac tissues after 2.5 h or 3 weeks of heat injury. (D) Representative immunofluorescence images of ABCC5 in cardiac sections from PPARγ-cKO mice after HS). (E–F) Representative immunofluorescence images of PPARγ and ABCC5 in cardiac sections from PPARγ-cKO mice at 3 weeks after HS). Error bars represent mean ± SD (n = 3). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, and ∗∗∗∗ P < 0.0001 versus the sham group (B–C). Statistical comparisons were performed using Student's t-test (B) or one-way ANOVA (C).

Article Snippet: For immunofluorescence, tissues and cells were fixed in 4% paraformaldehyde, permeabilized with 0.5% Triton X-100, and blocked with 5% normal goat serum in PBS for 1 h. Sections and cells were then incubated overnight at 4 °C with primary antibodies against PPARγ (Proteintech, 66936-1-1g) and ABCC5 (Bioss, bs-1437R), followed by incubation with appropriate secondary antibodies for 1 h. Images were acquired using a fluorescence microscope (Invitrogen EVOS M5000, Thermo Fisher Scientific, Waltham, MA, USA), and fluorescence intensity was quantified with ImageJ Pro Plus software.

Techniques: Expressing, In Vivo, Immunofluorescence, Immunohistochemical staining, Staining, Quantitative RT-PCR

Journal: Redox Biology

Article Title: PPARγ contributes to cardioprotection against heat stroke through ABCC5-dependent lipid metabolism

doi: 10.1016/j.redox.2026.104113

Figure Lengend Snippet: ABCC5 siRNA abolishes the cardioprotective effects of PPARγ overexpression against HS ​. (A) Luciferase activity in cells co-transfected with ABCC5 wild-type or mutant (Mut1/2/3) reporter plasmids and adenovirus expressing PPARγ. (B) CUT&Tag assay using a PPARγ-specific antibody to detect PPARγ binding to the ABCC5 promoter. (C) RT-qPCR analysis of ABCC5 mRNA in cells transfected with control siRNA or ABCC5 siRNA. (D – F) Cell morphology and viability in cells transfected with ABCC5 siRNA and/or PPARγ overexpression vector under HS conditions. (G – H) Apoptosis levels measured by flow cytometry in cells transfected with ABCC5 siRNA and PPARγ-OE under HS conditions. (I – J) DCFH-DA staining for ROS detection in cells transfected with ABCC5 siRNA and PPARγ-OE under HS conditions. (K – L) Mitochondrial membrane potential assessed by JC-1 fluorescence in the indicated groups. (M) Western blot analysis of PPARγ, ABCC5, ABCC1, Leptin, and β-actin (loading control) in cells treated as follows: PPARγ-NC + HS, PPARγ-OE + HS, and PPARγ-OE + ABCC5 siRNA + HS. Molecular weight markers are shown on the right. (N) Quantification of protein levels normalized to β-actin, corresponding to the blots in (M). Data are presented as mean ± SD (n = 3). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001 versus the indicated control, PPARγ + ABCC5 group (A–B), control siRNA group (C), PPARγ-NC + HS group, PPARγ-OE + HS group, or PPARγ-OE + ABCC5 siRNA + HS group (D–L), or versus the PPARγ-NC + HS group and PPARγ-OE + HS group (M − N). Statistical comparisons were performed using one-way ANOVA.

Article Snippet: For immunofluorescence, tissues and cells were fixed in 4% paraformaldehyde, permeabilized with 0.5% Triton X-100, and blocked with 5% normal goat serum in PBS for 1 h. Sections and cells were then incubated overnight at 4 °C with primary antibodies against PPARγ (Proteintech, 66936-1-1g) and ABCC5 (Bioss, bs-1437R), followed by incubation with appropriate secondary antibodies for 1 h. Images were acquired using a fluorescence microscope (Invitrogen EVOS M5000, Thermo Fisher Scientific, Waltham, MA, USA), and fluorescence intensity was quantified with ImageJ Pro Plus software.

