Data_Sheet_1_Language and face in interactions: emotion perception, social meanings, and communicative intentions.docx

IntroductionHuman emotions can be complex to interpret as they have multiple sources and are often times ambiguous, for example, when the signals sent by different channels of communication are inconsistent. Our study investigates the interaction of linguistic and facial expressions of emotions.MethodsIn two experiments, participants read short scenarios in German containing a direct utterance with positive or negative emotive markers, in combination with different facial expressions as still images of the speaker (i.e., the protagonist in the story). They answered questions about their perception regarding the intensity of the emotions (e.g., happiness, sadness), the properties of the expresser (e.g., honesty, warmth, likeability) and their relation to the addressee (e.g., closeness), as well as the expresser intention (e.g., irony, joke).ResultsThe findings suggest that facial expressions have a more dominant role in the emotion perception in comparison to emotive markers. Furthermore, consistent and inconsistent combinations of emotive markers and facial expressions convey distinct social meanings and communicative intentions.ConclusionThis research points to the importance to consider emotive markers in the emotional context that they occur in.</p

The role of PI3K/Akt signaling in the protection by fasudil was evaluated by using an Akt inhibitor, LY294002.

<p>Sham group, I/R group and I/R+fasudil group were either given LY294002 or placebo (n = 6 for each group rats treated with LY294002 for both time points, all the other rats are the same as shown in above). Western blotting was performed, targeting phosphorylation levels of Akt (representative protein bands shown in Panel A and quantified in bar graph in Panel B); JAK2 (Panel C & D), STAT3 (Panel E & F) and PLB (Panel G & H). SERCA protein expression levels (Panel I & J) were also analyzed. All data expressed as mean±SD. * denotes P<0.05 vs. Sham groups; †, P<0.05 vs. I/R group at the same time point and ‡, P<0.05 vs. I/R+fasudil group at the same time point.</p

SERCA activity, PLB phosphorylation and SERCA protein expression levels were measured.

<p>Using the same tissue obtained from each group as described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0048115#pone-0048115-g002" target="_blank">figure 2</a>, SERCA activity (Panel A), phosphorylation level of PLB (representative protein bands shown in Panel B and quantification in bar graph of Panel C) and SERCA protein expression level (Panel D & E) were quantified also shown. All data expressed as mean±SD. * denotes P<0.05 vs. Sham groups at the same time point and †, P<0.05 vs. I/R group at the same time point.</p

ROCK activity was measured in the presence of either PI3K/Akt inhibitor, LY294002, or JAK2 inhibitor, AG490, by quantifying the phosphorylation level of ERM.

<p>Representative bands for p-ERM and total ERM were shown for each group rats (n = 6 for either sham or I/R group rats treated with LY294001 or AG490, the other group rats are the same as shown above). All data expressed as mean±SD. * denotes P<0.05 vs. sham group.</p

The role for JAK2/STAT3 signaling pathway was also tested by using pharmacological inhibitor.

<p>Sham group, I/R group and I/R+fasudil group were either given AG490 or placebo (n = 6 for each group rats treated with AG490 for both time points, all the other rats are the same as shown in above). Western blotting was performed, targeting phosphorylation levels of Akt (Panel A showed representative protein bands for each group with quantification shown in bar graph in Panel B), JAK2 (Panel C & D), STAT3 (Panel E & F) and PLB (Panel G & H). SERCA protein expression levels (Panel I & J) were also analyzed. All data expressed as mean±SD. * denotes P<0.05 vs. Sham groups at the same time point; †, P<0.05 vs. I/R group at the same time point and ‡, P<0.05 vs. I/R+fasudil group at the same time point.</p

Data_Sheet_1_Cardioprotective Effect of Paeonol on Chronic Heart Failure Induced by Doxorubicin via Regulating the miR-21-5p/S-Phase Kinase-Associated Protein 2 Axis.PDF

BackgroundThis study primarily explored the role of paeonol in doxorubicin (DOX)-induced chronic heart failure (CHF), considering the cardioprotective effect of paeonol on an epirubicin-induced cardiac injury.MethodsDOX-induced CHF-modeled rats were treated with paeonol. Cardiac function and myocardial damage in rats were evaluated by using the multifunction instrument, and the histopathology, apoptosis, and the expression of miR-21-5p and S-phase kinase-associated protein 2 (SKP2) in myocardium were detected. The target gene of miR-21-5p was confirmed by a dual-luciferase reporter assay. After the required transfection or paeonol treatment, the viability, apoptosis, mitochondrial membrane potential (MMP), and reactive oxygen species (ROS) of the DOX-induced cardiomyocytes were determined. Reverse-transcription quantitative-PCR (RT-qPCR) and Western blot were performed to quantify the expressions of miR-21-5p, SKP2, and apoptosis-related factors.ResultsPaeonol improved cardiac function and also ameliorated the cardiac damage of CHF-modeled rats, where the downregulation of abnormally elevated myocardial damage markers, including brain natriuretic peptide, lactate dehydrogenase, renin, angiotensin II, aldosterone, and endothelin 1, was observed. Paeonol alleviated the histopathological injury and suppressed the apoptosis in CHF-modeled rats, inhibited miR-21-5p expression, and upregulated SKP2 expression in vitro and in vivo. miR-21-5p targeted SKP2. Paeonol and SKP2 increased the viability and MMP, but reduced apoptosis and ROS in the DOX-induced cardiomyocytes. miR-21-5p exerted effects opposite to PAE and SKP2, and it downregulated the expression of Bcl-2 and mitochondrion-Cytochrome c (Cyt c) and upregulated the expression of Bax, C-caspase-3, and cytoplasm-Cyt c. miR-21-5p reversed the effects of paeonol, and its effects were further reversed by SKP2.ConclusionPaeonol shows a cardioprotective effect on DOX-induced CHF via regulating the miR-21-5p/SKP2 axis.</p

Both PI3K/Akt and JAK2/STAT3 pathway activities were quantified.

