Fig. 4 Analysis of ISO response in vitro in neonatal cardiomyocytes.

Slides:



Advertisements
Similar presentations
Fig. 1. TP is highly expressed in myeloma.
Advertisements

Fig. 7. Downstream effects of α-synuclein on mitochondria.
Fig. 3. Ultrasound-mediated BMP-6 gene delivery to mini-pig tibial bone fractures. Ultrasound-mediated BMP-6 gene delivery to mini-pig tibial bone fractures.
Fig. 5. Circulating PPi concentration does not correlate with severity of calcification phenotype in mice. Circulating PPi concentration does not correlate.
Fig. 4. Intramuscular injection of AAV9-Cas9/sgRNA-51 corrects dystrophin expression. Intramuscular injection of AAV9-Cas9/sgRNA-51 corrects dystrophin.
In vivo function of MeTro sealants using rat incision model of lungs
Fig. 8. Gene and protein changes in ALK-dependent STING pathways in human sepsis. Gene and protein changes in ALK-dependent STING pathways in human sepsis.
Fig. 5. Correlation of tail and long bone growth velocities with Cxm serum concentrations in mice. Correlation of tail and long bone growth velocities.
β-ARs signal cooperatively with mutant EGFR and inactivate LKB1
Fig. 4. Biomechanical properties of treated tibiae.
Fig. 4. aPD-1 mAb transfer to macrophages is mediated by FcγRs.
Chd5 deficiency in NSCs leads to premature activation.
Analysis of brain and spinal cord of treated Gaa−/− mice and controls
Fig. 3. A circadian rhythm in fibroblast wound-healing response.
Fig. 4 Infection-induced CLV dysfunction is associated with decreased LMC coverage. Infection-induced CLV dysfunction is associated with decreased LMC.
Expression of CD36 and psap in a TMA of human ovarian cancer patients
Fig. 6. Effects of CD31-NP targeting in perfused human kidneys.
Fig. 4. Specific versus nonspecific NP accumulation.
Dot plots of trisomic versus fetal fractions for cohorts 1 and 2
Fig. 7 Gel scaffold for inhibition of postsurgical recurrence of B16F10 tumors. Gel scaffold for inhibition of postsurgical recurrence of B16F10 tumors.
Fig. 5 Acute loss of mitochondrial content after impact is prevented by inhibition of electron transport or critical redox events. Acute loss of mitochondrial.
Fig. 6. A circadian rhythm in keratinocyte wound healing and a diurnal variation in human burn healing outcome. A circadian rhythm in keratinocyte wound.
Fig. 1. Generation of the ΔEx50 mouse model.
Disrupted dynamics of early stages of differentiation perturbs neural cell fate specification. Disrupted dynamics of early stages of differentiation perturbs.
Fig. 2 In vitro assessment of hESC-RPE cell sheets.
Fig. 2 STED microscopy of isolated cardiomyocytes from mice treated with MP-rhodamine–loaded CaPs. STED microscopy of isolated cardiomyocytes from mice.
Fig. 2. Best model fits. Best model fits. Illustration of the best model fits for the (A) basic, (B) continuous, and (C) cluster models. See Table 1 and.
Fig. 1. Muscles of LAMA2 MD patients and dyW/dyW mice contain high amounts of laminin-α4 and show deficits in BM. Muscles of LAMA2 MD patients and dyW/dyW.
Fig. 6. Apoptotic MSCs exert in vivo immunosuppression in a TH2-type inflammation model in the absence of cytotoxic cells. Apoptotic MSCs exert in vivo.
Fig. 4. Expression of HGF in liver ECs cooperates with NOX4 inhibition to enhance engraftment of regenerative hepatocytes. Expression of HGF in liver ECs.
Fig. 4. Actin polymerization rhythms are required for circadian regulation of adhesion and wound-healing efficacy by fibroblasts. Actin polymerization.
Mitochondrial homeostasis.
Fig. 3. β-AR signaling induces IL-6 in NSCLC cells via activation of PKC and CREB. β-AR signaling induces IL-6 in NSCLC cells via activation of PKC and.
Fig. 3. Differential mPFC PV neuron activity during exploratory behaviors in CNTNAP2 KO and WT mice. Differential mPFC PV neuron activity during exploratory.
P53 inhibition impairs expansion of HSCs with VPA by increasing ROS levels. p53 inhibition impairs expansion of HSCs with VPA by increasing ROS levels.
Fig. 5 Local gel scaffold for T cell memory response.
Fig. 2 Fas controls IL-1RA–sEV secretion in murine MSCs.
Fig. 1 BX795 suppresses HSV-1 infection.
Fig. 7 Improvement of clinical score and axon pathology by nasal IL-4 treatment during chronic EAE. Improvement of clinical score and axon pathology by.
Fig. 8 SQLE inhibitor terbinafine suppresses NAFLD-HCC growth in vitro and in vivo. SQLE inhibitor terbinafine suppresses NAFLD-HCC growth in vitro and.
Fig. 5. Nutlin-3 treatment rescues the proliferation and differentiation of NPCs in vitro. Nutlin-3 treatment rescues the proliferation and differentiation.
Fig. 4 TNF-α up-regulates Fas/Fap-1 expression to promote IL-1RA–sEV release in murine MSCs. TNF-α up-regulates Fas/Fap-1 expression to promote IL-1RA–sEV.
Fig. 3 Chronic work overload leads to mitochondrial calcium overload.
Fig. 6. Rolling neutrophils extract membranes from fragile remnant PS+ platelets. Rolling neutrophils extract membranes from fragile remnant PS+ platelets.
Fig. 3 Tetrode trials and behavioral study in rats.
Fig. 1. β-APP overexpression or exposure to inflammatory mediators induces sIBM-like pathology in cultured rat myocytes that is abrogated by arimoclomol.
Fig. 7. NAC in breast cancer patients promotes TMEM assembly and increased MENAINV expression. NAC in breast cancer patients promotes TMEM assembly and.
Fig. 4. The effect of single-dose rozanolixizumab on the concentration of IgG subtypes in healthy subjects. The effect of single-dose rozanolixizumab on.
Fig. 6 Anticancer effects in PyMT-MMTV syngeneic and MDA-MB-231 xenograft-bearing mice. Anticancer effects in PyMT-MMTV syngeneic and MDA-MB-231 xenograft-bearing.
Fig. 2 In vitro and preclinical study with 18F-MPG.
Fig. 3 CSF1 is expressed in human melanoma.
Fig. 6 DMF inhibits NF-κB translocation upon infection.
Fig. 7. Scale-up of AAV vector–mediated liver gene transfer of secretable GAA to nonhuman primates. Scale-up of AAV vector–mediated liver gene transfer.
Fig. 1 LB100 and LB102 specifically inhibit PP2A phosphatase activity and the growth of BCR-ABL+ cells. LB100 and LB102 specifically inhibit PP2A phosphatase.
Correlation of reovirus RNA/protein with proliferating tumor cells
Fig. 2. Thorase variants cause impaired GluA2 endocytosis and trafficking in mouse primary cortical neurons. Thorase variants cause impaired GluA2 endocytosis.
Nuclear DNA signal is altered in Chd5-deficient NSCs.
MAPK14 regulates ROS generation in GS cells.
Fig. 3 Chronic work overload leads to mitochondrial calcium overload.
Chd5 deficiency leads to compromised expression of the repressive histone mark H3K27me3 and up-regulation of ribosomal protein genes. Chd5 deficiency leads.
High-affinity mutants of β3 integrin fail to stimulate RhoA activity and fibronectin fibrillogenesis. High-affinity mutants of β3 integrin fail to stimulate.
PGC-1α silencing in RPE cells promotes mitochondrial dysfunction and oxidative stress. PGC-1α silencing in RPE cells promotes mitochondrial dysfunction.
Volume 23, Issue 6, Pages (May 2018)
Fig. 6 Reduced mitochondrial respiration upon Lkb1 loss does not affect glial differentiation. Reduced mitochondrial respiration upon Lkb1 loss does not.
Fig. 2 In vitro and preclinical study with 18F-MPG.
Fig. 5 C9orf72 knockdown disrupts autophagy induction.
NRAS-mediated resistance to vemurafenib (Vem) is associated with restored glycolysis and can be overcome by combination with a glycolysis inhibitor. NRAS-mediated.
Fig. 7 Heart-specific OMA1 down-regulation protects from hypertrophy induced by TAC. Heart-specific OMA1 down-regulation protects from hypertrophy induced.
Fig. 2 BX795 is nontoxic to HCE cells at therapeutic concentration.
Fig. 3 TDP1 promotes OXPHOS at basal and high ATP demands.
Presentation transcript:

