Journal articles on the topic 'Heart cells Molecular aspects'
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Shlyakhto, Е. V. "MOLECULAR AND GENETIC ASPECTS OF HEART FAILURE IN DIABETIC PATIENTS." Annals of the Russian academy of medical sciences 67, no. 1 (January 22, 2012): 31–37. http://dx.doi.org/10.15690/vramn.v67i1.107.
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This article deals with peculiarities of development and clinical course of heart failure (HF) in diabetic patients, influence of diabetic cardiopathy on HF formation., role of genetic predictors of diabetes mellitus (DM) and HF formation, also the importance of treatment response predictors, the significance of a more «personalized» exposure in order to optimize treatment. The role of stationary and dynamic genomics was analyzed,especially molecular visualization that allows the earliest possible intervention. The article also includes examples of molecular visualization use in diagnosis of myocardial dysfunction, disease monitoring, and treatment efficacy assessment. Authors give an analysis of targeted treatment methods on the example of targeted delivery of medications to the target-organ (myocard). Discuss means of anti-ischemic myocardial protection, perspectives of metformin use in order to enhance efficacy of myocardial ischemic pre- and postconditioning mechanisms. Presented perspectives of study of molecular and genetic mechanisms involved in the pathogenesis of HF in diabetic patients, in particular, study of key biological features of stem cells, cell interactions, stem cell plasticity (in vitro direction of differentiation) and their paracrine function evaluation. Given information about identification of genes with partly altered expression due to chronic exposure of mesenchymal stem cells to the high concentration of glucose, and upon decreased ability of mesenchymal stem cells of proangiogenic factors with simultaneous increase of inflammatory markers production (IL8). In whole this article reviews modern state of HF in diabetic patients development mechanisms study with the use of molecular and genetic technologies, and of perspectives of development of this area.
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Łój, Magdalena, Magdalena Garncarz, and Michał Jank. "Genomic and genetic aspects of heart failure in dogs — A review." Acta Veterinaria Hungarica 60, no. 1 (March 1, 2012): 17–26. http://dx.doi.org/10.1556/avet.2012.002.
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The most common causes of heart failure in dogs are valvular disease, predominantly endocardiosis, and myocardial disease, predominantly dilated cardiomyopathy. They are related to changes in the expression of several genes in the heart muscle and in peripheral blood nuclear cells which could be considered as prognostic or diagnostic markers of heart disease in dogs. Since many human genetic markers of heart failure have turned out to be useless in dogs, the screening for genomic markers of canine heart failure could give more insight into the molecular pathology of these diseases and aid the development of new treatment strategies.
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Takemura, Genzou, and Hisayoshi Fujiwara. "Morphological aspects of apoptosis in heart diseases." Journal of Cellular and Molecular Medicine 10, no. 1 (January 2006): 56–75. http://dx.doi.org/10.1111/j.1582-4934.2006.tb00291.x.
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Kostyunin, A. E. "Molecular aspects of the pathological activation and differentiation of valvular interstitial cells during the development of calcific aortic stenosis." Siberian Medical Journal 34, no. 3 (November 4, 2019): 66–72. http://dx.doi.org/10.29001/2073-8552-2019-34-3-66-72.
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Calcific aortic stenosis is the most common valvular heart disease. The pathogenesis of this disease is complex and resembles the atherosclerotic process in the blood vessels. It is known that valvular interstitial cell activation and subsequent differentiation into osteoblast- and myofibroblast-like cells is the main driving force of fibrous and calcified aortic valve tissue. However, the molecular mechanisms behind these processes are still not fully understood. Current information on this issue is collected and analyzed in this article. The main molecular pathways mediating the pathological differentiation of the valvular interstitial cells and the reasons for their activation are considered.
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Zhou, Yiqiu. "Excitation Contraction Coupling in Hypertrophy and Failing Heart Cells." E3S Web of Conferences 271 (2021): 03008. http://dx.doi.org/10.1051/e3sconf/202127103008.
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The contraction of the heart is dependent on a process named the excitation-contraction coupling (E-C coupling). In hypertrophy and failing heart models, the expression, phosphorylation and function of key calcium handling proteins involved in E-C coupling are altered. It’s important to figure out the relationship changes between calcium channel activity and calcium release from sarcoplasmic reticulum (SR). This review will therefore focus on novel components of E-C coupling dysfunction in hypertrophy and failing heart, such as L-type Ca2+ channel (LCC), ryanodine receptor type-2 channel (RyR2) and SR Ca ATPase (SERCA), and how these molecular modifications altered excitation-contraction coupling. A lot of literature was well read and sorted. Recent findings in E-C coupling during hypertrophy and heart failure were focused on. Most importantly, the electrophysiological and signal pathway data was carefully analyzed. This review summarizes key principles and highlights novel aspects of E-C coupling changes during hypertrophy and heart failure models. Although LCC activity changed little, the loss of notch in action potential, reduced Ca2+ transient amplitude and desynchronized Ca2+ sparks resulted in a decreased contraction strength in hypertrophy and heart failure models. What’s more, L-type Ca2+ current becomes ineffective in triggering RyR2 Ca2+ release from SR and the SR uptake is reduced in some models. It has great meanings in understanding the E-C coupling changes during different heart diseases. Theses novel changes suggest potential therapeutic approaches for certain types of hypertrophy and heart failure.
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Drakhlis, Lika, Santoshi Biswanath, Clara-Milena Farr, Victoria Lupanow, Jana Teske, Katharina Ritzenhoff, Annika Franke, et al. "Human heart-forming organoids recapitulate early heart and foregut development." Nature Biotechnology 39, no. 6 (February 8, 2021): 737–46. http://dx.doi.org/10.1038/s41587-021-00815-9.
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AbstractOrganoid models of early tissue development have been produced for the intestine, brain, kidney and other organs, but similar approaches for the heart have been lacking. Here we generate complex, highly structured, three-dimensional heart-forming organoids (HFOs) by embedding human pluripotent stem cell aggregates in Matrigel followed by directed cardiac differentiation via biphasic WNT pathway modulation with small molecules. HFOs are composed of a myocardial layer lined by endocardial-like cells and surrounded by septum-transversum-like anlagen; they further contain spatially and molecularly distinct anterior versus posterior foregut endoderm tissues and a vascular network. The architecture of HFOs closely resembles aspects of early native heart anlagen before heart tube formation, which is known to require an interplay with foregut endoderm development. We apply HFOs to study genetic defects in vitro by demonstrating that NKX2.5-knockout HFOs show a phenotype reminiscent of cardiac malformations previously observed in transgenic mice.
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Currie, R. William, and Robert M. Tanguay. "Analysis of RNA for transcripts for catalase and SP71 in rat hearts after in vivo hyperthermia." Biochemistry and Cell Biology 69, no. 5-6 (May 1, 1991): 375–82. http://dx.doi.org/10.1139/o91-057.
