Proteomic Sequencing of Stellate Ganglions in Rabbits With Myocardial Infarction.
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SUBMITTER: Cheng L
PROVIDER: S-EPMC8716754 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:The purpose of this study was to evaluate the changes of left stellate ganglionic nerve activity (SGNA) and left thoracic vagal nerve activity (VNA) after acute myocardial infarction (MI).Whether MI results in remodeling of extracardiac nerve activity remains unclear.We implanted radiotransmitters to record the SGNA, VNA, and electrocardiogram in 9 ambulatory dogs. After baseline monitoring, MI was created by 1-h balloon occlusion of the coronary arteries. The dogs were then continuously monitored for 2 months. Both stellate ganglia were stained for growth-associated protein 43 and synaptophysin. The stellate ganglia from 5 normal dogs were used as control.MI increased 24-h integrated SGNA from 7.44 ± 7.19 Ln(Vs)/day at baseline to 8.09 ± 7.75 Ln(Vs)/day after the MI (p < 0.05). The 24-h integrated VNA before and after the MI was 5.29 ± 5.04 Ln(Vs)/day and 5.58 ± 5.15 Ln(Vs)/day, respectively (p < 0.05). A significant 24-h circadian variation was noted for the SGNA (p < 0.05) but not the VNA. The SGNA/VNA ratio also showed significant circadian variation. The nerve densities from the left SG were 63,218 ± 34,719 ?m(2)/mm(2) and 20,623 ± 4,926 ?m(2)/mm(2) for growth-associated protein 43 (p < 0.05) and were 32,116 ± 8,190 ?m(2)/mm(2)and 16,326 ± 4,679 ?m(2)/mm(2) for synaptophysin (p < 0.05) in MI and control groups, respectively. The right SG also showed increased nerve density after MI (p < 0.05).MI results in persistent increase in the synaptic density of bilateral stellate ganglia and is associated with increased SGNA and VNA. There is a circadian variation of the SGNA/VNA ratio. These data indicate significant remodeling of the extracardiac autonomic nerve activity and structures after MI.
| S-EPMC3975658 | biostudies-literature
Project description:Background: Stress cardiomyopathy (SCM) is a unique form of LV dysfunction that more often occurs in women. Patients with SCM have a higher Troponin I/B-type natriuretic peptide ratio than AMI, but little is known about other circulating proteins. The goals of this study were to compare plasma proteins in SCM and AMI to learn about the pathophysiology of SCM and also to identify putative biomarkers of SCM. Methods: Blood was drawn in normal controls (n=6), women with AMI (n=12) or women with acute SCM (n=15). Two-week follow up samples were available in AMI (n=4) and SCM patients (n=11). Relative concentrations of 1310 serum proteins were measured in each of the 48 samples using the SOMAscan aptamer based assay. Women with AMI tended to be younger (57.87 ± 16.0 vs. 65.08 ± 9.11 years, p=0.12) and had a higher peak troponin I (AMI 32.03 ± 29.46 vs. SCM 2.68 ± 2.6 ng/mL, p=0.02). No differentially expressed proteins were detected (absolute log2 fold change>1; q<0.05) between AMI and SCM in the acute or recovery phase. In the normal vs. AMI comparison there was differential expression of 35 proteins. In the normal vs. SCM comparison there were 45 proteins with differential expression. Pathway analysis demonstrated activation of complement, coagulation, and inflammation in both AMI and SCM. Conclusions: The acute phase of SCM is characterized by a severe inflammatory response similar to AMI. Despite recovery of LV function in SCM at two weeks, differences in circulating proteins remain in comparison to normal controls.
