cpt1a  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc cpt1a
    Increased lipid synthesis is required for hyper-proliferation and survival of human PAH PAVSMC. (A–E) Early passage distal primary human PAVSMC from non-diseased (CTRL) and PAH subjects were serum-deprived for 48 hours and subjected to immunoblot analysis to detect indicated proteins. n = 5 (CTRL), n = 7 (PAH for P-ACLY, ACLY, see for additional immunoblots used for statistical analysis) or n = 5 (PAH for ACC, FASN, <t>CPT1A).</t> Data are means ± SE, fold to control. (F,G) Human PAH PAVSMC were incubated for 48 h in serum deprived media supplemented with regular (+ Lipids) or lipid-deprived (-Lipids) 0.1% BSA and subjected to fluorescent BODIPY 493/503 staining (green) to detect intracellular neutral lipids followed by DAPI (blue) staining to detect nuclei. Representative images with enlarged area (F) and statistical analysis (G) are shown. Bar equals 50 μm. Data are means ± SE from n = 5 subjects/group, fold to cells incubated in regular 0.1% BSA (+ Lipids) group. (H) Equal amount of human PAVSMC from five PAH and five control subjects were seeded to 6 well plates. 48 h later (day 0), media was changed to the serum-free media supplemented with regular (+ Lipids) or lipid-deprived (-Lipids) 0.1% BSA; six days later, cell count assay was performed. Data are means ± SE, n = 5 subjects/group. (I) PAH PAVSMC were treated with ACC inhibitor TOFA (20 μM) for 48 h followed by proliferation analysis (Ki-67). Data are means ± SE, percentage of Ki-67 positive cells/total number of cells, n = 5 subjects/group. (J) PAH PAVSMC were treated with ACC inhibitor TOFA (20 μM) for 48 h followed by apoptosis analysis. Data are means ± SE, percentage of TUNEL-positive cells/total number of cells, n = 5 subjects/group. * p < 0.05, ** p < 0.01 by Mann–Whitney U test.
    Cpt1a, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    cpt1a - by Bioz Stars, 2023-02
    94/100 stars

    Images

    1) Product Images from "Akt-Dependent Glycolysis-Driven Lipogenesis Supports Proliferation and Survival of Human Pulmonary Arterial Smooth Muscle Cells in Pulmonary Hypertension"

    Article Title: Akt-Dependent Glycolysis-Driven Lipogenesis Supports Proliferation and Survival of Human Pulmonary Arterial Smooth Muscle Cells in Pulmonary Hypertension

    Journal: Frontiers in Medicine

    doi: 10.3389/fmed.2022.886868

    Increased lipid synthesis is required for hyper-proliferation and survival of human PAH PAVSMC. (A–E) Early passage distal primary human PAVSMC from non-diseased (CTRL) and PAH subjects were serum-deprived for 48 hours and subjected to immunoblot analysis to detect indicated proteins. n = 5 (CTRL), n = 7 (PAH for P-ACLY, ACLY, see for additional immunoblots used for statistical analysis) or n = 5 (PAH for ACC, FASN, CPT1A). Data are means ± SE, fold to control. (F,G) Human PAH PAVSMC were incubated for 48 h in serum deprived media supplemented with regular (+ Lipids) or lipid-deprived (-Lipids) 0.1% BSA and subjected to fluorescent BODIPY 493/503 staining (green) to detect intracellular neutral lipids followed by DAPI (blue) staining to detect nuclei. Representative images with enlarged area (F) and statistical analysis (G) are shown. Bar equals 50 μm. Data are means ± SE from n = 5 subjects/group, fold to cells incubated in regular 0.1% BSA (+ Lipids) group. (H) Equal amount of human PAVSMC from five PAH and five control subjects were seeded to 6 well plates. 48 h later (day 0), media was changed to the serum-free media supplemented with regular (+ Lipids) or lipid-deprived (-Lipids) 0.1% BSA; six days later, cell count assay was performed. Data are means ± SE, n = 5 subjects/group. (I) PAH PAVSMC were treated with ACC inhibitor TOFA (20 μM) for 48 h followed by proliferation analysis (Ki-67). Data are means ± SE, percentage of Ki-67 positive cells/total number of cells, n = 5 subjects/group. (J) PAH PAVSMC were treated with ACC inhibitor TOFA (20 μM) for 48 h followed by apoptosis analysis. Data are means ± SE, percentage of TUNEL-positive cells/total number of cells, n = 5 subjects/group. * p < 0.05, ** p < 0.01 by Mann–Whitney U test.
    Figure Legend Snippet: Increased lipid synthesis is required for hyper-proliferation and survival of human PAH PAVSMC. (A–E) Early passage distal primary human PAVSMC from non-diseased (CTRL) and PAH subjects were serum-deprived for 48 hours and subjected to immunoblot analysis to detect indicated proteins. n = 5 (CTRL), n = 7 (PAH for P-ACLY, ACLY, see for additional immunoblots used for statistical analysis) or n = 5 (PAH for ACC, FASN, CPT1A). Data are means ± SE, fold to control. (F,G) Human PAH PAVSMC were incubated for 48 h in serum deprived media supplemented with regular (+ Lipids) or lipid-deprived (-Lipids) 0.1% BSA and subjected to fluorescent BODIPY 493/503 staining (green) to detect intracellular neutral lipids followed by DAPI (blue) staining to detect nuclei. Representative images with enlarged area (F) and statistical analysis (G) are shown. Bar equals 50 μm. Data are means ± SE from n = 5 subjects/group, fold to cells incubated in regular 0.1% BSA (+ Lipids) group. (H) Equal amount of human PAVSMC from five PAH and five control subjects were seeded to 6 well plates. 48 h later (day 0), media was changed to the serum-free media supplemented with regular (+ Lipids) or lipid-deprived (-Lipids) 0.1% BSA; six days later, cell count assay was performed. Data are means ± SE, n = 5 subjects/group. (I) PAH PAVSMC were treated with ACC inhibitor TOFA (20 μM) for 48 h followed by proliferation analysis (Ki-67). Data are means ± SE, percentage of Ki-67 positive cells/total number of cells, n = 5 subjects/group. (J) PAH PAVSMC were treated with ACC inhibitor TOFA (20 μM) for 48 h followed by apoptosis analysis. Data are means ± SE, percentage of TUNEL-positive cells/total number of cells, n = 5 subjects/group. * p < 0.05, ** p < 0.01 by Mann–Whitney U test.