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Hyperthermic stress induces synthesis of the major inducible (heat) stress protein (SP71) in all rat tissues. In addition, there is an increase in catalase activity in hearts at 24 and 48 h after the induction of the heat shock response. To more precisely define some of the molecular aspects of the induction of the heat shock response in hearts, we examined mRNA levels for the catalase, SP71 and HSP27. RNA was isolated from control hearts and at various time periods (0–24 h) of recovery after brief hyperthermic treatment and was analyzed by Northern blot analysis using as probes cDNA sequences for rat liver catalase, human HSP70 (inducible), and human HSP27. There was no detectable change in mRNA for catalase after heat shock or during recovery. Hyperthermic stress has no apparent effect on the regulation of transcription of mRNA coding for catalase, indicating that the increase in catalase activity is either translationally or post-translationally regulated. The human HSP70 cDNA did not hybridize to control heart RNA, but did hybridize to SP71 transcripts at 0, 1.5, and 3 h post heat shock. The mRNA level for SP71 peaked at 1.5 h, was reduced at 3 h, and became almost undetectable at 6 h post heat shock. Similarly, the human HSP27 cDNA did not hybridize to control heart RNA, but did hybridize to transcripts for HSP27 at 0, 1.5, 3, and up to 15 h post heat shock. Maximal signal for HSP27 was at 3 h post heat shock and was sharply reduced at 6 h post heat shock. The accumulation of transcripts for SP71 and HSP27 after hyperthermic stress is rapid, and degradation of the transcripts is almost complete by 6 h post heat shock.Key words: heat shock proteins, hyperthermia, catalase, heart, RNA.
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Lu, Pengfei, Mladen Veletić, Jacob Bergsland, and Ilangko Balasingham. "Theoretical Aspects of Resting-State Cardiomyocyte Communication for Multi-Nodal Nano-Actuator Pacemakers." Sensors 20, no. 10 (May 14, 2020): 2792. http://dx.doi.org/10.3390/s20102792.
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The heart consists of billions of cardiac muscle cells—cardiomyocytes—that work in a coordinated fashion to supply oxygen and nutrients to the body. Inter-connected specialized cardiomyocytes form signaling channels through which the electrical signals are propagated throughout the heart, controlling the heart’s beat to beat function of the other cardiac cells. In this paper, we study to what extent it is possible to use ordinary cardiomyocytes as communication channels between components of a recently proposed multi-nodal leadless pacemaker, to transmit data encoded in subthreshold membrane potentials. We analyze signal propagation in the cardiac infrastructure considering noise in the communication channel by performing numerical simulations based on the Luo-Rudy computational model. The Luo-Rudy model is an action potential model but describes the potential changes with time including membrane potential and action potential stages, separated by the thresholding mechanism. Demonstrating system performance, we show that cardiomyocytes can be used to establish an artificial communication system where data are reliably transmitted between 10 s of cells. The proposed subthreshold cardiac communication lays the foundation for a new intra-cardiac communication technique.
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Savi, Monia, Leonardo Bocchi, Stefano Rossi, Caterina Frati, Gallia Graiani, Costanza Lagrasta, Michele Miragoli, et al. "Antiarrhythmic effect of growth factor-supplemented cardiac progenitor cells in chronic infarcted heart." American Journal of Physiology-Heart and Circulatory Physiology 310, no. 11 (June 1, 2016): H1622—H1648. http://dx.doi.org/10.1152/ajpheart.00035.2015.
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c-Kitpos cardiac progenitor cells (CPCs) represent a successful approach in healing the infarcted heart and rescuing its mechanical function, but electrophysiological consequences are uncertain. CPC mobilization promoted by hepatocyte growth factor (HGF) and IGF-1 improved electrogenesis in myocardial infarction (MI). We hypothesized that locally delivered CPCs supplemented with HGF + IGF-1 (GFs) can concur in ameliorating electrical stability of the regenerated heart. Adult male Wistar rats (139 rats) with 4-wk-old MI or sham conditions were randomized to receive intramyocardial injection of GFs, CPCs, CPCs + GFs, or vehicle (V). Enhanced green fluorescent protein-tagged CPCs were used for cell tracking. Vulnerability to stress-induced arrhythmia was assessed by telemetry-ECG. Basic cardiac electrophysiological properties were examined by epicardial multiple-lead recording. Hemodynamic function was measured invasively. Hearts were subjected to anatomical, morphometric, immunohistochemical, and molecular biology analyses. Compared with V and at variance with individual CPCs, CPCs + GFs approximately halved arrhythmias in all animals, restoring cardiac anisotropy toward sham values. GFs alone reduced arrhythmias by less than CPCs + GFs, prolonging ventricular refractoriness without affecting conduction velocity. Concomitantly, CPCs + GFs reactivated the expression levels of Connexin-43 and Connexin-40 as well as channel proteins of key depolarizing and repolarizing ion currents differently than sole GFs. Mechanical function and anatomical remodeling were equally improved by all regenerative treatments, thus exhibiting a divergent behavior relative to electrical aspects. Conclusively, we provided evidence of distinctive antiarrhythmic action of locally injected GF-supplemented CPCs, likely attributable to retrieval of Connexin-43, Connexin-40, and Cav1.2 expression, favoring intercellular coupling and spread of excitation in mended heart.
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Lisy, Milan, Guenay Kalender, Katja Schenke-Layland, Kelvin G. M. Brockbank, Anna Biermann, and Ulrich Alfred Stock. "Allograft Heart Valves: Current Aspects and Future Applications." Biopreservation and Biobanking 15, no. 2 (April 2017): 148–57. http://dx.doi.org/10.1089/bio.2016.0070.
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Kidokoro, Hinako, Koji Tamura, Masataka Okabe, Gary C. Schoenwolf, and Yukio Saijoh. "Cellular aspects of LR asymmetric morphogenesis in early heart development." Developmental Biology 344, no. 1 (August 2010): 441–42. http://dx.doi.org/10.1016/j.ydbio.2010.05.121.
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Loréal, Olivier, Thibault Cavey, François Robin, Moussa Kenawi, Pascal Guggenbuhl, and Pierre Brissot. "Iron as a Therapeutic Target in HFE-Related Hemochromatosis: Usual and Novel Aspects." Pharmaceuticals 11, no. 4 (November 26, 2018): 131. http://dx.doi.org/10.3390/ph11040131.
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Genetic hemochromatosis is an iron overload disease that is mainly related to the C282Y mutation in the HFE gene. This gene controls the expression of hepcidin, a peptide secreted in plasma by the liver and regulates systemic iron distribution. Homozygous C282Y mutation induces hepcidin deficiency, leading to increased circulating transferrin saturation, and ultimately, iron accumulation in organs such as the liver, pancreas, heart, and bone. Iron in excess may induce or favor the development of complications such as cirrhosis, liver cancer, diabetes, heart failure, hypogonadism, but also complaints such as asthenia and disabling arthritis. Iron depletive treatment mainly consists of venesections that permit the removal of iron contained in red blood cells and the subsequent mobilization of stored iron in order to synthesize hemoglobin for new erythrocytes. It is highly efficient in removing excess iron and preventing most of the complications associated with excess iron in the body. However, this treatment does not target the biological mechanisms involved in the iron metabolism disturbance. New treatments based on the increase of hepcidin levels, by using hepcidin mimetics or inducers, or inhibitors of the iron export activity of ferroportin protein that is the target of hepcidin, if devoid of significant secondary effects, should be useful to better control iron parameters and symptoms, such as arthritis.