Fig. 4 Analysis of ISO response in vitro in neonatal cardiomyocytes. Analysis of ISO response in vitro in neonatal cardiomyocytes. (A) Mitochondrial respirometry analysis of neonatal cardiomyocytes upon different treatments measured by Seahorse and maximum respiration rate (MRR) quantification. FCCP, carbonyl cyanide p-trifluoromethoxyphenylhydrazone; FBS, fetal bovine serum; NAC, N-acetyl-l-cysteine; OCR, oxygen consumption rate. (B) 2′,7′-Dichlorofluorescein diacetate (H2-DCFDA)–mediated ROS quantification in neonatal cardiomyocytes upon different treatments. (C) Fura-2-acetoxymethyl ester (Fura-2 AM)–mediated intramitochondrial calcium quantification in neonatal cardiomyocytes upon different treatments. (D) Tetramethylrhodamine methyl ester perchlorate (TMRM)–mediated mitochondrial membrane potential determination in neonatal cardiomyocytes upon different treatments. (E) Analysis of OPA1 processing by Western blot. (F) Analysis of MCU expression by Western blot of mitochondrial lysate. SDHA and core2 are used as loading controls. (G) Kurtosis analysis as indicator of calcium distribution in the cardiomyocytes at the indicated treatments. Basal and final treatments correspond to time 0 and time 9 min, respectively. (H) Time-lapse images (40×) at the indicated time showing calcium (Fura-2 AM) and mitochondrial (MitoTracker Deep Red) distribution under different treatments. Scale bars, 20 μM. Data in upper and middle panels of (A) are given as means ± SEM and in the rest of graphics as scatter dot plots, and lines are means ± SD. Differences assessed by two-way ANOVA and Sidak’s multiple comparison test (A) or one-way ANOVA and Tukey’s multiple comparison test (B to F). N as described in table S1; *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001. Rebeca Acin-Perez et al., Sci Transl Med 2018;10:eaan4935 Published by AAAS