    Techniques Used: Western Blot, Incubation, Staining, Cell Counting, TUNEL Assay, MANN-WHITNEY

    cpt1a  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc cpt1a
    Increased lipid synthesis is required for hyper-proliferation and survival of human PAH PAVSMC. (A–E) Early passage distal primary human PAVSMC from non-diseased (CTRL) and PAH subjects were serum-deprived for 48 hours and subjected to immunoblot analysis to detect indicated proteins. n = 5 (CTRL), n = 7 (PAH for P-ACLY, ACLY, see for additional immunoblots used for statistical analysis) or n = 5 (PAH for ACC, FASN, <t>CPT1A).</t> Data are means ± SE, fold to control. (F,G) Human PAH PAVSMC were incubated for 48 h in serum deprived media supplemented with regular (+ Lipids) or lipid-deprived (-Lipids) 0.1% BSA and subjected to fluorescent BODIPY 493/503 staining (green) to detect intracellular neutral lipids followed by DAPI (blue) staining to detect nuclei. Representative images with enlarged area (F) and statistical analysis (G) are shown. Bar equals 50 μm. Data are means ± SE from n = 5 subjects/group, fold to cells incubated in regular 0.1% BSA (+ Lipids) group. (H) Equal amount of human PAVSMC from five PAH and five control subjects were seeded to 6 well plates. 48 h later (day 0), media was changed to the serum-free media supplemented with regular (+ Lipids) or lipid-deprived (-Lipids) 0.1% BSA; six days later, cell count assay was performed. Data are means ± SE, n = 5 subjects/group. (I) PAH PAVSMC were treated with ACC inhibitor TOFA (20 μM) for 48 h followed by proliferation analysis (Ki-67). Data are means ± SE, percentage of Ki-67 positive cells/total number of cells, n = 5 subjects/group. (J) PAH PAVSMC were treated with ACC inhibitor TOFA (20 μM) for 48 h followed by apoptosis analysis. Data are means ± SE, percentage of TUNEL-positive cells/total number of cells, n = 5 subjects/group. * p < 0.05, ** p < 0.01 by Mann–Whitney U test.
    Cpt1a, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Akt-Dependent Glycolysis-Driven Lipogenesis Supports Proliferation and Survival of Human Pulmonary Arterial Smooth Muscle Cells in Pulmonary Hypertension"

    Article Title: Akt-Dependent Glycolysis-Driven Lipogenesis Supports Proliferation and Survival of Human Pulmonary Arterial Smooth Muscle Cells in Pulmonary Hypertension

    Journal: Frontiers in Medicine

    doi: 10.3389/fmed.2022.886868

    Increased lipid synthesis is required for hyper-proliferation and survival of human PAH PAVSMC. (A–E) Early passage distal primary human PAVSMC from non-diseased (CTRL) and PAH subjects were serum-deprived for 48 hours and subjected to immunoblot analysis to detect indicated proteins. n = 5 (CTRL), n = 7 (PAH for P-ACLY, ACLY, see for additional immunoblots used for statistical analysis) or n = 5 (PAH for ACC, FASN, CPT1A). Data are means ± SE, fold to control. (F,G) Human PAH PAVSMC were incubated for 48 h in serum deprived media supplemented with regular (+ Lipids) or lipid-deprived (-Lipids) 0.1% BSA and subjected to fluorescent BODIPY 493/503 staining (green) to detect intracellular neutral lipids followed by DAPI (blue) staining to detect nuclei. Representative images with enlarged area (F) and statistical analysis (G) are shown. Bar equals 50 μm. Data are means ± SE from n = 5 subjects/group, fold to cells incubated in regular 0.1% BSA (+ Lipids) group. (H) Equal amount of human PAVSMC from five PAH and five control subjects were seeded to 6 well plates. 48 h later (day 0), media was changed to the serum-free media supplemented with regular (+ Lipids) or lipid-deprived (-Lipids) 0.1% BSA; six days later, cell count assay was performed. Data are means ± SE, n = 5 subjects/group. (I) PAH PAVSMC were treated with ACC inhibitor TOFA (20 μM) for 48 h followed by proliferation analysis (Ki-67). Data are means ± SE, percentage of Ki-67 positive cells/total number of cells, n = 5 subjects/group. (J) PAH PAVSMC were treated with ACC inhibitor TOFA (20 μM) for 48 h followed by apoptosis analysis. Data are means ± SE, percentage of TUNEL-positive cells/total number of cells, n = 5 subjects/group. * p < 0.05, ** p < 0.01 by Mann–Whitney U test.
    Figure Legend Snippet: Increased lipid synthesis is required for hyper-proliferation and survival of human PAH PAVSMC. (A–E) Early passage distal primary human PAVSMC from non-diseased (CTRL) and PAH subjects were serum-deprived for 48 hours and subjected to immunoblot analysis to detect indicated proteins. n = 5 (CTRL), n = 7 (PAH for P-ACLY, ACLY, see for additional immunoblots used for statistical analysis) or n = 5 (PAH for ACC, FASN, CPT1A). Data are means ± SE, fold to control. (F,G) Human PAH PAVSMC were incubated for 48 h in serum deprived media supplemented with regular (+ Lipids) or lipid-deprived (-Lipids) 0.1% BSA and subjected to fluorescent BODIPY 493/503 staining (green) to detect intracellular neutral lipids followed by DAPI (blue) staining to detect nuclei. Representative images with enlarged area (F) and statistical analysis (G) are shown. Bar equals 50 μm. Data are means ± SE from n = 5 subjects/group, fold to cells incubated in regular 0.1% BSA (+ Lipids) group. (H) Equal amount of human PAVSMC from five PAH and five control subjects were seeded to 6 well plates. 48 h later (day 0), media was changed to the serum-free media supplemented with regular (+ Lipids) or lipid-deprived (-Lipids) 0.1% BSA; six days later, cell count assay was performed. Data are means ± SE, n = 5 subjects/group. (I) PAH PAVSMC were treated with ACC inhibitor TOFA (20 μM) for 48 h followed by proliferation analysis (Ki-67). Data are means ± SE, percentage of Ki-67 positive cells/total number of cells, n = 5 subjects/group. (J) PAH PAVSMC were treated with ACC inhibitor TOFA (20 μM) for 48 h followed by apoptosis analysis. Data are means ± SE, percentage of TUNEL-positive cells/total number of cells, n = 5 subjects/group. * p < 0.05, ** p < 0.01 by Mann–Whitney U test.