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Seguret, Magali, Eva Vermersch, Charlène Jouve, and Jean-Sébastien Hulot. "Cardiac Organoids to Model and Heal Heart Failure and Cardiomyopathies." Biomedicines 9, no. 5 (May 18, 2021): 563. http://dx.doi.org/10.3390/biomedicines9050563.
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Cardiac tissue engineering aims at creating contractile structures that can optimally reproduce the features of human cardiac tissue. These constructs are becoming valuable tools to model some of the cardiac functions, to set preclinical platforms for drug testing, or to alternatively be used as therapies for cardiac repair approaches. Most of the recent developments in cardiac tissue engineering have been made possible by important advances regarding the efficient generation of cardiac cells from pluripotent stem cells and the use of novel biomaterials and microfabrication methods. Different combinations of cells, biomaterials, scaffolds, and geometries are however possible, which results in different types of structures with gradual complexities and abilities to mimic the native cardiac tissue. Here, we intend to cover key aspects of tissue engineering applied to cardiology and the consequent development of cardiac organoids. This review presents various facets of the construction of human cardiac 3D constructs, from the choice of the components to their patterning, the final geometry of generated tissues, and the subsequent readouts and applications to model and treat cardiac diseases.
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Bernardo, Bianca C., Jenny Y. Y. Ooi, Kate L. Weeks, Natalie L. Patterson, and Julie R. McMullen. "Understanding Key Mechanisms of Exercise-Induced Cardiac Protection to Mitigate Disease: Current Knowledge and Emerging Concepts." Physiological Reviews 98, no. 1 (January 1, 2018): 419–75. http://dx.doi.org/10.1152/physrev.00043.2016.
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The benefits of exercise on the heart are well recognized, and clinical studies have demonstrated that exercise is an intervention that can improve cardiac function in heart failure patients. This has led to significant research into understanding the key mechanisms responsible for exercise-induced cardiac protection. Here, we summarize molecular mechanisms that regulate exercise-induced cardiac myocyte growth and proliferation. We discuss in detail the effects of exercise on other cardiac cells, organelles, and systems that have received less or little attention and require further investigation. This includes cardiac excitation and contraction, mitochondrial adaptations, cellular stress responses to promote survival (heat shock response, ubiquitin-proteasome system, autophagy-lysosomal system, endoplasmic reticulum unfolded protein response, DNA damage response), extracellular matrix, inflammatory response, and organ-to-organ crosstalk. We summarize therapeutic strategies targeting known regulators of exercise-induced protection and the challenges translating findings from bench to bedside. We conclude that technological advancements that allow for in-depth profiling of the genome, transcriptome, proteome and metabolome, combined with animal and human studies, provide new opportunities for comprehensively defining the signaling and regulatory aspects of cell/organelle functions that underpin the protective properties of exercise. This is likely to lead to the identification of novel biomarkers and therapeutic targets for heart disease.
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Starosta, Alicja, and Patryk Konieczny. "Therapeutic aspects of cell signaling and communication in Duchenne muscular dystrophy." Cellular and Molecular Life Sciences 78, no. 11 (April 7, 2021): 4867–91. http://dx.doi.org/10.1007/s00018-021-03821-x.
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AbstractDuchenne muscular dystrophy (DMD) is a devastating chromosome X-linked disease that manifests predominantly in progressive skeletal muscle wasting and dysfunctions in the heart and diaphragm. Approximately 1/5000 boys and 1/50,000,000 girls suffer from DMD, and to date, the disease is incurable and leads to premature death. This phenotypic severity is due to mutations in the DMD gene, which result in the absence of functional dystrophin protein. Initially, dystrophin was thought to be a force transducer; however, it is now considered an essential component of the dystrophin-associated protein complex (DAPC), viewed as a multicomponent mechanical scaffold and a signal transduction hub. Modulating signal pathway activation or gene expression through epigenetic modifications has emerged at the forefront of therapeutic approaches as either an adjunct or stand-alone strategy. In this review, we propose a broader perspective by considering DMD to be a disease that affects myofibers and muscle stem (satellite) cells, as well as a disorder in which abrogated communication between different cell types occurs. We believe that by taking this systemic view, we can achieve safe and holistic treatments that can restore correct signal transmission and gene expression in diseased DMD tissues.
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CARAFOLI, E. "The export of Ca from heart cells: Recent advances in the study of the two systems responsible, with emphasis on molecular aspects." Journal of Molecular and Cellular Cardiology 18 (1986): 17. http://dx.doi.org/10.1016/s0022-2828(86)80082-7.
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Kaucka, Marketa, Bara Szarowska, Michaela Kavkova, Maria Eleni Kastriti, Polina Kameneva, Inga Schmidt, Lucie Peskova, et al. "Nerve-associated Schwann cell precursors contribute extracutaneous melanocytes to the heart, inner ear, supraorbital locations and brain meninges." Cellular and Molecular Life Sciences 78, no. 16 (July 18, 2021): 6033–49. http://dx.doi.org/10.1007/s00018-021-03885-9.
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AbstractMelanocytes are pigmented cells residing mostly in the skin and hair follicles of vertebrates, where they contribute to colouration and protection against UV-B radiation. However, the spectrum of their functions reaches far beyond that. For instance, these pigment-producing cells are found inside the inner ear, where they contribute to the hearing function, and in the heart, where they are involved in the electrical conductivity and support the stiffness of cardiac valves. The embryonic origin of such extracutaneous melanocytes is not clear. We took advantage of lineage-tracing experiments combined with 3D visualizations and gene knockout strategies to address this long-standing question. We revealed that Schwann cell precursors are recruited from the local innervation during embryonic development and give rise to extracutaneous melanocytes in the heart, brain meninges, inner ear, and other locations. In embryos with a knockout of the EdnrB receptor, a condition imitating Waardenburg syndrome, we observed only nerve-associated melanoblasts, which failed to detach from the nerves and to enter the inner ear. Finally, we looked into the evolutionary aspects of extracutaneous melanocytes and found that pigment cells are associated mainly with nerves and blood vessels in amphibians and fish. This new knowledge of the nerve-dependent origin of extracutaneous pigment cells might be directly relevant to the formation of extracutaneous melanoma in humans.