Techniques: Over Expression, Luciferase, Activity Assay, Transfection, Mutagenesis, Expressing, Binding Assay, Quantitative RT-PCR, Control, Plasmid Preparation, Flow Cytometry, Staining, Membrane, Fluorescence, Western Blot, Molecular Weight

Journal: Redox Biology

Article Title: PPARγ contributes to cardioprotection against heat stroke through ABCC5-dependent lipid metabolism

doi: 10.1016/j.redox.2026.104113

Figure Lengend Snippet: The PPARγ/ABCC5 pathway alleviates lipid accumulation in HS-injured mice ​. (A – D) Cardiac sections from sham mice and from mice at indicated time points after HS were stained with HE (A) , PSR (B) , Masson's trichrome (C) , or Oil Red O (D) (n = 3 per group). (E) Serum levels of HDL-C and LDL-C in sham mice and in mice 3 weeks after HS (n = 6–7 per group). Error bars represent mean ± SD. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, and ∗∗∗∗ P < 0.0001 versus the sham group. Statistical comparisons were performed using Student's t-test.

Article Snippet: For immunofluorescence, tissues and cells were fixed in 4% paraformaldehyde, permeabilized with 0.5% Triton X-100, and blocked with 5% normal goat serum in PBS for 1 h. Sections and cells were then incubated overnight at 4 °C with primary antibodies against PPARγ (Proteintech, 66936-1-1g) and ABCC5 (Bioss, bs-1437R), followed by incubation with appropriate secondary antibodies for 1 h. Images were acquired using a fluorescence microscope (Invitrogen EVOS M5000, Thermo Fisher Scientific, Waltham, MA, USA), and fluorescence intensity was quantified with ImageJ Pro Plus software.

Techniques: Staining

Journal: Redox Biology

Article Title: PPARγ contributes to cardioprotection against heat stroke through ABCC5-dependent lipid metabolism

doi: 10.1016/j.redox.2026.104113

Figure Lengend Snippet: Rosiglitazone pretreatment alleviates HS-induced myocardial injury via the PPARγ/ABCC5 pathway in HL-1 cells ​. (A – C) Cell viability and morphology in cells treated with different concentrations of rosiglitazone (5 μM, 10 μM, 20 μM, 40 μM) under HS conditions. (D – E) Apoptosis levels in cells treated with different concentrations of rosiglitazone under HS conditions. (F–I) DHE staining (F) and DCFH-DA staining (I) for ROS detection in cells treated with different concentrations of rosiglitazone under HS conditions. (J – K) Mitochondrial membrane potential assessed by JC-1 fluorescence in the indicated groups. (L) RT-qPCR analysis of PPARγ, ABCC5, Leptin, and SREBP-1c in cells treated with different concentrations of rosiglitazone under HS conditions. (M – N) Representative Western blots and quantification of PPARγ, ABCC5, ABCC1, ABCG1, ABCA1, and Leptin in cells treated with different concentrations of rosiglitazone under HS conditions. Error bars represent mean ± SD (n = 3). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, and ∗∗∗∗ P < 0.0001 versus the control group or the HS group. Statistical comparisons were performed using one-way ANOVA.

Article Snippet: For immunofluorescence, tissues and cells were fixed in 4% paraformaldehyde, permeabilized with 0.5% Triton X-100, and blocked with 5% normal goat serum in PBS for 1 h. Sections and cells were then incubated overnight at 4 °C with primary antibodies against PPARγ (Proteintech, 66936-1-1g) and ABCC5 (Bioss, bs-1437R), followed by incubation with appropriate secondary antibodies for 1 h. Images were acquired using a fluorescence microscope (Invitrogen EVOS M5000, Thermo Fisher Scientific, Waltham, MA, USA), and fluorescence intensity was quantified with ImageJ Pro Plus software.

Techniques: Staining, Membrane, Fluorescence, Quantitative RT-PCR, Western Blot, Control

Journal: Redox Biology

Article Title: PPARγ contributes to cardioprotection against heat stroke through ABCC5-dependent lipid metabolism

doi: 10.1016/j.redox.2026.104113

Figure Lengend Snippet: The PPARγ agonist rosiglitazone confers pharmacological protection against HS-induced myocardial dysfunction ​. (A – C) Cell viability and morphology in cells transfected with PPARγ siRNA and pretreated with rosiglitazone under HS conditions. (D – E) Apoptosis levels measured by flow cytometry in cells transfected with PPARγ siRNA and pretreated with rosiglitazone under HS conditions. (F) LDH release in cells transfected with PPARγ siRNA and pretreated with rosiglitazone under HS conditions. (G – H) DCFH-DA staining for ROS detection in cells transfected with PPARγ siRNA and pretreated with rosiglitazone under HS conditions. (I – J) Mitochondrial membrane potential assessed by JC-1 fluorescence in the indicated groups. (K) RT-qPCR analysis of PPARγ and CPT1β mRNA in cells transfected with PPARγ siRNA and pretreated with rosiglitazone under HS conditions. (L) Representative Western blots and quantification of PPARγ, ABCC5, PGC-1α, and PPARγ in cells transfected with PPARγ siRNA and pretreated with rosiglitazone under HS conditions. Error bars represent mean ± SD (n = 3). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, and ∗∗∗∗ P < 0.0001 versus the control group, the HS group, or the ROSI + HS group as indicated. Statistical comparisons were performed using one-way ANOVA.