    Techniques Used: Western Blot, Incubation, Staining, Cell Counting, TUNEL Assay, MANN-WHITNEY

    rabbit anti cpt1a antibody  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc rabbit anti cpt1a antibody
    Transcriptomic and metabolomic analysis of UUO-induced rat kidneys. Rats were operated and treated in the same manner as in . Total RNA extracted from kidney samples was used for transcriptomic analysis, and acetonitrile extract from kidney samples was used for metabolomic analysis. ( A ) KEGG enrichment pathways of differential genes between UUO and sham rats with q-value < 0.05 and log 2 (FoldChange) > 1; RNA sequencing analysis of genes associated with ( B ) fibrosis ( n = 4) and ( C ) fatty acid metabolism ( n = 4); mRNA expressions associated with ( D ) fibrosis (Col1a1, Col3a1,Col4a1, TGF-β, Vim, Acta2, Fn1 and Twist1) and ( E ) fatty acid metabolism <t>(Cpt1a,</t> Cpt1b, Acot1, Decr1, Echs1 and Cpt2) in rat kidney samples were determined ( n = 5); ( F ) heatmap of metabolites in rat kidney samples ( n = 8); ( G ) KEGG enrichment pathways of differential metabolites between UUO and sham rats with VIP > 1 and p < 0.05; ( H ) network diagram of Twist1 gene, Cpt1a gene and differential metabolites in kidney of UUO and sham rats. Data were expressed as mean ± SD. ## p < 0.01, ### p < 0.001, vs. sham rats; * p < 0.05, ** p < 0.01, vs. UUO rats.
    Rabbit Anti Cpt1a Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Rhein Improves Renal Fibrosis by Restoring Cpt1a-Mediated Fatty Acid Oxidation through SirT1/STAT3/twist1 Pathway"

    Article Title: Rhein Improves Renal Fibrosis by Restoring Cpt1a-Mediated Fatty Acid Oxidation through SirT1/STAT3/twist1 Pathway

    Journal: Molecules

    doi: 10.3390/molecules27072344

    Transcriptomic and metabolomic analysis of UUO-induced rat kidneys. Rats were operated and treated in the same manner as in . Total RNA extracted from kidney samples was used for transcriptomic analysis, and acetonitrile extract from kidney samples was used for metabolomic analysis. ( A ) KEGG enrichment pathways of differential genes between UUO and sham rats with q-value < 0.05 and log 2 (FoldChange) > 1; RNA sequencing analysis of genes associated with ( B ) fibrosis ( n = 4) and ( C ) fatty acid metabolism ( n = 4); mRNA expressions associated with ( D ) fibrosis (Col1a1, Col3a1,Col4a1, TGF-β, Vim, Acta2, Fn1 and Twist1) and ( E ) fatty acid metabolism (Cpt1a, Cpt1b, Acot1, Decr1, Echs1 and Cpt2) in rat kidney samples were determined ( n = 5); ( F ) heatmap of metabolites in rat kidney samples ( n = 8); ( G ) KEGG enrichment pathways of differential metabolites between UUO and sham rats with VIP > 1 and p < 0.05; ( H ) network diagram of Twist1 gene, Cpt1a gene and differential metabolites in kidney of UUO and sham rats. Data were expressed as mean ± SD. ## p < 0.01, ### p < 0.001, vs. sham rats; * p < 0.05, ** p < 0.01, vs. UUO rats.
    Figure Legend Snippet: Transcriptomic and metabolomic analysis of UUO-induced rat kidneys. Rats were operated and treated in the same manner as in . Total RNA extracted from kidney samples was used for transcriptomic analysis, and acetonitrile extract from kidney samples was used for metabolomic analysis. ( A ) KEGG enrichment pathways of differential genes between UUO and sham rats with q-value < 0.05 and log 2 (FoldChange) > 1; RNA sequencing analysis of genes associated with ( B ) fibrosis ( n = 4) and ( C ) fatty acid metabolism ( n = 4); mRNA expressions associated with ( D ) fibrosis (Col1a1, Col3a1,Col4a1, TGF-β, Vim, Acta2, Fn1 and Twist1) and ( E ) fatty acid metabolism (Cpt1a, Cpt1b, Acot1, Decr1, Echs1 and Cpt2) in rat kidney samples were determined ( n = 5); ( F ) heatmap of metabolites in rat kidney samples ( n = 8); ( G ) KEGG enrichment pathways of differential metabolites between UUO and sham rats with VIP > 1 and p < 0.05; ( H ) network diagram of Twist1 gene, Cpt1a gene and differential metabolites in kidney of UUO and sham rats. Data were expressed as mean ± SD. ## p < 0.01, ### p < 0.001, vs. sham rats; * p < 0.05, ** p < 0.01, vs. UUO rats.

    Techniques Used: RNA Sequencing Assay

    Rhein reverses TGF-β-induced EMT in RTE cells by promoting Cpt1a activity. ( A ) Cell viability in RTE cells incubated with rhein at indicated concentrations for 24 h. RTE cells were incubated with 10 ng/mL TGF-β and rhein at indicated concentrations for 24 h, ( B ) protein expressions of E-cadherin, α-SMA and Col1A; ( C ) representative cell images of lipid droplets stained with BODIPY (rhein at 50 μmol/L, ×630). ( D ) Intracellular ATP levels in RTE cells incubated with 10 ng/mL TGF-β and 50 μmol/L rhein, or with 40 μmol/L etomoxir, for 24 h. RTE cells were incubated with 10 ng/mL TGF-β and 10 or 50 μmol/L rhein for 24 h, ( E ) protein expression and ( F ) activity of Cpt1. RTE cells were incubated with 10 ng/mL TGF-β and 50 μmol/L rhein or 0.5 mmol/L carnitine, or with 40 μmol/L etomoxir, for 24 h, ( G , I ) mRNA expressions of E-cadherin, vimentin, Acta2 and Col1a1; ( H ) Cpt1 activity. RTE cells were incubated with 10 ng/mL TGF-β and 50 μmol/L for 24 h, ( J ) mRNA expressions of Cpt1a, Cpt1b and Cpt1c; ( K ) representative images of cells immunostained with Cpt1a (×630). Data were expressed as mean ± SD ( n = 5). # p < 0.05, ## p < 0.01, ### p < 0.001, vs. blank cells; * p < 0.05, ** p < 0.01, *** p < 0.001, vs. TGF-β- or etomoxir-induced cells.
    Figure Legend Snippet: Rhein reverses TGF-β-induced EMT in RTE cells by promoting Cpt1a activity. ( A ) Cell viability in RTE cells incubated with rhein at indicated concentrations for 24 h. RTE cells were incubated with 10 ng/mL TGF-β and rhein at indicated concentrations for 24 h, ( B ) protein expressions of E-cadherin, α-SMA and Col1A; ( C ) representative cell images of lipid droplets stained with BODIPY (rhein at 50 μmol/L, ×630). ( D ) Intracellular ATP levels in RTE cells incubated with 10 ng/mL TGF-β and 50 μmol/L rhein, or with 40 μmol/L etomoxir, for 24 h. RTE cells were incubated with 10 ng/mL TGF-β and 10 or 50 μmol/L rhein for 24 h, ( E ) protein expression and ( F ) activity of Cpt1. RTE cells were incubated with 10 ng/mL TGF-β and 50 μmol/L rhein or 0.5 mmol/L carnitine, or with 40 μmol/L etomoxir, for 24 h, ( G , I ) mRNA expressions of E-cadherin, vimentin, Acta2 and Col1a1; ( H ) Cpt1 activity. RTE cells were incubated with 10 ng/mL TGF-β and 50 μmol/L for 24 h, ( J ) mRNA expressions of Cpt1a, Cpt1b and Cpt1c; ( K ) representative images of cells immunostained with Cpt1a (×630). Data were expressed as mean ± SD ( n = 5). # p < 0.05, ## p < 0.01, ### p < 0.001, vs. blank cells; * p < 0.05, ** p < 0.01, *** p < 0.001, vs. TGF-β- or etomoxir-induced cells.