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Kiss, Eva, Carolin Fischer, Jan-Mischa Sauter, Jinmeng Sun, and Nina D. Ullrich. "The Structural and the Functional Aspects of Intercellular Communication in iPSC-Cardiomyocytes." International Journal of Molecular Sciences 23, no. 8 (April 18, 2022): 4460. http://dx.doi.org/10.3390/ijms23084460.
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Recent advances in the technology of producing novel cardiomyocytes from induced pluripotent stem cells (iPSC-cardiomyocytes) fuel new hope for future clinical applications. The use of iPSC-cardiomyocytes is particularly promising for the therapy of cardiac diseases such as myocardial infarction, where these cells could replace scar tissue and restore the functionality of the heart. Despite successful cardiogenic differentiation, medical applications of iPSC-cardiomyocytes are currently limited by their pronounced immature structural and functional phenotype. This review focuses on gap junction function in iPSC-cardiomyocytes and portrays our current understanding around the structural and the functional limitations of intercellular coupling and viable cardiac graft formation involving these novel cardiac muscle cells. We further highlight the role of the gap junction protein connexin 43 as a potential target for improving cell–cell communication and electrical signal propagation across cardiac tissue engineered from iPSC-cardiomyocytes. Better insight into the mechanisms that promote functional intercellular coupling is the foundation that will allow the development of novel strategies to combat the immaturity of iPSC-cardiomyocytes and pave the way toward cardiac tissue regeneration.
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Sacks, Michael S., and Ajit P. Yoganathan. "Heart valve function: a biomechanical perspective." Philosophical Transactions of the Royal Society B: Biological Sciences 362, no. 1484 (June 22, 2007): 1369–91. http://dx.doi.org/10.1098/rstb.2007.2122.
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Heart valves (HVs) are cardiac structures whose physiological function is to ensure directed blood flow through the heart over the cardiac cycle. While primarily passive structures that are driven by forces exerted by the surrounding blood and heart, this description does not adequately describe their elegant and complex biomechanical function. Moreover, they must replicate their cyclic function over an entire lifetime, with an estimated total functional demand of least 3×10 9 cycles. As in many physiological systems, one can approach HV biomechanics from a multi-length-scale approach, since mechanical stimuli occur and have biological impact at the organ, tissue and cellular scales. The present review focuses on the functional biomechanics of HVs. Specifically, we refer to the unique aspects of valvular function, and how the mechanical and mechanobiological behaviours of the constituent biological materials (e.g. extracellular matrix proteins and cells) achieve this remarkable feat. While we focus on the work from the authors' respective laboratories, the works of most investigators known to the authors have been included whenever appropriate. We conclude with a summary and underscore important future trends.
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Douglas, Michael R., Karen E. Morrison, Michael Salmon, and Christopher D. Buckley. "Why does inflammation persist: a dominant role for the stromal microenvironment?" Expert Reviews in Molecular Medicine 4, no. 25 (December 9, 2002): 1–18. http://dx.doi.org/10.1017/s1462399402005264.
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Inflammatory responses occur within tissue microenvironments, with functional contributions from both haematopoietic (lymphocytic) cells and stromal cells (including macrophages and fibroblasts). These environments are complex – a compound of many different cell types at different stages of activation and differentiation. Traditional models of inflammatory disease highlight the role of antigen-specific lymphocyte responses and attempt to identify causative agents. However, recent studies have indicated the importance of tissue microenvironments and the innate immune response in perpetuating the inflammatory process. The prominent role of stromal cells in the generation and maintenance of these environments has begun to challenge the primacy of the lymphocyte in regulating chronic inflammatory processes. Sensible enquiries into factors regulating the persistence of inflammatory disease necessitate an understanding of the mechanisms regulating tissue homeostasis and remodelling during inflammation. This article highlights recent insights into the factors regulating dynamic aspects of inflammation, focusing particularly on mononuclear cell infiltrates, their interactions with stromal cells in tissues and the relevance of these interactions to existing and possible future therapies. A key feature of current research has been a growing appreciation that disordered spatial and temporal interactions between infiltrating immune cells and resident stromal cells lie at the heart of disease persistence.
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Rochette, Luc, Geoffrey Dogon, Marianne Zeller, Yves Cottin, and Catherine Vergely. "GDF15 and Cardiac Cells: Current Concepts and New Insights." International Journal of Molecular Sciences 22, no. 16 (August 18, 2021): 8889. http://dx.doi.org/10.3390/ijms22168889.
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Growth and differentiation factor 15 (GDF15) belongs to the transforming growth factor-β (TGF-β) superfamily of proteins. Glial-derived neurotrophic factor (GDNF) family receptor α-like (GFRAL) is an endogenous receptor for GDF15 detected selectively in the brain. GDF15 is not normally expressed in the tissue but is prominently induced by “injury”. Serum levels of GDF15 are also increased by aging and in response to cellular stress and mitochondrial dysfunction. It acts as an inflammatory marker and plays a role in the pathogenesis of cardiovascular diseases, metabolic disorders, and neurodegenerative processes. Identified as a new heart-derived endocrine hormone that regulates body growth, GDF15 has a local cardioprotective role, presumably due to its autocrine/paracrine properties: antioxidative, anti-inflammatory, antiapoptotic. GDF15 expression is highly induced in cardiomyocytes after ischemia/reperfusion and in the heart within hours after myocardial infarction (MI). Recent studies show associations between GDF15, inflammation, and cardiac fibrosis during heart failure and MI. However, the reason for this increase in GDF15 production has not been clearly identified. Experimental and clinical studies support the potential use of GDF15 as a novel therapeutic target (1) by modulating metabolic activity and (2) promoting an adaptive angiogenesis and cardiac regenerative process during cardiovascular diseases. In this review, we comment on new aspects of the biology of GDF15 as a cardiac hormone and show that GDF15 may be a predictive biomarker of adverse cardiac events.
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Melo, Rossana C. N. "Acute heart inflammation: ultrastructural and functional aspects of macrophages elicited by Trypanosoma cruzi infection." Journal of Cellular and Molecular Medicine 13, no. 2 (July 9, 2008): 279–94. http://dx.doi.org/10.1111/j.1582-4934.2008.00388.x.
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Bondarenko, Vladimir E., and Randall L. Rasmusson. "Simulations of propagated mouse ventricular action potentials: effects of molecular heterogeneity." American Journal of Physiology-Heart and Circulatory Physiology 293, no. 3 (September 2007): H1816—H1832. http://dx.doi.org/10.1152/ajpheart.00471.2007.