<p>Using the same heart tissue described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0048115#pone-0048115-g002" target="_blank">figure 2</a>, western blotting was performed for each group targeting phosphorylation levels of Akt (representative protein bands shown in Panel A and quantified in bar graph in Panel B), phosphorylation levels of JAK2 (Panel C and D) and STAT3 (Panel E and F). All data expressed as mean±SD. * denotes P<0.05 vs. Sham groups; †, P<0.05 vs. I/R group at the same time point and #, P<0.05 vs. I/R+fasudil group at 3 hours of reperfusion.</p

Different SERCA isoform expressions were quantified.

<p>Using the same heart tissue described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0048115#pone-0048115-g002" target="_blank">figure 2</a>, western blotting was performed using specific antibodies to measure the expression levels of different isoforms of SERCA. Panel A showed representative bands of SERCA2a for each group rats with quantification shown in bar graph, Panel B showed quantification of SERCA2b, and Panel C for SERCA3. All data expressed as mean±SD. * denotes P<0.05 vs. Sham groups; †, P<0.05 vs. I/R group at the same time point.</p

Fasudil Protects the Heart against Ischemia-Reperfusion Injury by Attenuating Endoplasmic Reticulum Stress and Modulating SERCA Activity: The Differential Role for PI3K/Akt and JAK2/STAT3 Signaling Pathways

<div><p>Disordered calcium homeostasis can lead to endoplasmic reticulum (ER) stress. Our previous data showed that time course activation of ER stress contributes to time-related increase in ischemia-reperfusion (I/R) injury. However, it has not been tested whether PI3K/Akt and JAK2/STAT3 pathways play differential roles in reducing ER stress to protect the heart. In the present study, using fasudil which is a specific inhibitor of ROCK, we aimed to investigate whether improved SERCA expression and activity accounts for reduced ER stress by ROCK inhibition, specifically whether PI3K/Akt and JAK2/STAT3 pathways are differentially involved in modulating SERCA activity to reduce ER stress and hence I/R injury. The results showed that during the reperfusion period following 45 min of coronary ligation the infarct size (IS) increased from 3 h of reperfusion (45.4±5.57%) to 24 h reperfusion (64.21±5.43, P<0.05), which was associated with ER stress dependent apoptosis signaling activation including CHOP, Caspase-12 and JNK (P<0.05, respectively).The dynamic ER stress activation was also related to impaired SERCA activity at 24 h of reperfusion. Administration of fasudil at 10 mg/Kg significantly attenuated ROCK activation during reperfusion and resulted in an improved SERCA activity which was closely associated with decreases in temporal activation of ER stress and IS changes. Interestingly, while both PI3K/Akt and JAK2/STAT3 signaling pathways played equal role in the protection offered by ROCK inhibition at 3 h of reperfusion, the rescued SERCA expression and activity at 24 h of reperfusion by fasudil was mainly due to JAK2/STAT3 activation, in which PI3K/Akt signaling shared much less roles.</p> </div

Image_1_Cardioprotective Effect of Paeonol on Chronic Heart Failure Induced by Doxorubicin via Regulating the miR-21-5p/S-Phase Kinase-Associated Protein 2 Axis.TIF

BackgroundThis study primarily explored the role of paeonol in doxorubicin (DOX)-induced chronic heart failure (CHF), considering the cardioprotective effect of paeonol on an epirubicin-induced cardiac injury.MethodsDOX-induced CHF-modeled rats were treated with paeonol. Cardiac function and myocardial damage in rats were evaluated by using the multifunction instrument, and the histopathology, apoptosis, and the expression of miR-21-5p and S-phase kinase-associated protein 2 (SKP2) in myocardium were detected. The target gene of miR-21-5p was confirmed by a dual-luciferase reporter assay. After the required transfection or paeonol treatment, the viability, apoptosis, mitochondrial membrane potential (MMP), and reactive oxygen species (ROS) of the DOX-induced cardiomyocytes were determined. Reverse-transcription quantitative-PCR (RT-qPCR) and Western blot were performed to quantify the expressions of miR-21-5p, SKP2, and apoptosis-related factors.ResultsPaeonol improved cardiac function and also ameliorated the cardiac damage of CHF-modeled rats, where the downregulation of abnormally elevated myocardial damage markers, including brain natriuretic peptide, lactate dehydrogenase, renin, angiotensin II, aldosterone, and endothelin 1, was observed. Paeonol alleviated the histopathological injury and suppressed the apoptosis in CHF-modeled rats, inhibited miR-21-5p expression, and upregulated SKP2 expression in vitro and in vivo. miR-21-5p targeted SKP2. Paeonol and SKP2 increased the viability and MMP, but reduced apoptosis and ROS in the DOX-induced cardiomyocytes. miR-21-5p exerted effects opposite to PAE and SKP2, and it downregulated the expression of Bcl-2 and mitochondrion-Cytochrome c (Cyt c) and upregulated the expression of Bax, C-caspase-3, and cytoplasm-Cyt c. miR-21-5p reversed the effects of paeonol, and its effects were further reversed by SKP2.ConclusionPaeonol shows a cardioprotective effect on DOX-induced CHF via regulating the miR-21-5p/SKP2 axis.</p