    Techniques Used: Activity Assay, Incubation, Staining, Expressing

    Twist1 is essential for Cpt1a-mediated FAO depression in RTE cells. ( A ) mRNA and ( B ) protein expression of Twist1 in RTE cells incubated with 10 ng/mL TGF-β and 10 or 50 μmol/L rhein for 24 h. After Twist1 transfection, RTE cells were incubated with 10 ng/mL TGF-β and 50 μmol/L rhein for 24 h, ( C ) mRNA and ( D ) protein expressions of E-cadherin, vimentin, Acta2 and Col1a1, ( E ) Cpt1a mRNA and ( F ) Cpt1 activity were detected; ( G , H ) representative images of cells immunostained with Cpt1a or stained with BODIPY (×630); ( I ) intracellular ATP levels. Data were expressed as mean ± SD ( n = 5). ## p < 0.01, ### p < 0.001, vs. blank cells; * p < 0.05, ** p < 0.01, vs. TGF-β-induced cells.
    Figure Legend Snippet: Twist1 is essential for Cpt1a-mediated FAO depression in RTE cells. ( A ) mRNA and ( B ) protein expression of Twist1 in RTE cells incubated with 10 ng/mL TGF-β and 10 or 50 μmol/L rhein for 24 h. After Twist1 transfection, RTE cells were incubated with 10 ng/mL TGF-β and 50 μmol/L rhein for 24 h, ( C ) mRNA and ( D ) protein expressions of E-cadherin, vimentin, Acta2 and Col1a1, ( E ) Cpt1a mRNA and ( F ) Cpt1 activity were detected; ( G , H ) representative images of cells immunostained with Cpt1a or stained with BODIPY (×630); ( I ) intracellular ATP levels. Data were expressed as mean ± SD ( n = 5). ## p < 0.01, ### p < 0.001, vs. blank cells; * p < 0.05, ** p < 0.01, vs. TGF-β-induced cells.

    Techniques Used: Expressing, Incubation, Transfection, Activity Assay, Staining

    Rhein promotes Cpt1a-mediated FAO via SirT1/STAT3/Twist1 pathway in UUO-induced rats. Rat UUO operation was in the same manner as in . The rats were i.g. administered with or without rhein at 100 mg/kg or resveratrol at 20 mg/kg per day from days 1 to 14, ( A ) protein expressions E-cadherin, α-SMA and Col1A of kidney samples; ( B , C ) representative images of kidney samples stained with BODIPY and immunostained with Cpt1a and Twist1 (×630, n = 3); ( D ) mRNA expression of Cpt1a; ( E ) protein expressions for Twist1, SirT1, p -STAT3 and acetylated STAT3. Data were expressed as mean ± SD ( n = 5). ## p < 0.01, ### p < 0.001, vs. sham rats; * p < 0.05, ** p < 0.01, *** p < 0.001, vs. UUO rats.
    Figure Legend Snippet: Rhein promotes Cpt1a-mediated FAO via SirT1/STAT3/Twist1 pathway in UUO-induced rats. Rat UUO operation was in the same manner as in . The rats were i.g. administered with or without rhein at 100 mg/kg or resveratrol at 20 mg/kg per day from days 1 to 14, ( A ) protein expressions E-cadherin, α-SMA and Col1A of kidney samples; ( B , C ) representative images of kidney samples stained with BODIPY and immunostained with Cpt1a and Twist1 (×630, n = 3); ( D ) mRNA expression of Cpt1a; ( E ) protein expressions for Twist1, SirT1, p -STAT3 and acetylated STAT3. Data were expressed as mean ± SD ( n = 5). ## p < 0.01, ### p < 0.001, vs. sham rats; * p < 0.05, ** p < 0.01, *** p < 0.001, vs. UUO rats.

    Techniques Used: Staining, Expressing

    rabbit anti cpt1a monoclonal antibody  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc rabbit anti cpt1a monoclonal antibody
    Rabbit Anti Cpt1a Monoclonal Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti cpt1a monoclonal antibody/product/Cell Signaling Technology Inc
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit anti cpt1a monoclonal antibody - by Bioz Stars, 2023-02
    94/100 stars

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    cpt1a  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc cpt1a
    A Protein expression of SREBP-1c, ACC, FASN, CPT-1, MCAD, GLUT-1, and β-catenin in the tumor tissues of mouse models inoculated with wild-type HCT116 cells or HCT116 TLR4-KO cells under different dietary interventions. B–D In iTRAQ proteomics study, the gene ontology (GO) pathway enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis of the biological functions of the differentially expressed proteins in the wild-type HCT116 or HCT116 TLR4-KO tumor tissues dissected from HFD mice. E STRING analysis of the highlighted metabolic enzymes that show significant differences between the wild-type HCT116 or HCT116 TLR4-KO tumor tissues. F ATP levels of the tumor tissues of the mouse models inoculated with wild-type HCT116 cells or HCT116 TLR4-KO cells under the dietary intervention. G Quantification of the β-catenin expressions in the tumor tissues of mouse models inoculated with wild-type HCT116 cells or HCT116 TLR4-KO cells under different dietary interventions. Data are shown as means ± SEM. n = 4 and 5 mice in each group. * p < 0.05, ** p < 0.01 compared with CD-HCT116, a < 0.05 compared with CD-HCT116 TLR4-KO , b < 0.05, bb <0.01 compared with HFD-HCT116 TLR4-KO . CD-HCT116 TLR4-KO mice inoculated with TLR4-KO HCT116 cells had CD diet, HFD-HCT116 TLR4-KO mice inoculated with TLR4-KO HCT116 cells had HFD diet, CD-HCT116 mice inoculated with HCT116 cells had CD diet, HFD-HCT116 mice inoculated with HCT116 cells had HFD diet. ACC acetyl-CoA carboxylase, FASN fatty acid synthase, <t>CPT1</t> carnitine palmitoyltransferase-1, MCAD medium-chain acyl-CoA dehydrogenase, GLUT1 glucose transporter, SREBP-1c sterol regulatory element-binding transcription factor-1.
    Cpt1a, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 94 stars, based on 1 article reviews
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    1) Product Images from "Toll-like receptor 4 is a master regulator for colorectal cancer growth under high-fat diet by programming cancer metabolism"