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The molecular heterogeneity of repolarizing currents produces significant spatial heterogeneity and/or dispersion of repolarization in many mammalian cardiac tissues. Transgenic mice are prominent experimental models for the study of the molecular basis of repolarization and arrhythmias. However, it is debated whether the small mouse heart can sustain physiologically relevant heterogeneity of repolarization. We used a comprehensive model of the mouse action potential (AP) to predict how small a region of the cardiac tissue can maintain spatial gradients of repolarization due to differential expression of channels. Our simulations of a one-dimensional multicellular ring or cable predict that substantial gradients in repolarization and intracellular Ca2+ concentration transients can be maintained through heterogeneity of expression of K+ channels in distances of ∼10 cells that are sufficient to block propagation. The abruptness of expression gradients and the site of stimulation can cause Ca2+ transient oscillations and affect the stability of Ca2+ dynamics and AP propagation. Two different mechanisms of instability of AP propagation in one-dimensional cable occur at fast pacing rates. Transitions from periodic activity to alternans or to irregular behavior were observed. Abrupt gradients of channel expression can cause alternans at slower pacing rates than gradual changes. Our simulations demonstrate the importance of incorporating realistic Ca2+ dynamics and current densities into models of propagated AP. They also emphasize that microscopic aspects of tissue organization are important for predicting large-scale propagation phenomena. Finally, our results predict that the mouse heart should be able to sustain substantial molecularly based heterogeneity of repolarization.
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Perez, Camilo, and Christine Ziegler. "Mechanistic aspects of sodium-binding sites in LeuT-like fold symporters." Biological Chemistry 394, no. 5 (May 1, 2013): 641–48. http://dx.doi.org/10.1515/hsz-2012-0336.
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Abstract Secondary active transporters are of paramount biological impact in all living cells, facilitating the movement of many different substrates across the membrane against a concentration gradient. The uphill transport of one substrate is coupled to the downhill transport of another and driven by the electrochemical gradient. In the last decade, an increasing number of atomic structures of secondary transporters have been reported, confirming a very fundamental mechanistic concept known as the alternating-access cycle. The wealth of structures of transporters sharing the so-called LeuT-like fold that is characterized by two five-transmembrane-helix repeats sharing a 2-fold inverted pseudo symmetry has raised big hopes to finally describe alternating access on a molecular level. Although comparing the individual transporter states of different LeuT-like fold transporters revealed striking similarities, the coupling process, which represents the heart of secondary transport, is far from being understood. Here, we review the structural, functional, and biophysical validation of sodium-binding sites in four different LeuT-like fold transporters. The conservation of sodium sites is discussed in light of their role as key elements connecting symmetry-related structural domains, which are involved in substrate translocation. Moreover, we highlight their crucial roles in conformational changes of LeuT-like fold transporters and their implication on a unifying mechanism in secondary transport.
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Krasińska, Aleksandra, Agata Brązert, and Jarosław Kocięcki. "The history of research of the ophthalmic aspects of hypertension." Medical Journal of Cell Biology 9, no. 1 (March 1, 2021): 14–18. http://dx.doi.org/10.2478/acb-2021-0003.
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Abstract The awareness of the widespread influence of hypertension on various organ systems is ever increasing. Changes associated with this disease can be observed in the heart, brain, kidneys, but also the organ of vision. These usual microvascular changes are defined as hypertensive retinopathy. During a funduscopic examination, abnormalities such as narrowing of arterioles, symptoms of arteriole and vein intersection, cotton wool spots, intra-retinal exudates, retinal haemorrhages, and in severe cases even swelling of the optic disc and macula. This review presents an overview of the changes at the fundus of the eye that may occur in patients with hypertension, as well as problems with the classification of hypertensive retinopathy over the years, and the development of diagnostic methods in ophthalmology and fundoscopic imaging. Running title: The history of hypertensive retinopathy research
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Yamada, Yoichi, Masato Nagashima, Masaaki Tsutsuura, Takeshi Kobayashi, Sumihiko Seki, Naomasa Makita, Yoshinobu Horio, and Noritsugu Tohse. "Cloning of a Functional Splice Variant of L-type Calcium Channel β2Subunit from Rat Heart." Journal of Biological Chemistry 276, no. 50 (October 16, 2001): 47163–70. http://dx.doi.org/10.1074/jbc.m108049200.
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L-type Ca2+channels are heteromultimeric and finely tuned by auxiliary subunits in different tissues and regions. Among auxiliary subunits, β subunit has been shown to play important roles in many functional aspects of Ca2+channel. Rat heart was reported to specifically express β2asubunit. However, the slow inactivation rates of Ca2+currents recorded from recombinant Ca2+channels with the β2asubunit, and the reported inability to detect β2asubunit in rabbit heart by reverse transcription-PCR analysis raise the possibility of the existence of other β subunits. We cloned a splice variant of β2subunit from rat heart, using rapid amplification of cDNA 5′ ends. The splice variant is highly similar to human β2csubunit that was cloned from human ventricle. Northern blot analysis detected the rat β2csubunit abundantly in rat heart and brain. The deduced amino acid sequence of the β2csubunit was different from that of the β2asubunit only in the N-terminal region. When the β2csubunit was expressed along with α1cand α2δ subunits in baby hamster kidney cells, the inactivation rates were comparable with those from native cardiac myocytes, although those with the β2asubunit were slow. Taken together, these observations suggest that the β2csubunit is a functional β2subunit expressed in heart and that the short N-terminal region plays a major role in modifying inactivation kinetics.
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Noden, D. M. "Origins and patterning of avian outflow tract endocardium." Development 111, no. 4 (April 1, 1991): 867–76. http://dx.doi.org/10.1242/dev.111.4.867.
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Outflow tract endocardium links the atrioventricular lining, which develops from cardiogenic plate mesoderm, with aortic arches, whose lining forms collectively from splanchnopleuric endothelial channels, local endothelial vesicles, and invasive angioblasts. At two discrete sites, outflow tract endocardial cells participate in morphogenetic events not within the repertoire of neighboring endocardium: they form mesenchymal precursors of endocardial cushions. The objectives of this research were to document the history of outflow tract endocardium in the avian embryo immediately prior to development of the heart, and to ascertain which, if any, aspects of this history are necessary to acquire cushion-forming potential. Paraxial and lateral mesodermal tissues from between somitomere 3 (midbrain level) and somite 5 were grafted from quail into chick embryos at 3–10 somite stages and, after 2–5 days incubation, survivors were fixed and sectioned. Tissues were stained with the Feulgen reaction to visualize the quail nuclear marker or with antibodies (monoclonal QH1 or polyclonals) that recognize quail but not chick cells. Many quail endothelial cells lose the characteristic nuclear heterochromatin marker, but they retain the species-specific epitope recognized by these antibodies. Precursors of outflow tract but not atrioventricular endocardium are present in cephalic paraxial and lateral mesoderm, with their greatest concentration at the level of the otic placode. Furthermore, the ventral movement of individual angiogenic cells is a normal antecedent to outflow tract formation. Cardiac myocytes were never derived from grafted head mesoderm. Thus, unlike the atrioventricular regions of the heart, outflow tract endocardial and myocardial precursors do not share a congruent embryonic history. The results of heterotopic transplantation, in which trunk paraxial or lateral mesoderm was grafted into the head, were identical, including the formation of cushion mesenchyme. This means that cushion positioning and inductive influences must operate locally within the developing heart tubes.
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Wolters, Renélyn, Ray Deepe, Jenna Drummond, Andrew B. Harvey, Emilye Hiriart, Marie M. Lockhart, Maurice J. B. van den Hoff, Russell A. Norris, and Andy Wessels. "Role of the Epicardium in the Development of the Atrioventricular Valves and Its Relevance to the Pathogenesis of Myxomatous Valve Disease." Journal of Cardiovascular Development and Disease 8, no. 5 (May 12, 2021): 54. http://dx.doi.org/10.3390/jcdd8050054.
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This paper is dedicated to the memory of Dr. Adriana “Adri” Gittenberger-de Groot and in appreciation of her work in the field of developmental cardiovascular biology and the legacy that she has left behind. During her impressive career, Dr. Gittenberger-de Groot studied many aspects of heart development, including aspects of cardiac valve formation and disease and the role of the epicardium in the formation of the heart. In this contribution, we review some of the work on the role of epicardially-derived cells (EPDCs) in the development of the atrioventricular valves and their potential involvement in the pathogenesis of myxomatous valve disease (MVD). We provide an overview of critical events in the development of the atrioventricular junction, discuss the role of the epicardium in these events, and illustrate how interfering with molecular mechanisms that are involved in the epicardial-dependent formation of the atrioventricular junction leads to a number of abnormalities. These abnormalities include defects of the AV valves that resemble those observed in humans that suffer from MVD. The studies demonstrate the importance of the epicardium for the proper formation and maturation of the AV valves and show that the possibility of epicardial-associated developmental defects should be taken into consideration when determining the genetic origin and pathogenesis of MVD.
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Castro, L. E., C. C. Guimarães, and J. M. R. Faria. "Physiological, cellular and molecular aspects of the desiccation tolerance in Anadenanthera colubrina seeds during germination." Brazilian Journal of Biology 77, no. 4 (May 25, 2017): 774–80. http://dx.doi.org/10.1590/1519-6984.00616.
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Abstract During germination, orthodox seeds become gradually intolerant to desiccation, and for this reason, they are a good model for recalcitrance studies. In the present work, physiological, biochemical, and ultrastructural aspects of the desiccation tolerance were characterized during the germination process of Anadenanthera colubrina seeds. The seeds were imbibed during zero (control), 2, 8, 12 (no germinated seeds), and 18 hours (germinated seeds with 1 mm protruded radicle); then they were dried for 72 hours, rehydrated and evaluated for survivorship. Along the imbibition, cytometric and ultrastructural analysis were performed, besides the extraction of the heat-stable proteins. Posteriorly to imbibition and drying, the evaluation of ultrastructural damages was performed. Desiccation tolerance was fully lost after root protrusion. There was no increase in 4C DNA content after the loss of desiccation tolerance. Ultrastructural characteristics of cells from 1mm roots resembled those found in the recalcitrant seeds, in both hydrated and dehydrated states. The loss of desiccation tolerance coincided with the reduction of heat-stable proteins.
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Freire, Ana G., Tatiana P. Resende, and Perpétua Pinto-do-Ó. "Building and Repairing the Heart: What Can We Learn from Embryonic Development?" BioMed Research International 2014 (2014): 1–8. http://dx.doi.org/10.1155/2014/679168.
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Mammalian heart formation is a complex morphogenetic event that depends on the correct temporal and spatial contribution of distinct cell sources. During cardiac formation, cellular specification, differentiation, and rearrangement are tightly regulated by an intricate signaling network. Over the last years, many aspects of this network have been uncovered not only due to advances in cardiac development comprehension but also due to the use of embryonic stem cells (ESCs)in vitromodel system. Additionally, several of these pathways have been shown to be functional or reactivated in the setting of cardiac disease. Knowledge withdrawn from studying heart development, ESCs differentiation, and cardiac pathophysiology may be helpful to envisage new strategies for improved cardiac repair/regeneration. In this review, we provide a comparative synopsis of the major signaling pathways required for cardiac lineage commitment in the embryo and murine ESCs. The involvement and possible reactivation of these pathways following heart injury and their role in tissue recovery will also be discussed.
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Leinonen, Jussi V., Päivi Leinikka, Miikka Tarkia, Milla Lampinen, Avishag K. Emanuelov, Ronen Beeri, Esko Kankuri, and Eero Mervaala. "Structural and Functional Support by Left Atrial Appendage Transplant to the Left Ventricle after a Myocardial Infarction." International Journal of Molecular Sciences 23, no. 9 (April 22, 2022): 4661. http://dx.doi.org/10.3390/ijms23094661.
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The left atrial appendage (LAA) of the adult heart has been shown to contain cardiac and myeloid progenitor cells. The resident myeloid progenitor population expresses an array of pro-regenerative paracrine factors. Cardiac constructs have been shown to inhibit deleterious remodeling of the heart using physical support. Due to these aspects, LAA holds promise as a regenerative transplant. LAAs from adult mT/mG mice were transplanted to the recipient 129X1-SvJ mice simultaneously as myocardial infarction (MI) was performed. A decellularized LAA patch was implanted in the control group. Two weeks after MI, the LAA patch had integrated to the ventricular wall, and migrated cells were seen in the MI area. The cells had two main phenotypes: small F4/80+ cells and large troponin C+ cells. After follow-up at 8 weeks, the LAA patch remained viable, and the functional status of the heart improved. Cardiac echo demonstrated that, after 6 weeks, the mice in the LAA-patch-treated group showed an increasing and statistically significant improvement in cardiac performance when compared to the MI and MI + decellularized patch controls. Physical patch-support (LAA and decellularized LAA patch) had an equal effect on the inhibition of deleterious remodeling, but only the LAA patch inhibited the hypertrophic response. Our study demonstrates that the LAA transplantation has the potential for use as a treatment for myocardial infarction. This method can putatively combine cell therapy (regenerative effect) and physical support (inhibition of deleterious remodeling).
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Yelon, Deborah, Sally A. Horne, and Didier Y. R. Stainier. "Restricted Expression of Cardiac Myosin Genes Reveals Regulated Aspects of Heart Tube Assembly in Zebrafish." Developmental Biology 214, no. 1 (October 1999): 23–37. http://dx.doi.org/10.1006/dbio.1999.9406.
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Anwar, Sidra, Awais Ur Rehman, Asma Hussain, Abdul Rahman Abid, Sobia ,. Saeed, and Hafiza Sobia Ramzan. "Assessment of Serum Levels of Oxidative Stress Markers and Heat Shock Proteins in Myocardial Infraction Patients." Pakistan Journal of Medical and Health Sciences 16, no. 6 (June 30, 2022): 912–15. http://dx.doi.org/10.53350/pjmhs22166912.
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Introduction: Heat stress proteins also known as shock proteins are the molecular chaperones due to various stimuli response to heat and ischemic injury to the cells. They are important in folding and degradation of other proteins involved in genesis of cardiovascular pathologies. Objectives: The main aim is to upgrade the role of oxidative markers and these stress proteins not only in development but also in evolution related to heart disease. Material and methods: Subjects were selected as diagnosed myocardial infarction in Faisalabad institute of cardiology, Faisalabad Division, Punjab. All subjects were further categorized as risk group and non-risk group on the basis of their risk factors history using ACC/AHC 2017 guided criteria for detection of myocardial infarction included chest pain, ECG finding and cardiac enzymes. Results: Data clearly depicts the demographical and hematological profile i-e complete blood picture of patients with diagnosed myocardial infraction and control subject. Hemoglobin as a highly advanced allosteric protein present in the form of HbA with two α and two β chains while globin chains are synthesized in erythrocytes cytosol. Conclusion: Despite of increasing evidence from the recent data, it is recommended that functions of these heat shock proteins related to guard cells against programmed apoptosis from stressful aspects e.g. infection, mechanical stress, oxidized low density lipoprotein and oxidants are also known as stress proteins. Keywords: Stress Proteins, Atherosclerosis, Apoptosis, Myocardial Infarction, Oxidative Markers
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Palazzuoli, Alberto, Francesco Tramonte, and Matteo Beltrami. "Laboratory and Metabolomic Fingerprint in Heart Failure with Preserved Ejection Fraction: From Clinical Classification to Biomarker Signature." Biomolecules 13, no. 1 (January 13, 2023): 173. http://dx.doi.org/10.3390/biom13010173.
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Heart failure with preserved ejection fraction (HFpEF) remains a poorly characterized syndrome with many unknown aspects related to different patient profiles, various associated risk factors and a wide range of aetiologies. It comprises several pathophysiological pathways, such as endothelial dysfunction, myocardial fibrosis, extracellular matrix deposition and intense inflammatory system activation. Until now, HFpEF has only been described with regard to clinical features and its most commonly associated risk factors, disregarding all biological mechanisms responsible for cardiovascular deteriorations. Recently, innovations in laboratory and metabolomic findings have shown that HFpEF appears to be strictly related to specific cells and molecular mechanisms’ dysregulation. Indeed, some biomarkers are efficient in early identification of these processes, adding new insights into diagnosis and risk stratification. Moreover, recent advances in intermediate metabolites provide relevant information on intrinsic cellular and energetic substrate alterations. Therefore, a systematic combination of clinical imaging and laboratory findings may lead to a ‘precision medicine’ approach providing prognostic and therapeutic advantages. The current review reports traditional and emerging biomarkers in HFpEF and it purposes a new diagnostic approach based on integrative information achieved from risk factor burden, hemodynamic dysfunction and biomarkers’ signature partnership.
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Radisic, M., H. Park, S. Gerecht, C. Cannizzaro, R. Langer, and G. Vunjak-Novakovic. "Biomimetic approach to cardiac tissue engineering." Philosophical Transactions of the Royal Society B: Biological Sciences 362, no. 1484 (June 26, 2007): 1357–68. http://dx.doi.org/10.1098/rstb.2007.2121.
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Here, we review an approach to tissue engineering of functional myocardium that is biomimetic in nature, as it involves the use of culture systems designed to recapitulate some aspects of the actual in vivo environment. To mimic the capillary network, subpopulations of neonatal rat heart cells were cultured on a highly porous elastomer scaffold with a parallel array of channels perfused with culture medium. To mimic oxygen supply by haemoglobin, the culture medium was supplemented with a perfluorocarbon (PFC) emulsion. Constructs cultivated in the presence of PFC contained higher amounts of DNA and cardiac markers and had significantly better contractile properties than control constructs cultured without PFC. To induce synchronous contractions of cultured constructs, electrical signals mimicking those in native heart were applied. Over only 8 days of cultivation, electrical stimulation induced cell alignment and coupling, markedly increased the amplitude of synchronous construct contractions and resulted in a remarkable level of ultrastructural organization. The biomimetic approach is discussed in the overall context of cardiac tissue engineering, and the possibility to engineer functional human cardiac grafts based on human stem cells.
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Hsu, Sheng-Kai, Chien-Chih Chiu, Hans-Uwe Dahms, Chon-Kit Chou, Chih-Mei Cheng, Wen-Tsan Chang, Kai-Chun Cheng, Hui-Min David Wang, and I.-Ling Lin. "Unfolded Protein Response (UPR) in Survival, Dormancy, Immunosuppression, Metastasis, and Treatments of Cancer Cells." International Journal of Molecular Sciences 20, no. 10 (May 22, 2019): 2518. http://dx.doi.org/10.3390/ijms20102518.
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The endoplasmic reticulum (ER) has diverse functions, and especially misfolded protein modification is in the focus of this review paper. With a highly regulatory mechanism, called unfolded protein response (UPR), it protects cells from the accumulation of misfolded proteins. Nevertheless, not only does UPR modify improper proteins, but it also degrades proteins that are unable to recover. Three pathways of UPR, namely PERK, IRE-1, and ATF6, have a significant role in regulating stress-induced physiological responses in cells. The dysregulated UPR may be involved in diseases, such as atherosclerosis, heart diseases, amyotrophic lateral sclerosis (ALS), and cancer. Here, we discuss the relation between UPR and cancer, considering several aspects including survival, dormancy, immunosuppression, angiogenesis, and metastasis of cancer cells. Although several moderate adversities can subject cancer cells to a hostile environment, UPR can ensure their survival. Excessive unfavorable conditions, such as overloading with misfolded proteins and nutrient deprivation, tend to trigger cancer cell death signaling. Regarding dormancy and immunosuppression, cancer cells can survive chemotherapies and acquire drug resistance through dormancy and immunosuppression. Cancer cells can also regulate the downstream of UPR to modulate angiogenesis and promote metastasis. In the end, regulating UPR through different molecular mechanisms may provide promising anticancer treatment options by suppressing cancer proliferation and progression.
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Marino, Fabiola, Mariangela Scalise, Eleonora Cianflone, Luca Salerno, Donato Cappetta, Nadia Salerno, Antonella De Angelis, Daniele Torella, and Konrad Urbanek. "Physical Exercise and Cardiac Repair: The Potential Role of Nitric Oxide in Boosting Stem Cell Regenerative Biology." Antioxidants 10, no. 7 (June 23, 2021): 1002. http://dx.doi.org/10.3390/antiox10071002.
