Fig. 3 Chronic work overload leads to mitochondrial calcium overload.

Slides:



Advertisements
Similar presentations
Fig. 4. Primary human metastatic melanomas contain CCL21-expressing LECs, and expression of VEGFC positively correlates with hallmarks of tumor inflammation.
Advertisements

John D. Widdrington, PhD, MRCP, Aurora Gomez-Duran, PhD, Jannetta S
Fig. 3. Copy number loss as a potential resistance mechanism in an independent cohort. Copy number loss as a potential resistance mechanism in an independent.
Fig. 5. Blocking LTB4 during initial lymphangiogenesis period abrogates the therapeutic benefit of LTB4 antagonism. Blocking LTB4 during initial lymphangiogenesis.
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.
BET inhibition and depletion repress the expression of BRCA1 and RAD51
Fig. 4. Bexarotene promotes PPARδ activation of target genes in mouse brain and muscle. Bexarotene promotes PPARδ activation of target genes in mouse brain.
Fig. 2. Mechanism of PD-L1 down-regulation in NOD HSPCs.
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. 3. Obese IFN-γ−/− mice develop accelerated NAFLD with fibrosis.
Fig. 2. Engraftment of CART-EGFRvIII and cytokine modulation in the peripheral blood. Engraftment of CART-EGFRvIII and cytokine modulation in the peripheral.
Comparison of N. gonorrhoeae gene expression during infection in men and women in vivo. Comparison of N. gonorrhoeae gene expression during infection in.
Fig. 6. Treatment with a DLK inhibitor is neuroprotective and reverses stress-induced gene expression changes. Treatment with a DLK inhibitor is neuroprotective.
Fig. 5. Wisper is associated with TIA1-related protein and regulates lysyl hydroxylase 2 expression. Wisper is associated with TIA1-related protein and.
Analysis of brain and spinal cord of treated Gaa−/− mice and controls
Fig. 1. Identification of SE-associated lncRNAs.
Fig. 5. Antitumor efficacy of ERY974 in immunocompetent human CD3 transgenic mice. Antitumor efficacy of ERY974 in immunocompetent human CD3 transgenic.
Fig. 5 A competent Fc is required for the antitumor immune response.
Analysis of total and polysomal RNA clk-1(qm30) and clk-1(qm30)+WT.
Fig. 5. Vascularization of human liver seed grafts.
Dot plots of trisomic versus fetal fractions for cohorts 1 and 2
Identification of bioactive compounds modulating STING activation
Fig. 7 Gel scaffold for inhibition of postsurgical recurrence of B16F10 tumors. Gel scaffold for inhibition of postsurgical recurrence of B16F10 tumors.
Fig. 1. Generation of the ΔEx50 mouse model.
Fig. 2 STED microscopy of isolated cardiomyocytes from mice treated with MP-rhodamine–loaded CaPs. STED microscopy of isolated cardiomyocytes from mice.
Fig. 6 Malaria and l-arginine induce changes in the expression of inflammatory and angiogenic mediators in placental tissue by reverse transcription PCR.
Fig. 3 Fbln4E57K/E57K mice develop large artery stiffness and systolic hypertension. Fbln4E57K/E57K mice develop large artery stiffness and systolic hypertension.
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.
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. 5 Local gel scaffold for T cell memory response.
Fig. 2 Fas controls IL-1RA–sEV secretion in murine MSCs.
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. 1. PGBD5-expressing cells do not tolerate deficiency of nonhomologous end-joining DNA repair. PGBD5-expressing cells do not tolerate deficiency of.
Fig. 5. Nutlin-3 treatment rescues the proliferation and differentiation of NPCs in vitro. Nutlin-3 treatment rescues the proliferation and differentiation.
Stroke induces atheroprogression via the RAGE-signaling pathway
Volume 22, Issue 3, Pages (January 2018)
Fig. 7. Genetic ablation of UCP2 compromised the protective effect of exogenous irisin on lung IR injury. Genetic ablation of UCP2 compromised the protective.
Fig. 3. TKI sensitivity assessed by the MANO method.
Fig. 2 In vitro and preclinical study with 18F-MPG.
Fig. 3. VEGFR-3 signaling increases infiltration of naïve T cells in a CCR7-dependent manner. VEGFR-3 signaling increases infiltration of naïve T cells.
Fig. 4 Analysis of ISO response in vitro in neonatal cardiomyocytes.
Significant differences in translational efficiencies of DNA damage repair pathway genes between patient clusters. Significant differences in translational.
Fig. 1 Differentiation of human peripheral blood monocytes into MDMi cells induces a microglial gene expression and functional phenotype. Differentiation.
Fig. 6 DMF inhibits NF-κB translocation upon infection.
Fig. 5 Early and modest immune response at day 3 after exposure in Delayed animals. Early and modest immune response at day 3 after exposure in Delayed.
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.
Daple is required for activation of Gαi3, Rac1, and AKT signals and in the antagonistic inhibition of β-catenin–dependent Wnt signals downstream of EGF/EGFR.
Fig. 7 Correlation of NHP and human ISGs.
Ingenuity pathway analysis of the genes enriched in both 96-h-induced MMs and human ccRCC. Ingenuity pathway analysis of the genes enriched in both 96-h-induced.
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.
Genetic maintenance of histone acetylation prevents gene expression changes in the promoters of genes responding to acute mtDNA depletion. Genetic maintenance.
Phospho-proteomic analysis of acutely and chronically stimulated PDGFRα signaling. Phospho-proteomic analysis of acutely and chronically stimulated PDGFRα.
Thomas Münzel et al. JACC 2018;71:
Fig. 5 A competent Fc is required for the antitumor immune response.
(A) Western blot probing nuclear extract from wild-type (wt) and the newly generated ACF1 mutant (AcfC) embryos (0–16 h). (A) Western blot probing nuclear.
The CREBBP-modulated network is enriched in signaling pathways upregulated in the light zone (LZ). The CREBBP-modulated network is enriched in signaling.
Fig. 5 Transcriptional changes in dKO mice after HFD regimen.
Loss of BAP1 blocks T cell differentiation at the DN3 stage in vitro.
Fig. 5 n-HA regulates gene expressions related to tumor suppression, calcium homeostasis, and immune response. n-HA regulates gene expressions related.
Fig. 3 Transcriptional changes in dKO mice.
Fig. 7 Heart-specific OMA1 down-regulation protects from hypertrophy induced by TAC. Heart-specific OMA1 down-regulation protects from hypertrophy induced.
Panobinostat induces reversible perturbations in PBMC gene expression patterns. Panobinostat induces reversible perturbations in PBMC gene expression patterns.
Fig. 6 Pharmacologic alterations of β-AR signaling regulate cardiomyocyte abscission and endowment. Pharmacologic alterations of β-AR signaling regulate.
Cxxc1-deficient TH17 cells exhibit a Treg cell–like expression profile
Presentation transcript:

Fig. 3 Chronic work overload leads to mitochondrial calcium overload. Chronic work overload leads to mitochondrial calcium overload. (A) Principal component (PC) analysis of RNA sequencing data from the hearts of control and ISO-treated mice (7 days). CPM, continuous phase modulation. (B) Most relevant Ingenuity Canonical Pathways (ICPs) enriched using the differentially expressed genes in OMA1KO ISO versus control. The inner bar circle represents the fold enrichment and the overall changes as a z score. The outer circle displays the logFC of the differentially expressed genes belonging to each category. eNOS, endothelial nitric oxide synthase; mTOR, mammalian target of rapamycin; NO, nitric oxide; iNOS, inducible nitric oxide synthase; ATM, ataxia-telangiectasia mutated. (C) Detailed relationship between changed genes [abs(logFC) ≥ 1 in any contrast] and the pathways selected by Chord Plots [left: logFC of genes in the contrasts ISO versus control of WT (inner) and OMA1KO (outer) mice; right: ICPs connected to the genes]. For (B) and (C), red represents up-regulated genes, and blue represents down-regulated genes. (D) Western blot analysis of mitochondrial lysated and quantification of mitochondrial calcium uniporter (MCU) components (MCU and M1CU1) after short chronic (7 days) ISO administration. (E) Western blot analysis and quantification of MCU expression modulation by mitochondrial ROS (mtROS) after chronic (28 days) ISO administration. (F to H) Effects of mitochondrial fission blockade with Mdivi1. (I to K) Effects of ryanodine receptor 2 (RyR2) activation with caffeine. (L to N) Effects of RyR2 blockade with dantrolene. (F, I, and L) Cardiac contractility (% EF and HR); (G, J, and M) Mitochondrial ATP synthesis; (H, K, and N) OPA1 processing and MCU expression. Loading controls were SDHA, core1, core2, MnSOD, and Tom20. Data are given as scatter dot plots, and lines are means ± SD. Differences assessed by one-way ANOVA and Tukey’s multiple comparison test. 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