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Ultrastructural Abnormalities of the Heart During Diabetes
Published in Grant N. Pierce, Robert E. Beamish, Naranjan S. Dhalla, Heart Dysfunction in Diabetes, 2019
Grant N. Pierce, Robert E. Beamish, Naranjan S. Dhalla
Numerous techniques are available to examine the structure of the myocardium.3–7 One of the most informative methods employs the electron microscope for imaging cell structure. Several references are available which describe the use of the electron microscope in examining the structure of the myocardial cell.3,7,8 A representative electron micrograph of a cardiac muscle cell in longitudinal section is presented in Figure 1. The reader is also referred to the work of McNutt and Fawcett9 for an excellent treatise of myocardial ultrastructure in the healthy, control heart. Clearly visible in the electron micrograph shown in Figure 1 are distinctly separate organelles within the myocardial cell. The principal organelles which have been identified are the contractile proteins, the mitochondria, the sarcoplasmic reticulum (SR), the transverse tubular system, and the nucleus. Each organelle has a unique function which contributes to maintaining the myocardial cell in a functional and viable state. A lesion in any of these subcellular organelles would leave the cell in a compromised condition and eventually result in significant functional defects. The lesion may be identified biochemically or through an examination of the ultrastructure. Available are many examples of studies which have identified alterations in the ultrastructure of subcellular organelles within the myocardial cell under conditions of disease or pathological challenge.8,10–12
Ion Transport and Left Ventricular Hypertrophy in Essential Hypertension
Published in Antonio Coca, Ricardo P. Garay, Ionic Transport in Hypertension: New Perspectives, 2019
Antonio Coca, Alejandro De la Sierra, Alvaro Urbano-Márquez
The molecular mechanisms of pressure-overload LVH are not well understood.64 An increase in intraventricular pressure from 0 to 25 mmHg has been proved to increase the rate of protein synthesis in rat hearts.68 These and other related findings support the hypothesis that stretch of the ventricular wall initiates a signal transduction pathway that leads to enhanced protein synthesis. Mechanical stretch and cell deformation generate a wide range of intracellular signals that may modify rates of RNA and protein synthesis (Table 2). Cardiac muscle cell membranes contain nonselective mechanotransducer ion channels that are either activated or inactivated by stretch.69 Thus, high blood pressure levels probably activate me-chanoreceptors of the myocardial plasma membrane, inducing transmembrane ionic movements as effector mechanisms of hypertrophy.69 Some studies have identified a deformation-dependent Na+ influx and a Ca2+ stretch-dependent uptake in isolated perfused rat hearts as early signals of the protein synthetic pathway.64
Cardiovascular Toxicology
Published in Frank A. Barile, Barile’s Clinical Toxicology, 2019
The appearance of an action potential in cardiac muscle cell membrane is coupled with a muscle contraction. This process occurs in two steps:1.Ca2+ enters the cell during Phase 2 of the action potential and provides approximately 20% of Ca2+ required for contraction.2.The influx of extracellular Ca2+ triggers the release of additional Ca2+ from the SR (i.e., Ca2+-induced Ca2+ release). As a result, muscle cell contraction continues through Phases 2 and 3 (depolarization; Figure 20.1). Intracellular Ca2+ is then sequestered by the SR or pumped out of the cell, leading to cardiac muscle relaxation (repolarization; Figure 20.1).
Cardioprotective effect of rosmarinic acid against myocardial ischaemia/reperfusion injury via suppression of the NF-κB inflammatory signalling pathway and ROS production in mice
Published in Pharmaceutical Biology, 2021
Wei Quan, Hui-xian Liu, Wei Zhang, Wei-juan Lou, Yang-ze Gong, Chong Yuan, Qing Shao, Na Wang, Chao Guo, Fei Liu
Cells of the cardiac muscle cell line HL-1 were cultured in DMEM supplemented with 10% FBS, streptomycin (100 μg/mL), and penicillin (100 U/mL) at 37 °C and 5% CO2. HL-1 cells were processed under conditions of oxygen glucose deprivation followed by reperfusion (OGD/R) to induce a simulated ischaemia/reperfusion injury model in vitro. Cells were exposed to hypoxia for 6 h in low-glucose DMEM, after which hypoxia was induced in a hypoxia incubator chamber saturated with a 5% CO2 and N2 balance. Non-OGD control groups were maintained at normoxia in high-glucose DMEM with 10% FBS. Subsequently, all of the sample groups were reoxygenated in a 21% O2/5% CO2/N2 balance and resupplied with nutrients in high-glucose DMEM with 10% FBS.
Cardioprotective potential of Spinacia oleracea (Spinach) against isoproterenol-induced myocardial infarction in rats
Published in Archives of Physiology and Biochemistry, 2022
Vandana Panda, Nikhil Bhandare, Kinjal Mistry, Sudhamani S., Payal Dande
Cardiac troponin T (cTnT) and troponin I (cTnI) are cardiac regulatory proteins that control the calcium mediated interaction between actin and myosin to cause muscle contraction (Sharma et al. 2004). cTnI has been found to be present only in the myocardium, hence, was used as a specific MI marker in the present study. Upon cardiac muscle cell death, cTnI is released into the blood from the heart. Hence, an elevated cTnI was noted in the serum of ISO treated animals due to myocardial necrosis caused by ISO. NAOE and rutin could protect the heart from ISO mediated free radical damage by its free radical scavenging activity as was witnessed by attenuation of the ISO-elevated cTnI levels.
Differential expression of exosomal microRNAs in fresh and senescent apheresis platelet concentrates
Published in Platelets, 2022
Ziyue Mi, Li Gong, Yujie Kong, Peizhe Zhao, Yonghua Yin, Haixia Xu, Li Tian, Zhong Liu
Based on the microarray results and subsequent validation, nine microRNAs (hsa-miR-22-3p, hsa-miR-223-3p, hsa-miR-21-5p, hsa-miR-23a-3p, hsa-miR-320b, hsa-let-7a-5p, hsa-miR-25-3p, hsa-miR-126-3p, and hsa-miR-320c) (fold change > 5.0, P < .001) were selected for a functional study in the two groups (day 1 and day 5). The target genes of the nine microRNAs were predicted by miWalk and miRDB. Figure 5 shows the network of the nine microRNAs and target genes. GO analysis is summarized in Figure 6A; it predicts that the target genes are primarily involved in positive regulation of cardiac muscle cell proliferation, nervous system development, and transcription from RNA polymerase II promoter in terms of biological process and synapse, dendrite cytoplasm, and axon in terms of cellular component. They also relate to transcription factor activity, RNA polymerase II core promoter sequence-specific DNA binding, and transcriptional activator activity in terms of molecular function. KEGG pathway analysis was conducted to better understand the biological functions and reveal the main pathways in which the candidate genes might be relevant (Figure 6B). The target genes are mainly enriched in regulating pluripotency of stem cells signaling pathway, prolactin signaling pathway, longevity signaling pathway, FoxO signaling pathway, etc. And they also play a role in axon guidance and apoptosis. The most significant immune-related pathway was the prolactin signaling pathway, which is associated with cell proliferation, metabolism, and immune response in T and B lymphocytes and macrophages. The target genes were mainly enriched for the FoxO signaling pathway, ErbB signaling pathway, and TNF signaling pathway. All of these are correlated with various cellular functions, including cell apoptosis, differentiation, and inflammatory cytokine release.