    Article Title: Toll-like receptor 4 is a master regulator for colorectal cancer growth under high-fat diet by programming cancer metabolism

    Journal: Cell Death & Disease

    doi: 10.1038/s41419-021-04076-x

    A Protein expression of SREBP-1c, ACC, FASN, CPT-1, MCAD, GLUT-1, and β-catenin in the tumor tissues of mouse models inoculated with wild-type HCT116 cells or HCT116 TLR4-KO cells under different dietary interventions. B–D In iTRAQ proteomics study, the gene ontology (GO) pathway enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis of the biological functions of the differentially expressed proteins in the wild-type HCT116 or HCT116 TLR4-KO tumor tissues dissected from HFD mice. E STRING analysis of the highlighted metabolic enzymes that show significant differences between the wild-type HCT116 or HCT116 TLR4-KO tumor tissues. F ATP levels of the tumor tissues of the mouse models inoculated with wild-type HCT116 cells or HCT116 TLR4-KO cells under the dietary intervention. G Quantification of the β-catenin expressions in the tumor tissues of mouse models inoculated with wild-type HCT116 cells or HCT116 TLR4-KO cells under different dietary interventions. Data are shown as means ± SEM. n = 4 and 5 mice in each group. * p < 0.05, ** p < 0.01 compared with CD-HCT116, a < 0.05 compared with CD-HCT116 TLR4-KO , b < 0.05, bb <0.01 compared with HFD-HCT116 TLR4-KO . CD-HCT116 TLR4-KO mice inoculated with TLR4-KO HCT116 cells had CD diet, HFD-HCT116 TLR4-KO mice inoculated with TLR4-KO HCT116 cells had HFD diet, CD-HCT116 mice inoculated with HCT116 cells had CD diet, HFD-HCT116 mice inoculated with HCT116 cells had HFD diet. ACC acetyl-CoA carboxylase, FASN fatty acid synthase, CPT1 carnitine palmitoyltransferase-1, MCAD medium-chain acyl-CoA dehydrogenase, GLUT1 glucose transporter, SREBP-1c sterol regulatory element-binding transcription factor-1.
    Figure Legend Snippet: A Protein expression of SREBP-1c, ACC, FASN, CPT-1, MCAD, GLUT-1, and β-catenin in the tumor tissues of mouse models inoculated with wild-type HCT116 cells or HCT116 TLR4-KO cells under different dietary interventions. B–D In iTRAQ proteomics study, the gene ontology (GO) pathway enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis of the biological functions of the differentially expressed proteins in the wild-type HCT116 or HCT116 TLR4-KO tumor tissues dissected from HFD mice. E STRING analysis of the highlighted metabolic enzymes that show significant differences between the wild-type HCT116 or HCT116 TLR4-KO tumor tissues. F ATP levels of the tumor tissues of the mouse models inoculated with wild-type HCT116 cells or HCT116 TLR4-KO cells under the dietary intervention. G Quantification of the β-catenin expressions in the tumor tissues of mouse models inoculated with wild-type HCT116 cells or HCT116 TLR4-KO cells under different dietary interventions. Data are shown as means ± SEM. n = 4 and 5 mice in each group. * p < 0.05, ** p < 0.01 compared with CD-HCT116, a < 0.05 compared with CD-HCT116 TLR4-KO , b < 0.05, bb <0.01 compared with HFD-HCT116 TLR4-KO . CD-HCT116 TLR4-KO mice inoculated with TLR4-KO HCT116 cells had CD diet, HFD-HCT116 TLR4-KO mice inoculated with TLR4-KO HCT116 cells had HFD diet, CD-HCT116 mice inoculated with HCT116 cells had CD diet, HFD-HCT116 mice inoculated with HCT116 cells had HFD diet. ACC acetyl-CoA carboxylase, FASN fatty acid synthase, CPT1 carnitine palmitoyltransferase-1, MCAD medium-chain acyl-CoA dehydrogenase, GLUT1 glucose transporter, SREBP-1c sterol regulatory element-binding transcription factor-1.