Article Snippet: For immunofluorescence, tissues and cells were fixed in 4% paraformaldehyde, permeabilized with 0.5% Triton X-100, and blocked with 5% normal goat serum in PBS for 1 h. Sections and cells were then incubated overnight at 4 °C with primary antibodies against PPARγ (Proteintech, 66936-1-1g) and ABCC5 (Bioss, bs-1437R), followed by incubation with appropriate secondary antibodies for 1 h. Images were acquired using a fluorescence microscope (Invitrogen EVOS M5000, Thermo Fisher Scientific, Waltham, MA, USA), and fluorescence intensity was quantified with ImageJ Pro Plus software.

Techniques: Transfection, Flow Cytometry, Staining, Membrane, Fluorescence, Quantitative RT-PCR, Western Blot, Control

Journal: Redox Biology

Article Title: PPARγ contributes to cardioprotection against heat stroke through ABCC5-dependent lipid metabolism

doi: 10.1016/j.redox.2026.104113

Figure Lengend Snippet: The proposed scheme describing the signaling pathway of PPARγ/ABCC5-elicted cardioprotective effect against HS.

Article Snippet: For immunofluorescence, tissues and cells were fixed in 4% paraformaldehyde, permeabilized with 0.5% Triton X-100, and blocked with 5% normal goat serum in PBS for 1 h. Sections and cells were then incubated overnight at 4 °C with primary antibodies against PPARγ (Proteintech, 66936-1-1g) and ABCC5 (Bioss, bs-1437R), followed by incubation with appropriate secondary antibodies for 1 h. Images were acquired using a fluorescence microscope (Invitrogen EVOS M5000, Thermo Fisher Scientific, Waltham, MA, USA), and fluorescence intensity was quantified with ImageJ Pro Plus software.

Techniques:

Journal: Journal of Ocular Pharmacology and Therapeutics

Article Title: Expression of Multidrug Resistance Associated Protein 5 (MRP5) on Cornea and Its Role in Drug Efflux

doi: 10.1089/jop.2008.0084

Figure Lengend Snippet: Efflux of active drug PMEA from MDCKII-wt, MDR1, MRP2, and MRP5 cells preloaded with prodrug Bis (POM)-PMEA. HBSS with glucose was used to measure the relative efflux of transporters. Statistical significance was tested by two-factor ANOVA. **P ≤ 0.01 (n = 5).

Article Snippet: 18 MRP5 primers were designed from human MRP5 cDNA (Genbank Accession No: {"type":"entrez-nucleotide","attrs":{"text":"AB209454","term_id":"62088487","term_text":"AB209454"}} AB209454 ; http://www.ncbi.nlm.nih.gov/Genbank ; made available in the public domain by the National Center for Biotechnology Information [NCBI], Bethesda, MD).

Techniques:

Journal: Journal of Ocular Pharmacology and Therapeutics

Article Title: Expression of Multidrug Resistance Associated Protein 5 (MRP5) on Cornea and Its Role in Drug Efflux

doi: 10.1089/jop.2008.0084

Figure Lengend Snippet: (A) RT-PCR confirming the presence of MRP5 in rPCEC, SIRC, MDCKII-MRP5 (positive control), and GAPDH (internal control). A specific band at ~228 bp corresponding to MRP5 can be observed in all cell lines. A band at 294 bp represents internal control. (B) RT-PCR confirming the presence of MRP5 in SV40-HCEC (228 bp) and GAPDH (294 bp).

Article Snippet: 18 MRP5 primers were designed from human MRP5 cDNA (Genbank Accession No: {"type":"entrez-nucleotide","attrs":{"text":"AB209454","term_id":"62088487","term_text":"AB209454"}} AB209454 ; http://www.ncbi.nlm.nih.gov/Genbank ; made available in the public domain by the National Center for Biotechnology Information [NCBI], Bethesda, MD).

