Browsing by Subject "Cardiomyocyte"
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- PublicationOpen AccessAnti-apoptotic effects and mechanisms of salvianolic acid A on cardiomyocytes in ischemia-reperfusion injury(Universidad de Murcia. Departamento de Biología Celular e Histología, 2019) Qian, Wei; Wang, Zilong; Xu, Tongda; Li, DongyePrompt myocardial reperfusion during acute myocardial infarction by fibrinolytic therapy, percutaneous coronary intervention, or coronary artery bypass grafting limits the affected area and improves prognosis. However, reperfusion itself can cause cardiomyocyte damage and decrease treatment efficacy. No treatments that effectively prevent myocardial ischemia/reperfusion (I/R) injury are currently available, and are therefore the focus of ongoing research. Salvianolic acid A (SAA), the active ingredient of the traditional Chinese herbal remedy Salvia miltiorrhiza, has anti-thrombotic activity, anti-inflammatory, and anticancer activity; regulates blood lipids and provides hepatic and neural protection. Recent studies demonstrated that SAA inhibits cardiomyocyte apoptosis in response to I/R by the PI3K/Akt, GSK-3β, JNK, and ERK1/2 pathways, and by JNK-ERK1/2 crosstalk. The mechanisms for SAA attenuating cardiomyocytes apoptosis during I/R injury through the P38 MAPK, caspase, JAK/STAT, NF-κB and LOX-1 signaling pathways need further illustration. There may be potential crosstalks between PI3K/Akt and JNK, and Akt/GSK-3β and ERK1/2 in the process of SAA against I/R-incuced cardiomyocytes apoptosis. This review summarizes the recent evidence of the anti-apoptotic effects and mechanisms of SAA against myocardial I/R injury and discusses the basis of potential clinical applications of SAA.
- PublicationOpen AccessDimensions of compartments and membrane surfaces in the intact rabbit heart of importance in studies on intramyocardial transfer of blood-borne substances(Universidad de Murcia. Departamento de Biología Celular e Histología, 2016) van der Vusse, Ger J.; Verheyen, Fons; Reneman, Robert S.; Arts, TheoCardiac studies on the uptake, storage and intramyocardial transfer of blood-borne substances require detailed information on the geometric ultrastructural dimensions of myocardial compartments and parts thereof, and the membranes separating these compartments. Such a specific ultrastructural set of data of the heart is yet lacking. In the present study, we quantitatively assessed these dimensions in glutaraldehyde-perfusion fixed rabbit hearts by means of histological and tailored mathematical techniques. We showed the true ellipsoid nature of the myocardial capillary cross section and estimated the mean capillary diameter dcap. After correction for the ellipsoid shape, dcap was found to be 5.21±1.41 μm. Effective widths of the endothelial cell and the pericapillary interstitium (is1), dimensions of importance in diffusion, amounted to 187±7 and 160±10 nm, respectively. The fractional volume of the large vessels (arteries and veins larger than 10 µm), capillaries, endothelium, is1, cardiomyocytes, non-pericapillary interstitium is2, t-tubular compartment and interstitial cells amounted on average to 5.92%, 9.36%, 1.83%, 1.94%, 73.07%, 5.97%, 0.95% and 0.96%, respectively, of total myocardial volume, defined as the cardiac tissue volume, the large blood vessels included. Normalized to total myocardial volume, the surface area of the luminal and abluminal endothelial membranes and of the cardiomyocyte membrane opposing the endothelial cells amounted to 75.2±5.5x103, 82.2±6.0x103 and 89.1±6.5x103 m2/m3, respectively. The present study provides quantitative information about ultrastructural dimensions of the adult rabbit heart, among others, of importance for studies on cardiac uptake, and intramyocardial transfer and storage of blood-supplied substances.
- PublicationOpen AccessGestational protein restriction: Study of the probable effects on cardiac muscle structure and function in adult rats(Universidad de Murcia. Departamento de Biología Celular e Histología, 2017) Amer, Mona G.; Mohamed, Nader M.; Shaalan, Aly A.M.Intrauterine growth restriction (IUGR) has been linked to heart disease in adulthood. This study aimed to examine the effect of gestational protein restriction during fetal and early postnatal life on the cardiac muscle structure and function in adult offspring. Pregnant female rats were randomly divided into two dietary groups: normal-protein diet (NP) and low-protein diet (LP). Fifteen male offspring from each group were included in the study. Offspring body weights were recorded at birth and monthly from weaning until 24 weeks of age while systolic blood pressure was measured weekly. At the end of the experiment, hearts were weighed and processed for light and electron microscopy and immunohistochemical study. Immunohistochemical staining for localization of inducible nitric oxide synthase (iNOS) and connexin 43 proteins was performed. The gestational protein restriction induced deleterious effects on adult offspring including decreased birth weight, heart weight, and heart rate, and increased systolic blood pressure. Histologically, the number of cardiomyocytes decreased and cardiac fibrosis increased. Signs of degeneration at both structural and ultra-structural levels of cardiomyocytes were also seen. The iNOS was up regulated in LP offspring which was a promoter for apoptosis, while connexin 43 was down regulated which would affect heart conductivity and contractility. Our results demonstrate that adult offspring body weight and cardiac muscle structure and function can be programmed by maternal gestational nutrition. These adverse outcomes suggest the criticality of dietary behavior during pregnancy on long-term offspring cardiac health.