    Techniques Used: Expressing, Binding Assay

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    • cpt1a  (Cell Signaling Technology Inc)
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    Cell Signaling Technology Inc cpt1a
    Increased lipid synthesis is required for hyper-proliferation and survival of human PAH PAVSMC. (A–E) Early passage distal primary human PAVSMC from non-diseased (CTRL) and PAH subjects were serum-deprived for 48 hours and subjected to immunoblot analysis to detect indicated proteins. n = 5 (CTRL), n = 7 (PAH for P-ACLY, ACLY, see for additional immunoblots used for statistical analysis) or n = 5 (PAH for ACC, FASN, <t>CPT1A).</t> Data are means ± SE, fold to control. (F,G) Human PAH PAVSMC were incubated for 48 h in serum deprived media supplemented with regular (+ Lipids) or lipid-deprived (-Lipids) 0.1% BSA and subjected to fluorescent BODIPY 493/503 staining (green) to detect intracellular neutral lipids followed by DAPI (blue) staining to detect nuclei. Representative images with enlarged area (F) and statistical analysis (G) are shown. Bar equals 50 μm. Data are means ± SE from n = 5 subjects/group, fold to cells incubated in regular 0.1% BSA (+ Lipids) group. (H) Equal amount of human PAVSMC from five PAH and five control subjects were seeded to 6 well plates. 48 h later (day 0), media was changed to the serum-free media supplemented with regular (+ Lipids) or lipid-deprived (-Lipids) 0.1% BSA; six days later, cell count assay was performed. Data are means ± SE, n = 5 subjects/group. (I) PAH PAVSMC were treated with ACC inhibitor TOFA (20 μM) for 48 h followed by proliferation analysis (Ki-67). Data are means ± SE, percentage of Ki-67 positive cells/total number of cells, n = 5 subjects/group. (J) PAH PAVSMC were treated with ACC inhibitor TOFA (20 μM) for 48 h followed by apoptosis analysis. Data are means ± SE, percentage of TUNEL-positive cells/total number of cells, n = 5 subjects/group. * p < 0.05, ** p < 0.01 by Mann–Whitney U test.
    Cpt1a, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    rabbit anti cpt1a antibody  (Cell Signaling Technology Inc)
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    Cell Signaling Technology Inc rabbit anti cpt1a antibody
    Transcriptomic and metabolomic analysis of UUO-induced rat kidneys. Rats were operated and treated in the same manner as in . Total RNA extracted from kidney samples was used for transcriptomic analysis, and acetonitrile extract from kidney samples was used for metabolomic analysis. ( A ) KEGG enrichment pathways of differential genes between UUO and sham rats with q-value < 0.05 and log 2 (FoldChange) > 1; RNA sequencing analysis of genes associated with ( B ) fibrosis ( n = 4) and ( C ) fatty acid metabolism ( n = 4); mRNA expressions associated with ( D ) fibrosis (Col1a1, Col3a1,Col4a1, TGF-β, Vim, Acta2, Fn1 and Twist1) and ( E ) fatty acid metabolism <t>(Cpt1a,</t> Cpt1b, Acot1, Decr1, Echs1 and Cpt2) in rat kidney samples were determined ( n = 5); ( F ) heatmap of metabolites in rat kidney samples ( n = 8); ( G ) KEGG enrichment pathways of differential metabolites between UUO and sham rats with VIP > 1 and p < 0.05; ( H ) network diagram of Twist1 gene, Cpt1a gene and differential metabolites in kidney of UUO and sham rats. Data were expressed as mean ± SD. ## p < 0.01, ### p < 0.001, vs. sham rats; * p < 0.05, ** p < 0.01, vs. UUO rats.
    Rabbit Anti Cpt1a Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    rabbit anti cpt1a monoclonal antibody  (Cell Signaling Technology Inc)
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    Cell Signaling Technology Inc rabbit anti cpt1a monoclonal antibody
    Transcriptomic and metabolomic analysis of UUO-induced rat kidneys. Rats were operated and treated in the same manner as in . Total RNA extracted from kidney samples was used for transcriptomic analysis, and acetonitrile extract from kidney samples was used for metabolomic analysis. ( A ) KEGG enrichment pathways of differential genes between UUO and sham rats with q-value < 0.05 and log 2 (FoldChange) > 1; RNA sequencing analysis of genes associated with ( B ) fibrosis ( n = 4) and ( C ) fatty acid metabolism ( n = 4); mRNA expressions associated with ( D ) fibrosis (Col1a1, Col3a1,Col4a1, TGF-β, Vim, Acta2, Fn1 and Twist1) and ( E ) fatty acid metabolism <t>(Cpt1a,</t> Cpt1b, Acot1, Decr1, Echs1 and Cpt2) in rat kidney samples were determined ( n = 5); ( F ) heatmap of metabolites in rat kidney samples ( n = 8); ( G ) KEGG enrichment pathways of differential metabolites between UUO and sham rats with VIP > 1 and p < 0.05; ( H ) network diagram of Twist1 gene, Cpt1a gene and differential metabolites in kidney of UUO and sham rats. Data were expressed as mean ± SD. ## p < 0.01, ### p < 0.001, vs. sham rats; * p < 0.05, ** p < 0.01, vs. UUO rats.
    Rabbit Anti Cpt1a Monoclonal Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Increased lipid synthesis is required for hyper-proliferation and survival of human PAH PAVSMC. (A–E) Early passage distal primary human PAVSMC from non-diseased (CTRL) and PAH subjects were serum-deprived for 48 hours and subjected to immunoblot analysis to detect indicated proteins. n = 5 (CTRL), n = 7 (PAH for P-ACLY, ACLY, see for additional immunoblots used for statistical analysis) or n = 5 (PAH for ACC, FASN, CPT1A). Data are means ± SE, fold to control. (F,G) Human PAH PAVSMC were incubated for 48 h in serum deprived media supplemented with regular (+ Lipids) or lipid-deprived (-Lipids) 0.1% BSA and subjected to fluorescent BODIPY 493/503 staining (green) to detect intracellular neutral lipids followed by DAPI (blue) staining to detect nuclei. Representative images with enlarged area (F) and statistical analysis (G) are shown. Bar equals 50 μm. Data are means ± SE from n = 5 subjects/group, fold to cells incubated in regular 0.1% BSA (+ Lipids) group. (H) Equal amount of human PAVSMC from five PAH and five control subjects were seeded to 6 well plates. 48 h later (day 0), media was changed to the serum-free media supplemented with regular (+ Lipids) or lipid-deprived (-Lipids) 0.1% BSA; six days later, cell count assay was performed. Data are means ± SE, n = 5 subjects/group. (I) PAH PAVSMC were treated with ACC inhibitor TOFA (20 μM) for 48 h followed by proliferation analysis (Ki-67). Data are means ± SE, percentage of Ki-67 positive cells/total number of cells, n = 5 subjects/group. (J) PAH PAVSMC were treated with ACC inhibitor TOFA (20 μM) for 48 h followed by apoptosis analysis. Data are means ± SE, percentage of TUNEL-positive cells/total number of cells, n = 5 subjects/group. * p < 0.05, ** p < 0.01 by Mann–Whitney U test.

    Journal: Frontiers in Medicine

    Article Title: Akt-Dependent Glycolysis-Driven Lipogenesis Supports Proliferation and Survival of Human Pulmonary Arterial Smooth Muscle Cells in Pulmonary Hypertension

    doi: 10.3389/fmed.2022.886868

    Figure Lengend Snippet: Increased lipid synthesis is required for hyper-proliferation and survival of human PAH PAVSMC. (A–E) Early passage distal primary human PAVSMC from non-diseased (CTRL) and PAH subjects were serum-deprived for 48 hours and subjected to immunoblot analysis to detect indicated proteins. n = 5 (CTRL), n = 7 (PAH for P-ACLY, ACLY, see for additional immunoblots used for statistical analysis) or n = 5 (PAH for ACC, FASN, CPT1A). Data are means ± SE, fold to control. (F,G) Human PAH PAVSMC were incubated for 48 h in serum deprived media supplemented with regular (+ Lipids) or lipid-deprived (-Lipids) 0.1% BSA and subjected to fluorescent BODIPY 493/503 staining (green) to detect intracellular neutral lipids followed by DAPI (blue) staining to detect nuclei. Representative images with enlarged area (F) and statistical analysis (G) are shown. Bar equals 50 μm. Data are means ± SE from n = 5 subjects/group, fold to cells incubated in regular 0.1% BSA (+ Lipids) group. (H) Equal amount of human PAVSMC from five PAH and five control subjects were seeded to 6 well plates. 48 h later (day 0), media was changed to the serum-free media supplemented with regular (+ Lipids) or lipid-deprived (-Lipids) 0.1% BSA; six days later, cell count assay was performed. Data are means ± SE, n = 5 subjects/group. (I) PAH PAVSMC were treated with ACC inhibitor TOFA (20 μM) for 48 h followed by proliferation analysis (Ki-67). Data are means ± SE, percentage of Ki-67 positive cells/total number of cells, n = 5 subjects/group. (J) PAH PAVSMC were treated with ACC inhibitor TOFA (20 μM) for 48 h followed by apoptosis analysis. Data are means ± SE, percentage of TUNEL-positive cells/total number of cells, n = 5 subjects/group. * p < 0.05, ** p < 0.01 by Mann–Whitney U test.