Techniques: Reverse Transcription Polymerase Chain Reaction, Positive Control, Control

Journal: Journal of Ocular Pharmacology and Therapeutics

Article Title: Expression of Multidrug Resistance Associated Protein 5 (MRP5) on Cornea and Its Role in Drug Efflux

doi: 10.1089/jop.2008.0084

Figure Lengend Snippet: Immunoprecipitation followed by Western blot indicating the presence of MRP5 in membrane fraction of SV40-HCEC and MDCKII-MRP5 (+ve control).

Article Snippet: 18 MRP5 primers were designed from human MRP5 cDNA (Genbank Accession No: {"type":"entrez-nucleotide","attrs":{"text":"AB209454","term_id":"62088487","term_text":"AB209454"}} AB209454 ; http://www.ncbi.nlm.nih.gov/Genbank ; made available in the public domain by the National Center for Biotechnology Information [NCBI], Bethesda, MD).

Techniques: Immunoprecipitation, Western Blot, Membrane, Control

Journal: Journal of Ocular Pharmacology and Therapeutics

Article Title: Expression of Multidrug Resistance Associated Protein 5 (MRP5) on Cornea and Its Role in Drug Efflux

doi: 10.1089/jop.2008.0084

Figure Lengend Snippet: Immunostaining of MRP5 on human cornea using the M511–54 monoclonal antibody. Specific staining can be observed on both apical and basolateral side of corneal epithelium and endothelium.

Article Snippet: 18 MRP5 primers were designed from human MRP5 cDNA (Genbank Accession No: {"type":"entrez-nucleotide","attrs":{"text":"AB209454","term_id":"62088487","term_text":"AB209454"}} AB209454 ; http://www.ncbi.nlm.nih.gov/Genbank ; made available in the public domain by the National Center for Biotechnology Information [NCBI], Bethesda, MD).

Techniques: Immunostaining, Staining

Journal: Journal of Ocular Pharmacology and Therapeutics

Article Title: Expression of Multidrug Resistance Associated Protein 5 (MRP5) on Cornea and Its Role in Drug Efflux

doi: 10.1089/jop.2008.0084

Figure Lengend Snippet: Efflux of active drug PMEA from MDCKII-MRP5 cells preloaded with prodrug Bis (POM)-PMEA in the presence and absence of Indomethacin (100 μM), MK-571 (25 μM), and Sulfinpyrazone (1 mM). Statistical significance was examined by two-factor ANOVA. **P ≤ 0.01 (n = 5).

Article Snippet: 18 MRP5 primers were designed from human MRP5 cDNA (Genbank Accession No: {"type":"entrez-nucleotide","attrs":{"text":"AB209454","term_id":"62088487","term_text":"AB209454"}} AB209454 ; http://www.ncbi.nlm.nih.gov/Genbank ; made available in the public domain by the National Center for Biotechnology Information [NCBI], Bethesda, MD).

Techniques:

Journal: Journal of Ocular Pharmacology and Therapeutics

Article Title: Expression of Multidrug Resistance Associated Protein 5 (MRP5) on Cornea and Its Role in Drug Efflux

doi: 10.1089/jop.2008.0084

Figure Lengend Snippet: Efflux of acyclovir was measured from MDCKII-MRP5, rPCEC, SIRC, and SV40-HCEC. Monolayers of cells were incubated with 3H-acyclovir under ATP-depleting conditions (10-mM sodium azide; 10-mM 2-deoxy-d-glucose) for 1 h at 37°C. HBSS with glucose was added, with and without 25, 50, 75 μM MK-571, and cumulative amount of acyclovir efflux was determined by measuring the radioactivity in the supernatant. Statistical significance was measured by two-factor ANOVA. **P ≤ 0.01 (n = 5).

Article Snippet: 18 MRP5 primers were designed from human MRP5 cDNA (Genbank Accession No: {"type":"entrez-nucleotide","attrs":{"text":"AB209454","term_id":"62088487","term_text":"AB209454"}} AB209454 ; http://www.ncbi.nlm.nih.gov/Genbank ; made available in the public domain by the National Center for Biotechnology Information [NCBI], Bethesda, MD).