- PublicationOpen AccessImmunolocalization of interleukin-1 receptor antagonist in healthy and infarcted myocardium(Murcia : F. Hernández, 2008) Bonetti, A.; Marchini, M.; Ortolani, F.Ischemic heart disease is a widespread cause of death. During infarction, myocardial injury is mediated by release of several pro-inflammatory cytokines including multifunctional interleukin-1 (IL-1). In various tissues, IL-1-mediated deleterious effects are known to be attenuated via the over-expression of natural anti-inflammatory cytokine IL-1 receptor antagonist (IL-1ra). In the present investigation, IL-1ra distribution in healthy and infarcted myocardium was studied by light and electron microscopy. After immunostaining, weak positivity resulted for cardiomyocytes in normal myocardium and, at higher degrees, in infarction border areas and ischemic ones. In ischemic areas, additional reactivity was displayed by the extracellular matrix and intravascular plasma. Immunogold labelling provided further details on intracytoplasmatic and extracellular distribution; in particular, noticeable gold particle distribution appeared on intercalated discs in normal and hypertrophic cardiomyocytes, as well as on thickened Z-lines for these latter. The present results suggest that cardiomyocytes represent a major source of IL-1ra in vivo, even though additional contribution by blood derived IL-1ra is to be taken in account in ischemic areas. In addition, ischemia-associated intracytoplasmic IL-1ra increase and its additional presence in the extracellular matrix is consistent with the concept that this cytokine plays a cardioprotective role at different levels and by distinct mechanisms.
- PublicationOpen AccessIntracellular Ca2+ Pools and Fluxes in Cardiac Muscle-Derived H9c2 Cells(2005-08) Lax Pérez, Antonio Manuel; Fernandez Belda, Francisco; Soler Pardo, Fernando; MedicinaRelevant Ca(2+) pools and fluxes in H9c2 cells have been studied using fluorescent indicators and Ca(2+)-mobilizing agents. Vasopressin produced a cytoplasmic Ca(2+) peak with half-maximal effective concentration of 6 nM, whereas thapsigargin-induced Ca(2+) increase showed half-maximal effect at 3 nM. Depolarization of the mitochondrial inner membrane by protonophore was also associated with an increase in cytoplasmic Ca(2+). Ionomycin induced a small and sustained depolarization, while thapsigargin had a small but transient effect. The thapsigargin-sensitive Ca(2+) pool was also sensitive to ionomycin, whereas the protonophore-sensitive Ca(2+) pool was not. The vasopressin-induced cytoplasmic Ca(2+) signal, which caused a reversible discharge of the sarco-endoplasmic reticulum Ca(2+) pool, was sensed as a mitochondrial Ca(2+) peak but was unaffected by the permeability transition pore inhibitor cyclosporin A. The mitochondrial Ca(2+) peak was affected by cyclosporin A when the Ca(2+) signal was induced by irreversible discharge of the intracellular Ca(2+) pool, i.e., adding thapsigargin. These observations indicate that the mitochondria interpret the cytoplasmic Ca(2+) signals generated in the reticular store.
- PublicationRestrictedMitochondrial damage as death inducer in heart-derived H9c2 cells: more than one way for an early demise(Springer, 2009-09-24) Lax Pérez, Antonio Manuel; Fernandez Belda, Francisco; Soler Pardo, Fernando; MedicinaThe release of cytochrome c from mitochondria induced by 10 microM thapsigargin was linked to rapid loss of the mitochondrial membrane potential whereas that induced by 50 nM staurosporine was mediated by Bax activation and occurred in polarized mitochondria. Similar levels of cytochrome c were observed when induced by either thapsigargin or staurosporine indicating that the release magnitude was independent of the mechanism involved in membrane permeabilization. In any case caspase 3 activation was subsequent to cytochrome c release. Mitochondrial dysfunction and release of cytochrome c occurred earlier when induced by thapsigargin even though morphological alteration of the cell and chromatin condensation were developed earlier in the presence of staurosporine. In addition, a general and irreversible caspase inhibitor did not protect against chromatin condensation induced by staurosporine. It is also shown that earlier mitochondrial damage does not always correlate with earlier cell demise. This can be attributed to the existence of alternative caspase-independent cell death programmes.
- PublicationOpen AccessNuclear localization of aldolase A in pig cardiomyocytes(Murcia : F. Hernández, 2004) Mamczur, P.; Dzugaj, A.The subcellular localization of the muscle aldolase (aldolase A) in cardiomyocytes was determined immunocytochemically by light and electron microscopy. The enzyme was localized in the cytoplasm and also in cardiomyocyte nuclei. Inside the nuclei it was preferentially localized in the heterochromatin region. The nuclear localization was confirmed by the measurement of aldolase activity in subcellular fractions of a heart muscle, and in isolated nuclei of cardiomyocytes. There was no detectable aldolase activity in isolated cardiomyocyte nuclei fractions if the fraction was not preincubated with a solution containing Triton X-100 and KCl. The calculated concentration of aldolase in the nucleus was about 0.6 µM. This paper is the first report on the localization of aldolase A inside cardiomyocyte nuclei.