    Article Snippet: Antibodies for ACLY (#4332), P-S79-ACC (#11818), ACC (#3676), FASN (#3180), P-S473-Akt (#4060), P-T450-Akt (#12178), Akt (#9272), PThr183/Tyr185-JNK (#4668), JNK (#9252), α/β-Tubulin (#2148), CPT1A (#97361), hexokinase II (HKII) (#2867), phosphofructokinase (PFKP) (#8164) were purchased from Cell Signaling (Danvers, MA, United States).

    Techniques: Western Blot, Incubation, Staining, Cell Counting, TUNEL Assay, MANN-WHITNEY

    Transcriptomic and metabolomic analysis of UUO-induced rat kidneys. Rats were operated and treated in the same manner as in . Total RNA extracted from kidney samples was used for transcriptomic analysis, and acetonitrile extract from kidney samples was used for metabolomic analysis. ( A ) KEGG enrichment pathways of differential genes between UUO and sham rats with q-value < 0.05 and log 2 (FoldChange) > 1; RNA sequencing analysis of genes associated with ( B ) fibrosis ( n = 4) and ( C ) fatty acid metabolism ( n = 4); mRNA expressions associated with ( D ) fibrosis (Col1a1, Col3a1,Col4a1, TGF-β, Vim, Acta2, Fn1 and Twist1) and ( E ) fatty acid metabolism (Cpt1a, Cpt1b, Acot1, Decr1, Echs1 and Cpt2) in rat kidney samples were determined ( n = 5); ( F ) heatmap of metabolites in rat kidney samples ( n = 8); ( G ) KEGG enrichment pathways of differential metabolites between UUO and sham rats with VIP > 1 and p < 0.05; ( H ) network diagram of Twist1 gene, Cpt1a gene and differential metabolites in kidney of UUO and sham rats. Data were expressed as mean ± SD. ## p < 0.01, ### p < 0.001, vs. sham rats; * p < 0.05, ** p < 0.01, vs. UUO rats.

    Journal: Molecules

    Article Title: Rhein Improves Renal Fibrosis by Restoring Cpt1a-Mediated Fatty Acid Oxidation through SirT1/STAT3/twist1 Pathway

    doi: 10.3390/molecules27072344

    Figure Lengend Snippet: Transcriptomic and metabolomic analysis of UUO-induced rat kidneys. Rats were operated and treated in the same manner as in . Total RNA extracted from kidney samples was used for transcriptomic analysis, and acetonitrile extract from kidney samples was used for metabolomic analysis. ( A ) KEGG enrichment pathways of differential genes between UUO and sham rats with q-value < 0.05 and log 2 (FoldChange) > 1; RNA sequencing analysis of genes associated with ( B ) fibrosis ( n = 4) and ( C ) fatty acid metabolism ( n = 4); mRNA expressions associated with ( D ) fibrosis (Col1a1, Col3a1,Col4a1, TGF-β, Vim, Acta2, Fn1 and Twist1) and ( E ) fatty acid metabolism (Cpt1a, Cpt1b, Acot1, Decr1, Echs1 and Cpt2) in rat kidney samples were determined ( n = 5); ( F ) heatmap of metabolites in rat kidney samples ( n = 8); ( G ) KEGG enrichment pathways of differential metabolites between UUO and sham rats with VIP > 1 and p < 0.05; ( H ) network diagram of Twist1 gene, Cpt1a gene and differential metabolites in kidney of UUO and sham rats. Data were expressed as mean ± SD. ## p < 0.01, ### p < 0.001, vs. sham rats; * p < 0.05, ** p < 0.01, vs. UUO rats.

    Article Snippet: Rabbit anti-α-SMA antibody (#19245), mouse anti-Col1A antibody (#66948), rabbit anti-Cpt1a antibody (#97361), anti-STAT3 rabbit polyclonal antibody (#12640), rabbit anti- p -STAT3 antibody (#9145), rabbit anti-acetylated-Lysine (#9441), rabbit anti-SirT1 antibody (#2496), FITC-goat anti-rabbit IgG (#4414) and Alexa-goat anti-mouse IgG (#4412) were purchased from Cell Signaling Technology (Beverly, CA, USA).

    Techniques: RNA Sequencing Assay

    Rhein reverses TGF-β-induced EMT in RTE cells by promoting Cpt1a activity. ( A ) Cell viability in RTE cells incubated with rhein at indicated concentrations for 24 h. RTE cells were incubated with 10 ng/mL TGF-β and rhein at indicated concentrations for 24 h, ( B ) protein expressions of E-cadherin, α-SMA and Col1A; ( C ) representative cell images of lipid droplets stained with BODIPY (rhein at 50 μmol/L, ×630). ( D ) Intracellular ATP levels in RTE cells incubated with 10 ng/mL TGF-β and 50 μmol/L rhein, or with 40 μmol/L etomoxir, for 24 h. RTE cells were incubated with 10 ng/mL TGF-β and 10 or 50 μmol/L rhein for 24 h, ( E ) protein expression and ( F ) activity of Cpt1. RTE cells were incubated with 10 ng/mL TGF-β and 50 μmol/L rhein or 0.5 mmol/L carnitine, or with 40 μmol/L etomoxir, for 24 h, ( G , I ) mRNA expressions of E-cadherin, vimentin, Acta2 and Col1a1; ( H ) Cpt1 activity. RTE cells were incubated with 10 ng/mL TGF-β and 50 μmol/L for 24 h, ( J ) mRNA expressions of Cpt1a, Cpt1b and Cpt1c; ( K ) representative images of cells immunostained with Cpt1a (×630). Data were expressed as mean ± SD ( n = 5). # p < 0.05, ## p < 0.01, ### p < 0.001, vs. blank cells; * p < 0.05, ** p < 0.01, *** p < 0.001, vs. TGF-β- or etomoxir-induced cells.

    Journal: Molecules

    Article Title: Rhein Improves Renal Fibrosis by Restoring Cpt1a-Mediated Fatty Acid Oxidation through SirT1/STAT3/twist1 Pathway

    doi: 10.3390/molecules27072344

    Figure Lengend Snippet: Rhein reverses TGF-β-induced EMT in RTE cells by promoting Cpt1a activity. ( A ) Cell viability in RTE cells incubated with rhein at indicated concentrations for 24 h. RTE cells were incubated with 10 ng/mL TGF-β and rhein at indicated concentrations for 24 h, ( B ) protein expressions of E-cadherin, α-SMA and Col1A; ( C ) representative cell images of lipid droplets stained with BODIPY (rhein at 50 μmol/L, ×630). ( D ) Intracellular ATP levels in RTE cells incubated with 10 ng/mL TGF-β and 50 μmol/L rhein, or with 40 μmol/L etomoxir, for 24 h. RTE cells were incubated with 10 ng/mL TGF-β and 10 or 50 μmol/L rhein for 24 h, ( E ) protein expression and ( F ) activity of Cpt1. RTE cells were incubated with 10 ng/mL TGF-β and 50 μmol/L rhein or 0.5 mmol/L carnitine, or with 40 μmol/L etomoxir, for 24 h, ( G , I ) mRNA expressions of E-cadherin, vimentin, Acta2 and Col1a1; ( H ) Cpt1 activity. RTE cells were incubated with 10 ng/mL TGF-β and 50 μmol/L for 24 h, ( J ) mRNA expressions of Cpt1a, Cpt1b and Cpt1c; ( K ) representative images of cells immunostained with Cpt1a (×630). Data were expressed as mean ± SD ( n = 5). # p < 0.05, ## p < 0.01, ### p < 0.001, vs. blank cells; * p < 0.05, ** p < 0.01, *** p < 0.001, vs. TGF-β- or etomoxir-induced cells.

