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Arraystar inc microarray analysis for cardiac mrna
(A) Predicted AP-1 (yellow) and KLF (framed) binding sites on mouse Ppara promoter. (B–C) Cardiac <t>mRNA</t> levels of Klf isoforms (B) and protein levels <t>of</t> <t>KLF5</t> and β-actin (C) in 10–12-weeks old C57BL/6 mice treated with 5 mg/kg LPS or saline (CTRL) (n=4–5; *P<0.05; **P<0.01; ***P<0.001 vs CTRL). (D–E) Ppara, Klf5 and Klf6 mRNA levels in HL-1 cells (D) treated with 1µg/ml LPS or saline (CTRL) for 9h (n=6; *p<0.05 vs. CTRL) or in aMHC-Pparg mice (E) treated with 5mg/kg LPS or saline (CTRL) for 8–10h (n=5; *p<0.05; **p<0.01 vs. CTRL).
Microarray Analysis For Cardiac Mrna, supplied by Arraystar inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Cardiac Myocyte KLF5 Regulates Ppara Expression and Cardiac Function"

Article Title: Cardiac Myocyte KLF5 Regulates Ppara Expression and Cardiac Function

Journal: Circulation research

doi: 10.1161/CIRCRESAHA.115.306383

(A) Predicted AP-1 (yellow) and KLF (framed) binding sites on mouse Ppara promoter. (B–C) Cardiac mRNA levels of Klf isoforms (B) and protein levels of KLF5 and β-actin (C) in 10–12-weeks old C57BL/6 mice treated with 5 mg/kg LPS or saline (CTRL) (n=4–5; *P<0.05; **P<0.01; ***P<0.001 vs CTRL). (D–E) Ppara, Klf5 and Klf6 mRNA levels in HL-1 cells (D) treated with 1µg/ml LPS or saline (CTRL) for 9h (n=6; *p<0.05 vs. CTRL) or in aMHC-Pparg mice (E) treated with 5mg/kg LPS or saline (CTRL) for 8–10h (n=5; *p<0.05; **p<0.01 vs. CTRL).
Figure Legend Snippet: (A) Predicted AP-1 (yellow) and KLF (framed) binding sites on mouse Ppara promoter. (B–C) Cardiac mRNA levels of Klf isoforms (B) and protein levels of KLF5 and β-actin (C) in 10–12-weeks old C57BL/6 mice treated with 5 mg/kg LPS or saline (CTRL) (n=4–5; *P<0.05; **P<0.01; ***P<0.001 vs CTRL). (D–E) Ppara, Klf5 and Klf6 mRNA levels in HL-1 cells (D) treated with 1µg/ml LPS or saline (CTRL) for 9h (n=6; *p<0.05 vs. CTRL) or in aMHC-Pparg mice (E) treated with 5mg/kg LPS or saline (CTRL) for 8–10h (n=5; *p<0.05; **p<0.01 vs. CTRL).

Techniques Used: Binding Assay, Saline

(A–D) Ppara and Klf5 mRNA (A, C) and protein (B, D) levels in HL-1 cells treated with Ad-cJunAsp (A, B) or Ad-KLF5 (C, D); (n=6; *p<0.05; **p<0.01; ***p<0.001 vs CTRL). (E–I) Enrichment of −792/−772 bp region (E, F) or −719/−698 bp region (G, H) of mouse Ppara promoter with c-Jun (E, G) or KLF5 (F, H) of chromatin samples from HL-1 cells treated with Ad-GFP (CTRL) and either Ad-cJunAsp (E, G) or Ad-KLF5 (F, H); **p<0.01 vs CTRL. (I) Enrichment of −792/−772 bp region of mouse Ppara promoter with c-Jun or KLF5 of chromatin samples from HL-1 cells treated with 1 µg/ml LPS or saline (CTRL); *p<0.05 vs CTRL. Data for all bar graphs are represented as means ± SEM (statistical analysis: t-test).
Figure Legend Snippet: (A–D) Ppara and Klf5 mRNA (A, C) and protein (B, D) levels in HL-1 cells treated with Ad-cJunAsp (A, B) or Ad-KLF5 (C, D); (n=6; *p<0.05; **p<0.01; ***p<0.001 vs CTRL). (E–I) Enrichment of −792/−772 bp region (E, F) or −719/−698 bp region (G, H) of mouse Ppara promoter with c-Jun (E, G) or KLF5 (F, H) of chromatin samples from HL-1 cells treated with Ad-GFP (CTRL) and either Ad-cJunAsp (E, G) or Ad-KLF5 (F, H); **p<0.01 vs CTRL. (I) Enrichment of −792/−772 bp region of mouse Ppara promoter with c-Jun or KLF5 of chromatin samples from HL-1 cells treated with 1 µg/ml LPS or saline (CTRL); *p<0.05 vs CTRL. Data for all bar graphs are represented as means ± SEM (statistical analysis: t-test).