2017-08-03 | GSE95368 | GEO
Project description:BackgroundDorsal root ganglion (DRG) neurons are primary sensory neurons that conduct neuronal impulses related to pain, touch and temperature senses. Plasma membrane (PM) of DRG cells plays important roles in their functions. PM proteins are main performers of the functions. However, mainly due to the very low amount of DRG that leads to the difficulties in PM sample collection, few proteomic analyses on the PM have been reported and it is a subject that demands further investigation.ResultsBy using aqueous polymer two-phase partition in combination with high salt and high pH washing, PMs were efficiently enriched, demonstrated by western blot analysis. A total of 954 non-redundant proteins were identified from the plasma membrane-enriched preparation with CapLC-MS/MS analysis subsequent to protein separation by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) or shotgun digestion. 205 (21.5%) of the identified proteins were unambiguously assigned as PM proteins, including a large number of signal proteins, receptors, ion channel and transporters.ConclusionThe aqueous polymer two-phase partition is a simple, rapid and relatively inexpensive method. It is well suitable for the purification of PMs from small amount of tissues. Therefore, it is reasonable for the DRG PM to be enriched by using aqueous two-phase partition as a preferred method. Proteomic analysis showed that DRG PM was rich in proteins involved in the fundamental biological processes including material exchange, energy transformation and information transmission, etc. These data would help to our further understanding of the fundamental DRG functions.
| S-EPMC2780401 | biostudies-literature
Project description:Aims. The molecular mechanisms of Chinese traditional medicine Wenxin Keli (WXKL) were unknown. This study was aimed at exploring the effects of WXKL on the gene expression profile and pathological alteration of rabbits with myocardial infarction. Methods. Twenty male adult rabbits were randomly divided into 4 groups: sham, model, WXKL, and captopril groups. Model, WXKL, and captopril groups underwent the ligation of the left anterior descending coronary artery while sham group went through an identical procedure without ligation. WXKL (817 mg/kg/d), captopril (8 mg/kg/d), and distilled water (to model and sham groups) were administered orally to each group. After 4 weeks, the rabbits were examined with echocardiography and the hearts were taken for expression chip and pathological staining (H&E, Masson, and Tunel) studies. Results. The data revealed that WXKL downregulated genes associated with inflammation (CX3CR1, MRC1, and FPR1), apoptosis (CTSC and TTC5), and neurohumoral system (ACE and EDN1) and upregulated angiogenesis promoting genes such as RSPO3. Moreover, the results also showed that WXKL improved cardiac function and prevented histopathological injury and apoptosis. Conclusion. The present study demonstrated that WXKL might play an important role in inhibiting inflammation, renin-angiotensin system, and apoptosis. It might be a promising Chinese medicine in the treatment of patients with myocardial infarction.
| S-EPMC5098077 | biostudies-literature
Project description:ObjectiveThis study tested the hypothesis that vasospasm can trigger coronary plaque injury and acute ischemic myocardial damage.Approach and resultsMyocardial infarction-prone strain of the Watanabe heritable hyperlipidemic rabbits received an intravenous bolus of ergonovine maleate (0.45 µmol/kg) during intravenous infusion of norepinephrine (12 nmol/kg per minute) to provoke coronary spasm in vivo. After this treatment, coronary angiography demonstrated vasospasm, and the ECG showed ischemic abnormalities (ST depression/elevation and T-wave inversion) in 77% of animals (23/30). These changes normalized after nitroglycerin injection. In rabbits that demonstrated these ECG findings for >20 minutes, echocardiograms showed left ventricular wall motion abnormality. Serum levels of heart-type fatty acid-binding protein, cardiac troponin-I, and myoglobin increased markedly 4 hours after spasm provocation. In coronary lesions of myocardial infarction-prone strain of the Watanabe heritable hyperlipidemic rabbits with provoked coronary spasm, we observed intimal injury in 60.9% in the form of endothelial cell protrusions (39.1%), denudation (30.4%), and macrophage extravasation (56.5%). Plaque disruption with luminal thrombus, however, was only seen in 2 of 23 animals (8.7%), and mural microthrombus was rarely observed (4.3%).ConclusionsThese observations show that provocation of vasospasm in myocardial infarction-prone strain of the Watanabe heritable hyperlipidemic rabbits associates with subsequent ischemic myocardial damage. Although treatment with spasmogens altered aspects of plaque morphology, for example, endothelial protrusion and macrophage emigration, thrombosis was rare in these animals with chronic atherosclerotic disease.