    Article Snippet: Rabbit anti-α-SMA antibody (#19245), mouse anti-Col1A antibody (#66948), rabbit anti-Cpt1a antibody (#97361), anti-STAT3 rabbit polyclonal antibody (#12640), rabbit anti- p -STAT3 antibody (#9145), rabbit anti-acetylated-Lysine (#9441), rabbit anti-SirT1 antibody (#2496), FITC-goat anti-rabbit IgG (#4414) and Alexa-goat anti-mouse IgG (#4412) were purchased from Cell Signaling Technology (Beverly, CA, USA).

    Techniques: Activity Assay, Incubation, Staining, Expressing

    Twist1 is essential for Cpt1a-mediated FAO depression in RTE cells. ( A ) mRNA and ( B ) protein expression of Twist1 in RTE cells incubated with 10 ng/mL TGF-β and 10 or 50 μmol/L rhein for 24 h. After Twist1 transfection, RTE cells were incubated with 10 ng/mL TGF-β and 50 μmol/L rhein for 24 h, ( C ) mRNA and ( D ) protein expressions of E-cadherin, vimentin, Acta2 and Col1a1, ( E ) Cpt1a mRNA and ( F ) Cpt1 activity were detected; ( G , H ) representative images of cells immunostained with Cpt1a or stained with BODIPY (×630); ( I ) intracellular ATP levels. Data were expressed as mean ± SD ( n = 5). ## p < 0.01, ### p < 0.001, vs. blank cells; * p < 0.05, ** p < 0.01, vs. TGF-β-induced cells.

    Journal: Molecules

    Article Title: Rhein Improves Renal Fibrosis by Restoring Cpt1a-Mediated Fatty Acid Oxidation through SirT1/STAT3/twist1 Pathway

    doi: 10.3390/molecules27072344

    Figure Lengend Snippet: Twist1 is essential for Cpt1a-mediated FAO depression in RTE cells. ( A ) mRNA and ( B ) protein expression of Twist1 in RTE cells incubated with 10 ng/mL TGF-β and 10 or 50 μmol/L rhein for 24 h. After Twist1 transfection, RTE cells were incubated with 10 ng/mL TGF-β and 50 μmol/L rhein for 24 h, ( C ) mRNA and ( D ) protein expressions of E-cadherin, vimentin, Acta2 and Col1a1, ( E ) Cpt1a mRNA and ( F ) Cpt1 activity were detected; ( G , H ) representative images of cells immunostained with Cpt1a or stained with BODIPY (×630); ( I ) intracellular ATP levels. Data were expressed as mean ± SD ( n = 5). ## p < 0.01, ### p < 0.001, vs. blank cells; * p < 0.05, ** p < 0.01, vs. TGF-β-induced cells.

    Article Snippet: Rabbit anti-α-SMA antibody (#19245), mouse anti-Col1A antibody (#66948), rabbit anti-Cpt1a antibody (#97361), anti-STAT3 rabbit polyclonal antibody (#12640), rabbit anti- p -STAT3 antibody (#9145), rabbit anti-acetylated-Lysine (#9441), rabbit anti-SirT1 antibody (#2496), FITC-goat anti-rabbit IgG (#4414) and Alexa-goat anti-mouse IgG (#4412) were purchased from Cell Signaling Technology (Beverly, CA, USA).

    Techniques: Expressing, Incubation, Transfection, Activity Assay, Staining

    Rhein promotes Cpt1a-mediated FAO via SirT1/STAT3/Twist1 pathway in UUO-induced rats. Rat UUO operation was in the same manner as in . The rats were i.g. administered with or without rhein at 100 mg/kg or resveratrol at 20 mg/kg per day from days 1 to 14, ( A ) protein expressions E-cadherin, α-SMA and Col1A of kidney samples; ( B , C ) representative images of kidney samples stained with BODIPY and immunostained with Cpt1a and Twist1 (×630, n = 3); ( D ) mRNA expression of Cpt1a; ( E ) protein expressions for Twist1, SirT1, p -STAT3 and acetylated STAT3. Data were expressed as mean ± SD ( n = 5). ## p < 0.01, ### p < 0.001, vs. sham rats; * p < 0.05, ** p < 0.01, *** p < 0.001, vs. UUO rats.

    Journal: Molecules

    Article Title: Rhein Improves Renal Fibrosis by Restoring Cpt1a-Mediated Fatty Acid Oxidation through SirT1/STAT3/twist1 Pathway

    doi: 10.3390/molecules27072344

    Figure Lengend Snippet: Rhein promotes Cpt1a-mediated FAO via SirT1/STAT3/Twist1 pathway in UUO-induced rats. Rat UUO operation was in the same manner as in . The rats were i.g. administered with or without rhein at 100 mg/kg or resveratrol at 20 mg/kg per day from days 1 to 14, ( A ) protein expressions E-cadherin, α-SMA and Col1A of kidney samples; ( B , C ) representative images of kidney samples stained with BODIPY and immunostained with Cpt1a and Twist1 (×630, n = 3); ( D ) mRNA expression of Cpt1a; ( E ) protein expressions for Twist1, SirT1, p -STAT3 and acetylated STAT3. Data were expressed as mean ± SD ( n = 5). ## p < 0.01, ### p < 0.001, vs. sham rats; * p < 0.05, ** p < 0.01, *** p < 0.001, vs. UUO rats.

    Article Snippet: Rabbit anti-α-SMA antibody (#19245), mouse anti-Col1A antibody (#66948), rabbit anti-Cpt1a antibody (#97361), anti-STAT3 rabbit polyclonal antibody (#12640), rabbit anti- p -STAT3 antibody (#9145), rabbit anti-acetylated-Lysine (#9441), rabbit anti-SirT1 antibody (#2496), FITC-goat anti-rabbit IgG (#4414) and Alexa-goat anti-mouse IgG (#4412) were purchased from Cell Signaling Technology (Beverly, CA, USA).

    Techniques: Staining, Expressing