Techniques Used: Saline

(A, B) Klf5 mRNA in the heart, skeletal muscle, intestine, kidney, white adipose tissue, brain (A) and primary cardiac myocytes (B) of aMHC-Klf5−/− mice (n=3; *p<0.05 vs floxed). (C) Hierarchical clustering for differentially expressed mRNAs detected by whole genome microarray analysis of cardiac mRNA obtained from aMHC-Klf5−/− mice and control floxed mice. Red color indicates high relative expression and blue color indicates low relative expression. (D–G) Gene ontology analysis for classification of the downregulated (D) or upregulated (E) genes based on the metabolic process that they are associated with and pathway analysis for downregulated (F) and upregulated (G) genes detected with whole genome microarray analysis of cardiac mRNA obtained from aMHC-Klf5−/− mice and control floxed mice. Data for all bar graphs are represented as means ± SEM (statistical analysis: t-test).
Figure Legend Snippet: (A, B) Klf5 mRNA in the heart, skeletal muscle, intestine, kidney, white adipose tissue, brain (A) and primary cardiac myocytes (B) of aMHC-Klf5−/− mice (n=3; *p<0.05 vs floxed). (C) Hierarchical clustering for differentially expressed mRNAs detected by whole genome microarray analysis of cardiac mRNA obtained from aMHC-Klf5−/− mice and control floxed mice. Red color indicates high relative expression and blue color indicates low relative expression. (D–G) Gene ontology analysis for classification of the downregulated (D) or upregulated (E) genes based on the metabolic process that they are associated with and pathway analysis for downregulated (F) and upregulated (G) genes detected with whole genome microarray analysis of cardiac mRNA obtained from aMHC-Klf5−/− mice and control floxed mice. Data for all bar graphs are represented as means ± SEM (statistical analysis: t-test).

Techniques Used: Microarray, Control, Expressing

(A) Ingenuity pathway analysis of genes regulated over 2-fold in the aMHC-Klf5−/− mouse array that are related to FA metabolism. (B) Cardiac Klf5 and Ppara mRNA levels of 10- to 12-week-old aMHC-Klf5−/− male and female mice (n=5; **p<0.01; ***p<0.001 vs same gender floxed mice). (C) Cardiac PPARα and β-actin protein levels of 10- to 12-week-old floxed and aMHC-Klf5−/− male mice. (D–F) Cardiac mRNA levels for FA oxidation- (Ppargc-1a, Ppargc-1β, Pparg, Ppard, Acox and Cpt1b) (D), lipid uptake- (Cd36, Lpl and Angptl4) (E) and lipid storage-related genes (Dgat1, Dgat2, Plin2, Plin5) (F) (n=5; *p<0.05, **p<0.01, ***p<0.001 vs same gender floxed mice). (G) Cardiac PGC-1, CPT-1, DGAT-1, ATGL, phosphorylated AMPK, total AMPK, and GAPDH protein levels of 10- to 12-week-old floxed and aMHC-Klf5−/− male mice. (H, I) [14C]-Palmitic acid (H) and [14C]-Glucose (I) oxidation levels in cardiac muscle of 10- to 12-week-old floxed and aMHC-Klf5−/− male mice (n=4–5; *p<0.05; **p<0.01 vs floxed mice). Data for all bar graphs are represented as means ± SEM (statistical analysis: t-test).
Figure Legend Snippet: (A) Ingenuity pathway analysis of genes regulated over 2-fold in the aMHC-Klf5−/− mouse array that are related to FA metabolism. (B) Cardiac Klf5 and Ppara mRNA levels of 10- to 12-week-old aMHC-Klf5−/− male and female mice (n=5; **p<0.01; ***p<0.001 vs same gender floxed mice). (C) Cardiac PPARα and β-actin protein levels of 10- to 12-week-old floxed and aMHC-Klf5−/− male mice. (D–F) Cardiac mRNA levels for FA oxidation- (Ppargc-1a, Ppargc-1β, Pparg, Ppard, Acox and Cpt1b) (D), lipid uptake- (Cd36, Lpl and Angptl4) (E) and lipid storage-related genes (Dgat1, Dgat2, Plin2, Plin5) (F) (n=5; *p<0.05, **p<0.01, ***p<0.001 vs same gender floxed mice). (G) Cardiac PGC-1, CPT-1, DGAT-1, ATGL, phosphorylated AMPK, total AMPK, and GAPDH protein levels of 10- to 12-week-old floxed and aMHC-Klf5−/− male mice. (H, I) [14C]-Palmitic acid (H) and [14C]-Glucose (I) oxidation levels in cardiac muscle of 10- to 12-week-old floxed and aMHC-Klf5−/− male mice (n=4–5; *p<0.05; **p<0.01 vs floxed mice). Data for all bar graphs are represented as means ± SEM (statistical analysis: t-test).

Techniques Used:

(A–F) Fractional shortening (A, D), left ventricular internal dimension during diastole (B, E), left ventricular internal dimension during systole (C, F), in 2–3 months old (A–C) and 6 months old (D–F) αMHC-Klf5−/− and floxed (WT) mice. (G–M) Photographs of echocardiograms (G), fractional shortening (H), left ventricular internal dimension during diastole (I), left ventricular internal dimension during systole (J) left ventricular posterior wall during diastole (K) left ventricular posterior wall during systole (L), and heart weight/tibia length ratio (M) in 8–12 months old αMHC-Klf5−/− and floxed (WT) mice (n=7–8; *p<0.05). (N, O) Cardiac mRNA levels for Bnp, Anf, αMHC and βMHC genes in 2–3 months old (N) and 11–12 months old (O) male floxed and αMHC-Klf5−/− mice (F) (n=5; *p<0.05, **p<0.01 vs floxed mice).
Figure Legend Snippet: (A–F) Fractional shortening (A, D), left ventricular internal dimension during diastole (B, E), left ventricular internal dimension during systole (C, F), in 2–3 months old (A–C) and 6 months old (D–F) αMHC-Klf5−/− and floxed (WT) mice. (G–M) Photographs of echocardiograms (G), fractional shortening (H), left ventricular internal dimension during diastole (I), left ventricular internal dimension during systole (J) left ventricular posterior wall during diastole (K) left ventricular posterior wall during systole (L), and heart weight/tibia length ratio (M) in 8–12 months old αMHC-Klf5−/− and floxed (WT) mice (n=7–8; *p<0.05). (N, O) Cardiac mRNA levels for Bnp, Anf, αMHC and βMHC genes in 2–3 months old (N) and 11–12 months old (O) male floxed and αMHC-Klf5−/− mice (F) (n=5; *p<0.05, **p<0.01 vs floxed mice).

Techniques Used:

(A) Ingenuity pathway analysis of cardiac genes regulated over 2-fold in the aMHC-Klf5−/− mouse array that have direct or indirect association with insulin signaling and glucose metabolism proteins. Highlighted with bold fonts within the diagram are proteins that modulate insulin signaling. (B) Fractional shortening of C57BL/6 mice 6 weeks post-STZ or saline (CTRL) administration (n=5; *p<0.05 vs CTRL). (C) Western blot analysis for cardiac KLF5 and β-actin protein levels in C57BL/6 mice 6 weeks post-STZ administration (n=3; ***p<0.001 vs CTRL). (D) Cardiac Klf5 and Ppara mRNA levels in floxed and aMHC-Klf5−/− mice 6 weeks post-STZ administration (n=5; *p<0.05, **p<0.01 vs CTRL). (E) Cardiac Klf5 and Ppara mRNA levels in 12 weeks old ob/ob mice compared with wild type C57BL/6 mice (n=4–5, *p<0.05, ***p<0.001 vs wt). (F–I) Plasma glucose levels (F, G) and cardiac Klf5 and Ppara mRNA levels (H, I) in wild type mice treated with STZ (6 weeks prior to glucose measurement), dapagliflozin (F, H), antisense oligonucleotides against SGLT2 (SGLT2-ASO) (G, I) and combination of either STZ with dapagliflozin (F, H) or STZ with SGLT2-ASO (G, I) (n=5, **p<0.01, ***p<0.001 vs CTRL).
Figure Legend Snippet: (A) Ingenuity pathway analysis of cardiac genes regulated over 2-fold in the aMHC-Klf5−/− mouse array that have direct or indirect association with insulin signaling and glucose metabolism proteins. Highlighted with bold fonts within the diagram are proteins that modulate insulin signaling. (B) Fractional shortening of C57BL/6 mice 6 weeks post-STZ or saline (CTRL) administration (n=5; *p<0.05 vs CTRL). (C) Western blot analysis for cardiac KLF5 and β-actin protein levels in C57BL/6 mice 6 weeks post-STZ administration (n=3; ***p<0.001 vs CTRL). (D) Cardiac Klf5 and Ppara mRNA levels in floxed and aMHC-Klf5−/− mice 6 weeks post-STZ administration (n=5; *p<0.05, **p<0.01 vs CTRL). (E) Cardiac Klf5 and Ppara mRNA levels in 12 weeks old ob/ob mice compared with wild type C57BL/6 mice (n=4–5, *p<0.05, ***p<0.001 vs wt). (F–I) Plasma glucose levels (F, G) and cardiac Klf5 and Ppara mRNA levels (H, I) in wild type mice treated with STZ (6 weeks prior to glucose measurement), dapagliflozin (F, H), antisense oligonucleotides against SGLT2 (SGLT2-ASO) (G, I) and combination of either STZ with dapagliflozin (F, H) or STZ with SGLT2-ASO (G, I) (n=5, **p<0.01, ***p<0.001 vs CTRL).

Techniques Used: Saline, Western Blot, Clinical Proteomics



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Arraystar inc microarray analysis for cardiac mrna
(A) Predicted AP-1 (yellow) and KLF (framed) binding sites on mouse Ppara promoter. (B–C) Cardiac <t>mRNA</t> levels of Klf isoforms (B) and protein levels <t>of</t> <t>KLF5</t> and β-actin (C) in 10–12-weeks old C57BL/6 mice treated with 5 mg/kg LPS or saline (CTRL) (n=4–5; *P<0.05; **P<0.01; ***P<0.001 vs CTRL). (D–E) Ppara, Klf5 and Klf6 mRNA levels in HL-1 cells (D) treated with 1µg/ml LPS or saline (CTRL) for 9h (n=6; *p<0.05 vs. CTRL) or in aMHC-Pparg mice (E) treated with 5mg/kg LPS or saline (CTRL) for 8–10h (n=5; *p<0.05; **p<0.01 vs. CTRL).
Microarray Analysis For Cardiac Mrna, supplied by Arraystar inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/microarray analysis for cardiac mrna/product/Arraystar inc
Average 90 stars, based on 1 article reviews
microarray analysis for cardiac mrna - by Bioz Stars, 2026-03
90/100 stars
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(A) Predicted AP-1 (yellow) and KLF (framed) binding sites on mouse Ppara promoter. (B–C) Cardiac mRNA levels of Klf isoforms (B) and protein levels of KLF5 and β-actin (C) in 10–12-weeks old C57BL/6 mice treated with 5 mg/kg LPS or saline (CTRL) (n=4–5; *P<0.05; **P<0.01; ***P<0.001 vs CTRL). (D–E) Ppara, Klf5 and Klf6 mRNA levels in HL-1 cells (D) treated with 1µg/ml LPS or saline (CTRL) for 9h (n=6; *p<0.05 vs. CTRL) or in aMHC-Pparg mice (E) treated with 5mg/kg LPS or saline (CTRL) for 8–10h (n=5; *p<0.05; **p<0.01 vs. CTRL).

Journal: Circulation research

Article Title: Cardiac Myocyte KLF5 Regulates Ppara Expression and Cardiac Function

doi: 10.1161/CIRCRESAHA.115.306383

Figure Lengend Snippet: (A) Predicted AP-1 (yellow) and KLF (framed) binding sites on mouse Ppara promoter. (B–C) Cardiac mRNA levels of Klf isoforms (B) and protein levels of KLF5 and β-actin (C) in 10–12-weeks old C57BL/6 mice treated with 5 mg/kg LPS or saline (CTRL) (n=4–5; *P<0.05; **P<0.01; ***P<0.001 vs CTRL). (D–E) Ppara, Klf5 and Klf6 mRNA levels in HL-1 cells (D) treated with 1µg/ml LPS or saline (CTRL) for 9h (n=6; *p<0.05 vs. CTRL) or in aMHC-Pparg mice (E) treated with 5mg/kg LPS or saline (CTRL) for 8–10h (n=5; *p<0.05; **p<0.01 vs. CTRL).

Article Snippet: The microarray analysis for cardiac mRNA obtained from α MHC-Klf5 −/− mice was performed by Arraystar (data deposited in {"type":"entrez-geo","attrs":{"text":"GSE63839","term_id":"63839"}} GSE63839 ).

Techniques: Binding Assay, Saline

(A–D) Ppara and Klf5 mRNA (A, C) and protein (B, D) levels in HL-1 cells treated with Ad-cJunAsp (A, B) or Ad-KLF5 (C, D); (n=6; *p<0.05; **p<0.01; ***p<0.001 vs CTRL). (E–I) Enrichment of −792/−772 bp region (E, F) or −719/−698 bp region (G, H) of mouse Ppara promoter with c-Jun (E, G) or KLF5 (F, H) of chromatin samples from HL-1 cells treated with Ad-GFP (CTRL) and either Ad-cJunAsp (E, G) or Ad-KLF5 (F, H); **p<0.01 vs CTRL. (I) Enrichment of −792/−772 bp region of mouse Ppara promoter with c-Jun or KLF5 of chromatin samples from HL-1 cells treated with 1 µg/ml LPS or saline (CTRL); *p<0.05 vs CTRL. Data for all bar graphs are represented as means ± SEM (statistical analysis: t-test).

Journal: Circulation research

Article Title: Cardiac Myocyte KLF5 Regulates Ppara Expression and Cardiac Function

doi: 10.1161/CIRCRESAHA.115.306383

Figure Lengend Snippet: (A–D) Ppara and Klf5 mRNA (A, C) and protein (B, D) levels in HL-1 cells treated with Ad-cJunAsp (A, B) or Ad-KLF5 (C, D); (n=6; *p<0.05; **p<0.01; ***p<0.001 vs CTRL). (E–I) Enrichment of −792/−772 bp region (E, F) or −719/−698 bp region (G, H) of mouse Ppara promoter with c-Jun (E, G) or KLF5 (F, H) of chromatin samples from HL-1 cells treated with Ad-GFP (CTRL) and either Ad-cJunAsp (E, G) or Ad-KLF5 (F, H); **p<0.01 vs CTRL. (I) Enrichment of −792/−772 bp region of mouse Ppara promoter with c-Jun or KLF5 of chromatin samples from HL-1 cells treated with 1 µg/ml LPS or saline (CTRL); *p<0.05 vs CTRL. Data for all bar graphs are represented as means ± SEM (statistical analysis: t-test).

Article Snippet: The microarray analysis for cardiac mRNA obtained from α MHC-Klf5 −/− mice was performed by Arraystar (data deposited in {"type":"entrez-geo","attrs":{"text":"GSE63839","term_id":"63839"}} GSE63839 ).

Techniques: Saline

(A, B) Klf5 mRNA in the heart, skeletal muscle, intestine, kidney, white adipose tissue, brain (A) and primary cardiac myocytes (B) of aMHC-Klf5−/− mice (n=3; *p<0.05 vs floxed). (C) Hierarchical clustering for differentially expressed mRNAs detected by whole genome microarray analysis of cardiac mRNA obtained from aMHC-Klf5−/− mice and control floxed mice. Red color indicates high relative expression and blue color indicates low relative expression. (D–G) Gene ontology analysis for classification of the downregulated (D) or upregulated (E) genes based on the metabolic process that they are associated with and pathway analysis for downregulated (F) and upregulated (G) genes detected with whole genome microarray analysis of cardiac mRNA obtained from aMHC-Klf5−/− mice and control floxed mice. Data for all bar graphs are represented as means ± SEM (statistical analysis: t-test).

Journal: Circulation research

Article Title: Cardiac Myocyte KLF5 Regulates Ppara Expression and Cardiac Function

doi: 10.1161/CIRCRESAHA.115.306383

Figure Lengend Snippet: (A, B) Klf5 mRNA in the heart, skeletal muscle, intestine, kidney, white adipose tissue, brain (A) and primary cardiac myocytes (B) of aMHC-Klf5−/− mice (n=3; *p<0.05 vs floxed). (C) Hierarchical clustering for differentially expressed mRNAs detected by whole genome microarray analysis of cardiac mRNA obtained from aMHC-Klf5−/− mice and control floxed mice. Red color indicates high relative expression and blue color indicates low relative expression. (D–G) Gene ontology analysis for classification of the downregulated (D) or upregulated (E) genes based on the metabolic process that they are associated with and pathway analysis for downregulated (F) and upregulated (G) genes detected with whole genome microarray analysis of cardiac mRNA obtained from aMHC-Klf5−/− mice and control floxed mice. Data for all bar graphs are represented as means ± SEM (statistical analysis: t-test).

Article Snippet: The microarray analysis for cardiac mRNA obtained from α MHC-Klf5 −/− mice was performed by Arraystar (data deposited in {"type":"entrez-geo","attrs":{"text":"GSE63839","term_id":"63839"}} GSE63839 ).

Techniques: Microarray, Control, Expressing

(A) Ingenuity pathway analysis of genes regulated over 2-fold in the aMHC-Klf5−/− mouse array that are related to FA metabolism. (B) Cardiac Klf5 and Ppara mRNA levels of 10- to 12-week-old aMHC-Klf5−/− male and female mice (n=5; **p<0.01; ***p<0.001 vs same gender floxed mice). (C) Cardiac PPARα and β-actin protein levels of 10- to 12-week-old floxed and aMHC-Klf5−/− male mice. (D–F) Cardiac mRNA levels for FA oxidation- (Ppargc-1a, Ppargc-1β, Pparg, Ppard, Acox and Cpt1b) (D), lipid uptake- (Cd36, Lpl and Angptl4) (E) and lipid storage-related genes (Dgat1, Dgat2, Plin2, Plin5) (F) (n=5; *p<0.05, **p<0.01, ***p<0.001 vs same gender floxed mice). (G) Cardiac PGC-1, CPT-1, DGAT-1, ATGL, phosphorylated AMPK, total AMPK, and GAPDH protein levels of 10- to 12-week-old floxed and aMHC-Klf5−/− male mice. (H, I) [14C]-Palmitic acid (H) and [14C]-Glucose (I) oxidation levels in cardiac muscle of 10- to 12-week-old floxed and aMHC-Klf5−/− male mice (n=4–5; *p<0.05; **p<0.01 vs floxed mice). Data for all bar graphs are represented as means ± SEM (statistical analysis: t-test).

Journal: Circulation research

Article Title: Cardiac Myocyte KLF5 Regulates Ppara Expression and Cardiac Function

doi: 10.1161/CIRCRESAHA.115.306383

Figure Lengend Snippet: (A) Ingenuity pathway analysis of genes regulated over 2-fold in the aMHC-Klf5−/− mouse array that are related to FA metabolism. (B) Cardiac Klf5 and Ppara mRNA levels of 10- to 12-week-old aMHC-Klf5−/− male and female mice (n=5; **p<0.01; ***p<0.001 vs same gender floxed mice). (C) Cardiac PPARα and β-actin protein levels of 10- to 12-week-old floxed and aMHC-Klf5−/− male mice. (D–F) Cardiac mRNA levels for FA oxidation- (Ppargc-1a, Ppargc-1β, Pparg, Ppard, Acox and Cpt1b) (D), lipid uptake- (Cd36, Lpl and Angptl4) (E) and lipid storage-related genes (Dgat1, Dgat2, Plin2, Plin5) (F) (n=5; *p<0.05, **p<0.01, ***p<0.001 vs same gender floxed mice). (G) Cardiac PGC-1, CPT-1, DGAT-1, ATGL, phosphorylated AMPK, total AMPK, and GAPDH protein levels of 10- to 12-week-old floxed and aMHC-Klf5−/− male mice. (H, I) [14C]-Palmitic acid (H) and [14C]-Glucose (I) oxidation levels in cardiac muscle of 10- to 12-week-old floxed and aMHC-Klf5−/− male mice (n=4–5; *p<0.05; **p<0.01 vs floxed mice). Data for all bar graphs are represented as means ± SEM (statistical analysis: t-test).

Article Snippet: The microarray analysis for cardiac mRNA obtained from α MHC-Klf5 −/− mice was performed by Arraystar (data deposited in {"type":"entrez-geo","attrs":{"text":"GSE63839","term_id":"63839"}} GSE63839 ).

Techniques:

(A–F) Fractional shortening (A, D), left ventricular internal dimension during diastole (B, E), left ventricular internal dimension during systole (C, F), in 2–3 months old (A–C) and 6 months old (D–F) αMHC-Klf5−/− and floxed (WT) mice. (G–M) Photographs of echocardiograms (G), fractional shortening (H), left ventricular internal dimension during diastole (I), left ventricular internal dimension during systole (J) left ventricular posterior wall during diastole (K) left ventricular posterior wall during systole (L), and heart weight/tibia length ratio (M) in 8–12 months old αMHC-Klf5−/− and floxed (WT) mice (n=7–8; *p<0.05). (N, O) Cardiac mRNA levels for Bnp, Anf, αMHC and βMHC genes in 2–3 months old (N) and 11–12 months old (O) male floxed and αMHC-Klf5−/− mice (F) (n=5; *p<0.05, **p<0.01 vs floxed mice).

Journal: Circulation research

Article Title: Cardiac Myocyte KLF5 Regulates Ppara Expression and Cardiac Function

doi: 10.1161/CIRCRESAHA.115.306383

Figure Lengend Snippet: (A–F) Fractional shortening (A, D), left ventricular internal dimension during diastole (B, E), left ventricular internal dimension during systole (C, F), in 2–3 months old (A–C) and 6 months old (D–F) αMHC-Klf5−/− and floxed (WT) mice. (G–M) Photographs of echocardiograms (G), fractional shortening (H), left ventricular internal dimension during diastole (I), left ventricular internal dimension during systole (J) left ventricular posterior wall during diastole (K) left ventricular posterior wall during systole (L), and heart weight/tibia length ratio (M) in 8–12 months old αMHC-Klf5−/− and floxed (WT) mice (n=7–8; *p<0.05). (N, O) Cardiac mRNA levels for Bnp, Anf, αMHC and βMHC genes in 2–3 months old (N) and 11–12 months old (O) male floxed and αMHC-Klf5−/− mice (F) (n=5; *p<0.05, **p<0.01 vs floxed mice).

Article Snippet: The microarray analysis for cardiac mRNA obtained from α MHC-Klf5 −/− mice was performed by Arraystar (data deposited in {"type":"entrez-geo","attrs":{"text":"GSE63839","term_id":"63839"}} GSE63839 ).

Techniques:

(A) Ingenuity pathway analysis of cardiac genes regulated over 2-fold in the aMHC-Klf5−/− mouse array that have direct or indirect association with insulin signaling and glucose metabolism proteins. Highlighted with bold fonts within the diagram are proteins that modulate insulin signaling. (B) Fractional shortening of C57BL/6 mice 6 weeks post-STZ or saline (CTRL) administration (n=5; *p<0.05 vs CTRL). (C) Western blot analysis for cardiac KLF5 and β-actin protein levels in C57BL/6 mice 6 weeks post-STZ administration (n=3; ***p<0.001 vs CTRL). (D) Cardiac Klf5 and Ppara mRNA levels in floxed and aMHC-Klf5−/− mice 6 weeks post-STZ administration (n=5; *p<0.05, **p<0.01 vs CTRL). (E) Cardiac Klf5 and Ppara mRNA levels in 12 weeks old ob/ob mice compared with wild type C57BL/6 mice (n=4–5, *p<0.05, ***p<0.001 vs wt). (F–I) Plasma glucose levels (F, G) and cardiac Klf5 and Ppara mRNA levels (H, I) in wild type mice treated with STZ (6 weeks prior to glucose measurement), dapagliflozin (F, H), antisense oligonucleotides against SGLT2 (SGLT2-ASO) (G, I) and combination of either STZ with dapagliflozin (F, H) or STZ with SGLT2-ASO (G, I) (n=5, **p<0.01, ***p<0.001 vs CTRL).

Journal: Circulation research

Article Title: Cardiac Myocyte KLF5 Regulates Ppara Expression and Cardiac Function

doi: 10.1161/CIRCRESAHA.115.306383

Figure Lengend Snippet: (A) Ingenuity pathway analysis of cardiac genes regulated over 2-fold in the aMHC-Klf5−/− mouse array that have direct or indirect association with insulin signaling and glucose metabolism proteins. Highlighted with bold fonts within the diagram are proteins that modulate insulin signaling. (B) Fractional shortening of C57BL/6 mice 6 weeks post-STZ or saline (CTRL) administration (n=5; *p<0.05 vs CTRL). (C) Western blot analysis for cardiac KLF5 and β-actin protein levels in C57BL/6 mice 6 weeks post-STZ administration (n=3; ***p<0.001 vs CTRL). (D) Cardiac Klf5 and Ppara mRNA levels in floxed and aMHC-Klf5−/− mice 6 weeks post-STZ administration (n=5; *p<0.05, **p<0.01 vs CTRL). (E) Cardiac Klf5 and Ppara mRNA levels in 12 weeks old ob/ob mice compared with wild type C57BL/6 mice (n=4–5, *p<0.05, ***p<0.001 vs wt). (F–I) Plasma glucose levels (F, G) and cardiac Klf5 and Ppara mRNA levels (H, I) in wild type mice treated with STZ (6 weeks prior to glucose measurement), dapagliflozin (F, H), antisense oligonucleotides against SGLT2 (SGLT2-ASO) (G, I) and combination of either STZ with dapagliflozin (F, H) or STZ with SGLT2-ASO (G, I) (n=5, **p<0.01, ***p<0.001 vs CTRL).

Article Snippet: The microarray analysis for cardiac mRNA obtained from α MHC-Klf5 −/− mice was performed by Arraystar (data deposited in {"type":"entrez-geo","attrs":{"text":"GSE63839","term_id":"63839"}} GSE63839 ).

Techniques: Saline, Western Blot, Clinical Proteomics