| S-EPMC4349325 | biostudies-literature
Project description:BackgroundPreclinical data suggest that an acute inflammatory response following myocardial infarction (MI) accelerates systemic atherosclerosis. Using combined positron emission and computed tomography, we investigated whether this phenomenon occurs in humans.Methods and resultsOverall, 40 patients with MI and 40 with stable angina underwent thoracic 18F-fluorodeoxyglucose combined positron emission and computed tomography scan. Radiotracer uptake was measured in aortic atheroma and nonvascular tissue (paraspinal muscle). In 1003 patients enrolled in the Global Registry of Acute Coronary Events, we assessed whether infarct size predicted early (≤30 days) and late (>30 days) recurrent coronary events. Compared with patients with stable angina, patients with MI had higher aortic 18F-fluorodeoxyglucose uptake (tissue-to-background ratio 2.15±0.30 versus 1.84±0.18, P<0.0001) and plasma C-reactive protein concentrations (6.50 [2.00 to 12.75] versus 2.00 [0.50 to 4.00] mg/dL, P=0.0005) despite having similar aortic (P=0.12) and less coronary (P=0.006) atherosclerotic burden and similar paraspinal muscular 18F-fluorodeoxyglucose uptake (P=0.52). Patients with ST-segment elevation MI had larger infarcts (peak plasma troponin 32 300 [10 200 to >50 000] versus 3800 [1000 to 9200] ng/L, P<0.0001) and greater aortic 18F-fluorodeoxyglucose uptake (2.24±0.32 versus 2.02±0.21, P=0.03) than those with non-ST-segment elevation MI. Peak plasma troponin concentrations correlated with aortic 18F-fluorodeoxyglucose uptake (r=0.43, P=0.01) and, on multivariate analysis, independently predicted early (tertile 3 versus tertile 1: relative risk 4.40 [95% CI 1.90 to 10.19], P=0.001), but not late, recurrent MI.ConclusionsThe presence and extent of MI is associated with increased aortic atherosclerotic inflammation and early recurrent MI. This finding supports the hypothesis that acute MI exacerbates systemic atherosclerotic inflammation and remote plaque destabilization: MI begets MI.Clinical trial registrationURL: https://www.clinicaltrials.gov. Unique identifier: NCT01749254.
| S-EPMC4599491 | biostudies-literature
Project description:Exercise has been shown to improve function of the left ventricle (LV) following myocardial infarction (MI). The mechanisms to explain this benefit have not been fully delineated, but may involve improved mechanics resulting in unloading effects and increased endothelial nitric oxide synthase levels [1,2]. Accordingly, the goal of this study was to determine how the LV infarct proteome is altered by a post-MI exercise regimen. Sprague-Dawley rats underwent ligation of the left descending coronary artery to induce MI. Exercise training was initiated four weeks post-MI and continued for 8 weeks in n=12 rats. Compared with the sedentary MI group (n=10), the infarct region of rats receiving exercise showed 20 protein spots with altered intensities in two-dimensional gels (15 increased and 5 decreased; p<0.05). Of 52 proteins identified in 20 spots, decreased levels of voltage-dependent anion-selective channel 2 and increased levels of glutathione perioxidase and manganese superoxide were confirmed by immunoblotting. Cardiac function was preserved in rats receiving exercise training, and the beneficial effect was linked with changes in these 3 proteins. In conclusion, our results suggest that post-MI exercise training increases anti-oxidant levels and decreases ion channel levels, which may explain, in part, the improved cardiac function seen with exercise.
| S-EPMC2939257 | biostudies-literature
Project description:Acute aortic dissection (AAD) and acute myocardial infarction (AMI) are both severe cardiovascular diseases that may cause sudden death. However, whether serum proteins are differentially expressed between AAD and AMI remains unclear. Here, we aimed to explore serum protein profiles between AAD and AMI patients. A total of 75 serum samples were collected, including AAD patients without AMI (n = 25), AMI patients without AAD (n = 25), and normal subjects (n = 25). Protein identities and expression levels were assessed by LC-MS/MS analysis and a label-free quantitation method, respectively. After depletion of albumin and IgG, a total of 117 proteins with differential expression (fold change ≥2 or ≤−2.0, p < 0.05) were identified, of which 60 were upregulated and 57 were downregulated in AAD sera as compared to AMI sera. Bioinformatic analysis revealed that the differentially expressed serum proteins were mainly derived from exosomes and the extracellular space, and their molecular functions and biological processes were primarily involved in the activity of transporters and complements and the immune response. In addition, the serum level of Cadherin-5, an identified protein with significant regulation in AAD, was further evaluated by ELISA and the results showed that Cadherin-5 in AAD sera was higher that in AMI and healthy sera. Collectively, these findings reveal the differential serum protein profiles between AAD and AMI, which may reflect the divergent pathophysiological progression between the two cardiovascular diseases.
| S-EPMC9855332 | biostudies-literature
Project description:Myocardial infarction (MI) induces neuroinflammation indirectly, chronic neuroinflammation may cause neurodegenerative diseases. Changes in the proteomics of heart and brain tissue after MI may shed new light on the mechanisms involved in neuroinflammation. This study explored brain and heart protein changes after MI with a data-independent acquisition (DIA) mode proteomics approach. Permanent ligation of the left anterior descending coronary artery (LAD) was performed in the heart of rats, and the immunofluorescence of microglia in the brain cortex was performed at 1d, 3d, 5d, and 7d after MI to detect the neuroinflammation. Then proteomics was accomplished to obtain the vital proteins in the heart and brain post-MI. The results show that the number of microglia was significantly increased in the Model-1d group, the Model-3d group, the Model-5d group, and the Model-7d group compared to the Sham group. Various proteins were obtained through DIA proteomics. Linking to key targets of brain disease, 14 proteins were obtained in the brain cortex. Among them, elongation of very long chain fatty acids protein 5 (ELOVL5) and ATP-binding cassette subfamily G member 4 (ABCG4) were verified through western blotting (WB). The results of WB were consistent with the proteomics results. Therefore, these proteins may be related to the pathogenesis of neuroinflammation after MI.
| S-EPMC10958002 | biostudies-literature
Project description:Myocardial infarction (MI) was induced by permanent ligation of the left anterior descending coronary artery (LAD) in 8 weeks C57BL/6 male mice. 1 day (1D), 1 week (1W), 8 weeks (8W) after MI, the mouse left ventricles were used to construct cDNA libraries. For RNA-sequencing, 1 μg of total RNA extracted from pooled mouse LV (left ventricle) of MI or sham animals was used to construct cDNA libraries using the TruSeq RNA library kit (Illumina). For small RNA-sequencing, 1 μg of total RNA from the pooled LV of MI and sham was isolated using a miRNeasy Mini kit (Qiagen) and libraries were prepared using a TruSeq RNA library preparation kit (Illumina). Total RNA and small RNA profiles were generated by deep sequencing, in triplicate, using Illumina HiSeq 2000 sequencer. The reads from the RNA-seq were aligned to Mus musculus (mm10) using Tophat v2.0.13 which incorporates the Bowtie v2.2.3 algorithm. After aligning the reads to the genome, Cufflinks v2.2.1 was used to assemble aligned reads into transcripts and to estimate their abundance. The reads from small RNA-seq were aligned to Mus musculus matured and precursor miRNAs obtained from miRBase v21 using the miRDeep2 algorithm. qRT–PCR validation was performed using SYBR Green assays. The mean numbers of the total mapped reads by RNA-seq were 33,951,175 and the overall read mapping ratios were 96.84%. For the transcript expression quantification in RNA-seq, the number of reads for the genes were normalized to FPKM. Scatter plots of the normalized read counts of all mRNA (R2 > 0.99) showed high degrees of correlation between biological replicates, indicating their high levels of reproducibility.
2020-04-14 | GSE114695 | GEO