Techniques: Incubation, Radioactivity

Journal: Journal of Ocular Pharmacology and Therapeutics

Article Title: Expression of Multidrug Resistance Associated Protein 5 (MRP5) on Cornea and Its Role in Drug Efflux

doi: 10.1089/jop.2008.0084

Figure Lengend Snippet: Efflux of PMEA from MDCKII-MRP5 cells preloaded with Bis (POM)-PMEA under ATP-depleting conditions (10-mM sodium azide; 10-mM 2-deoxy-d-glucose) for 1 h at 37°C. HBSS with glucose was added, with and without bimatoprost, latanoprost, and efflux was determined. Statistical significance was determined by two-factor ANOVA. **P ≤ 0.01 (n = 5).

Article Snippet: 18 MRP5 primers were designed from human MRP5 cDNA (Genbank Accession No: {"type":"entrez-nucleotide","attrs":{"text":"AB209454","term_id":"62088487","term_text":"AB209454"}} AB209454 ; http://www.ncbi.nlm.nih.gov/Genbank ; made available in the public domain by the National Center for Biotechnology Information [NCBI], Bethesda, MD).

Techniques:

Journal: Journal of Ocular Pharmacology and Therapeutics

Article Title: Expression of Multidrug Resistance Associated Protein 5 (MRP5) on Cornea and Its Role in Drug Efflux

doi: 10.1089/jop.2008.0084

Figure Lengend Snippet: TLC separation of PMEA and bis(POM)PMEA shown by autoradiography. MDCKII-MRP5, SV40-HCEC, and SIRC were loaded with 3H-bis(POM)PMEA and radioactivity present in the cellular extracts was quantified. Lane 1, bis(POM)PMEA standard; Lane 2, PMEA standard; Lane 3, donor, intracellular conversion of bis(POM)PMEA to PMEA in 60 min; Lane 4, MRP5; Lane 5, SV40-HCEC; Lane 6, SIRC.

Article Snippet: 18 MRP5 primers were designed from human MRP5 cDNA (Genbank Accession No: {"type":"entrez-nucleotide","attrs":{"text":"AB209454","term_id":"62088487","term_text":"AB209454"}} AB209454 ; http://www.ncbi.nlm.nih.gov/Genbank ; made available in the public domain by the National Center for Biotechnology Information [NCBI], Bethesda, MD).

Techniques: Autoradiography, Radioactivity

Journal: Journal of Ocular Pharmacology and Therapeutics

Article Title: Expression of Multidrug Resistance Associated Protein 5 (MRP5) on Cornea and Its Role in Drug Efflux

doi: 10.1089/jop.2008.0084

Figure Lengend Snippet: Efflux of drug was measured from MDCKII-wt, MDR1, MRP2, and MRP5 cells preloaded with 3H-acyclovir under ATP-depleting conditions (10 mM sodium azide; 10 mM 2-deoxy-d-glucose) for 1 h at 37°C. HBSS with glucose was added and comparative efflux of transporters was determined. Statistical significance was examined by two-factor ANOVA. **P ≤ 0.01 (n = 5).

Article Snippet: 18 MRP5 primers were designed from human MRP5 cDNA (Genbank Accession No: {"type":"entrez-nucleotide","attrs":{"text":"AB209454","term_id":"62088487","term_text":"AB209454"}} AB209454 ; http://www.ncbi.nlm.nih.gov/Genbank ; made available in the public domain by the National Center for Biotechnology Information [NCBI], Bethesda, MD).

Techniques:

Journal: In Silico Pharmacology

Article Title: Computational modeling to predict the functions and impact of drug transporters

doi: 10.1186/s40203-015-0012-3

Figure Lengend Snippet: Nomenclature and protein-based tissue expression of common drug transport proteins

Article Snippet: ABCC5 , MRP5 , Small intestine , Low , Human Protein Atlas.

Techniques: Expressing, Drug Transport Assay

Journal: Oxidative Medicine and Cellular Longevity

Article Title: Brusatol Enhances the Chemotherapy Efficacy of Gemcitabine in Pancreatic Cancer via the Nrf2 Signalling Pathway

doi: 10.1155/2018/2360427

Figure Lengend Snippet: Sequences of the primers used for quantitative real-time PCR.

Article Snippet: The antibodies used in this study were against Keap1 (AF5266), MDR1 (AF5185), and MRP5 (DF7149) (Affinity Biosciences, OH, USA); Nrf2 (ab62352), NQO1 (ab80588), HO-1 (ab68477), active caspase-3 (ab2302), and Ki-67 (ab16667) (Abcam Inc., MA, USA); and GAPDH (5174S), Bax (2772S), and Bcl-2 (15071S) (Cell Signaling Technology Inc., MA, USA).

Techniques: