Fig 1: MitoQ improves myotube atrophy and in vitro metabolism. (A,B) Myosin heavy chain (MyHC; green) and DAPI (blue) immunofluorescent staining in C2C12 myotubes exposed to unconditioned medium or 20% C26 CM (C26) and treated with 75 µM MitoQ or TPP for up to 48 h. Myotube size was determined by measuring the minimum diameter of 250–350 myotubes per experimental condition (n = 3). Scale bar, 100 µm. (C) Gene expression levels for Atrogin-1 Murf1, PDK4 and Lipe in C2C12 myotubes. Gene expression was normalized to TBP levels and expressed as fold change vs. TPP. (D,E) Representative Western blotting and quantification for phospho-AKT (pAKT), AKT, phospho-mTOR (pmTOR), mTOR, phospho-4EBP1 (p4EBP1), 4EBP1, PDK4, phospho-PDH (pPDH), PDH, expressed as fold change vs. TPP. Tubulin was used as loading control. Statistical significance was evaluated by two-way analysis of variance, and significant differences (at least p < 0.05) were reported as * p < 0.05, ** p < 0.01, *** p < 0.001 vs. TPP; $ p < 0.05, $$ p < 0.01, $$$ p < 0.001 vs. C26 + TPP.
Fig 2: PN upregulated the expression of ATP4a in cmECs. (A-C) The expression of ATP4a in cmECs, LPMC, and cmVECs; (D,E) the expression of ATP4a protein in the cell membranes and mitochondria; (F-H) the expression of ATP4a and PDK4 protein in cmECs. PN, panax notoginseng; ATP4a, ATPase H+/K+ Transporting Subunit Alpha; cmEC, colonic mucosal epithelial cells; LPMC, lamina propria mononuclear cells; cmVECs, colonic mucosal microvascular endothelial cells; PDK4, pyruvate dehydrogenase lipoamide kinase isozyme 4.
Fig 3: Mitochondrial functions and oxidative status are linked to retinoic acid insufficiency in the heart of the Bco2 -/- mice. (A) Assessment of mitochondrial DNA content via gene expression of Atp6, CytoxII, and Nd5 measured by real-time RT-PCR in the heart (left ventricle) of WT and Bco2 -/- female mice (n = 4–6 mice/genotype). Values are calculated using the 2-??CT method. (B) Immunoblot and quantification of the oxidative phosphorylation complexes I-V in the heart (left ventricle) of 12-14-week-old WT and Bco2 -/- female mice (n = 3 mice/genotype). (C) mRNA expression of genes regulating mitochondria dynamics (Fis1, Drp1, Pink1, Parkin, Mfn1, Mfn2) and (D) oxidative stress-related pathways (Alcat1, Prx3, Gpx1, p22phox, Sod1, Sod2) measured by real-time RT-PCR in the heart (left ventricle) of WT and Bco2 -/- female mice (n = 4–6 mice/genotype). Values are calculated using the 2-??CT method. Values are mean ± SD. Statistical analysis by t-test between genotypes within each gene; *p = .05. (E) Cardiac (whole heart) retinoic acid concentrations are measured by LC–MS/MS (n = 3–4 mice/genotype) in vehicle- (drinking water), or NAC-supplemented WT and Bco2 -/- female mice. (F) Pdk4 mRNA expression in the whole heart (n = 4–6 mice/genotype) of vehicle or NAC-supplemented WT and Bco2 -/- female mice. Values are expressed as mean ± SD. (G) Immunoblot and quantification of PDK4 (47 kDa) in the heart (left ventricle) of 12-14-week-old WT and Bco2 -/- female mice (n = 3 mice/genotype). Levels of vinculin (118 kDa) were used as the loading control. In E and F, normally distributed data were statistically analyzed with a two-way ANOVA. Different letters indicate a significant difference among the groups, p = .05.
Fig 4: MiR-107 targeted PDK4 to inhibit OC cell proliferation, migration and invasion. a. MiR-107 mimic and PDK4 overexpression plasmids were co-transfected into OC cells, and CCK-8 assay was used for examining cell proliferation after transfection. b. Western blot was used to detect PCNA and cyclin D1 protein expression levels. c & d. Transwell assays were used to detect cell migration and invasion after transfection. *P < 0.05, **P < 0.01 and ***P < 0.001
Fig 5: PDK1 and PDK2 expression levels are decreased in human visceral adipose tissue and are positively correlated with the PPAR? expression level.a Correlations between the mRNA expression of PDK1, PDK2, PDK3, and PDK4 and body mass index (BMI). b Correlations of PPAR? and SREBP-1c mRNA expression with BMI. c Correlations between the expression of PDK isoforms and that of PPAR?.
Supplier Page from Abcam for Anti-PDK4 antibody [EPR19727-245]