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Over the years strong evidence has been accumulated showing that aerobic physical exercise exerts beneficial effects on the prevention and reduction of cardiovascular risk. Exercise in healthy subjects fosters physiological remodeling of the adult heart. Concurrently, physical training can significantly slow-down or even reverse the maladaptive pathologic cardiac remodeling in cardiac diseases, improving heart function. The underlying cellular and molecular mechanisms of the beneficial effects of physical exercise on the heart are still a subject of intensive study. Aerobic activity increases cardiovascular nitric oxide (NO) released mainly through nitric oxidase synthase 3 activity, promoting endothelium-dependent vasodilation, reducing vascular resistance, and lowering blood pressure. On the reverse, an imbalance between increasing free radical production and decreased NO generation characterizes pathologic remodeling, which has been termed the “nitroso-redox imbalance”. Besides these classical evidence on the role of NO in cardiac physiology and pathology, accumulating data show that NO regulate different aspects of stem cell biology, including survival, proliferation, migration, differentiation, and secretion of pro-regenerative factors. Concurrently, it has been shown that physical exercise generates physiological remodeling while antagonizes pathologic remodeling also by fostering cardiac regeneration, including new cardiomyocyte formation. This review is therefore focused on the possible link between physical exercise, NO, and stem cell biology in the cardiac regenerative/reparative response to physiological or pathological load. Cellular and molecular mechanisms that generate an exercise-induced cardioprotective phenotype are discussed in regards with myocardial repair and regeneration. Aerobic training can benefit cells implicated in cardiovascular homeostasis and response to damage by NO-mediated pathways that protect stem cells in the hostile environment, enhance their activation and differentiation and, in turn, translate to more efficient myocardial tissue regeneration. Moreover, stem cell preconditioning by and/or local potentiation of NO signaling can be envisioned as promising approaches to improve the post-transplantation stem cell survival and the efficacy of cardiac stem cell therapy.
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Ferenczyová, Kristína, Lucia Kindernay, Jana Vlkovičová, Barbora Kaločayová, Tomáš Rajtík, and Monika Barteková. "Pharmacology of Catechins in Ischemia-Reperfusion Injury of the Heart." Antioxidants 10, no. 9 (August 30, 2021): 1390. http://dx.doi.org/10.3390/antiox10091390.
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Catechins represent a group of polyphenols that possesses various beneficial effects in the cardiovascular system, including protective effects in cardiac ischemia-reperfusion (I/R) injury, a major pathophysiology associated with ischemic heart disease, myocardial infarction, as well as with cardioplegic arrest during heart surgery. In particular, catechin, (−)-epicatechin, and epigallocatechin gallate (EGCG) have been reported to prevent cardiac myocytes from I/R-induced cell damage and I/R-associated molecular changes, finally, resulting in improved cell viability, reduced infarct size, and improved recovery of cardiac function after ischemic insult, which has been widely documented in experimental animal studies and cardiac-derived cell lines. Cardioprotective effects of catechins in I/R injury were mediated via multiple molecular mechanisms, including inhibition of apoptosis; activation of cardioprotective pathways, such as PI3K/Akt (RISK) pathway; and inhibition of stress-associated pathways, including JNK/p38-MAPK; preserving mitochondrial function; and/or modulating autophagy. Moreover, regulatory roles of several microRNAs, including miR-145, miR-384-5p, miR-30a, miR-92a, as well as lncRNA MIAT, were documented in effects of catechins in cardiac I/R. On the other hand, the majority of results come from cell-based experiments and healthy small animals, while studies in large animals and studies including comorbidities or co-medications are rare. Human studies are lacking completely. The dosages of compounds also vary in a broad scale, thus, pharmacological aspects of catechins usage in cardiac I/R are inconclusive so far. Therefore, the aim of this focused review is to summarize the most recent knowledge on the effects of catechins in cardiac I/R injury and bring deep insight into the molecular mechanisms involved and dosage-dependency of these effects, as well as to outline potential gaps for translation of catechin-based treatments into clinical practice.
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Vliegen, H. W., A. M. Vossepoel, A. van der Laarse, F. Eulderink, and C. J. Cornelisse. "Methodological aspects of flow cytometric analysis of DNA polyploidy in human heart tissue." Histochemistry 84, no. 4-6 (July 1986): 348–54. http://dx.doi.org/10.1007/bf00482962.
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Koh, Carolina Cattoni, Eula G. A. Neves, Thaiany Goulart de Souza-Silva, Ana Carolina Carvalho, Cecília Horta Ramalho Pinto, Alexsandro Galdino, Kenneth J. Gollob, and Walderez Ornelas Dutra. "Cytokine Networks as Targets for Preventing and Controlling Chagas Heart Disease." Pathogens 12, no. 2 (January 21, 2023): 171. http://dx.doi.org/10.3390/pathogens12020171.
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Chagas disease, a neglected disease caused by the protozoan Trypanosoma cruzi, is endemic in 21 Latin American countries, affecting 6–8 million people. Increasing numbers of Chagas disease cases have also been reported in non-endemic countries due to migration, contamination via blood transfusions or organ transplantation, characterizing Chagas as an emerging disease in such regions. While most individuals in the chronic phase of Chagas disease remain in an asymptomatic clinical form named indeterminate, approximately 30% of the patients develop a cardiomyopathy that is amongst the deadliest cardiopathies known. The clinical distinctions between the indeterminate and the cardiac clinical forms are associated with different immune responses mediated by innate and adaptive cells. In this review, we present a collection of studies focusing on the human disease, discussing several aspects that demonstrate the association between chemokines, cytokines, and cytotoxic molecules with the distinct clinical outcomes of human infection with Trypanosoma cruzi. In addition, we discuss the role of gene polymorphisms in the transcriptional control of these immunoregulatory molecules. Finally, we discuss the potential application of cytokine expression and gene polymorphisms as markers of susceptibility to developing the severe form of Chagas disease, and as targets for disease control.
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Masoud, Said, Fraser McDonald, Dirk Bister, Claire Kotecki, Martin D. Bootman, and Katja Rietdorf. "Examining Cardiomyocyte Dysfunction Using Acute Chemical Induction of an Ageing Phenotype." International Journal of Molecular Sciences 21, no. 1 (December 27, 2019): 197. http://dx.doi.org/10.3390/ijms21010197.
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Much effort is focussed on understanding the structural and functional changes in the heart that underlie age-dependent deterioration of cardiac performance. Longitudinal studies, using aged animals, have pinpointed changes occurring to the contractile myocytes within the heart. However, whilst longitudinal studies are important, other experimental approaches are being advanced that can recapitulate the phenotypic changes seen during ageing. This study investigated the induction of an ageing cardiomyocyte phenotypic change by incubation of cells with hydroxyurea for several days ex vivo. Hydroxyurea incubation has been demonstrated to phenocopy age- and senescence-induced changes in neurons, but its utility for ageing studies with cardiac cells has not been examined. Incubation of neonatal rat ventricular myocytes with hydroxyurea for up to 7 days replicated specific aspects of cardiac ageing including reduced systolic calcium responses, increased alternans and a lesser ability of the cells to follow electrical pacing. Additional functional and structural changes were observed within the myocytes that pointed to ageing-like remodelling, including lipofuscin granule accumulation, reduced mitochondrial membrane potential, increased production of reactive oxygen species, and altered ultrastructure, such as mitochondria with disrupted cristae and disorganised myofibres. These data highlight the utility of alternative approaches for exploring cellular ageing whilst avoiding the costs and co-morbid factors that can affect longitudinal studies.
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Lamberto, Federica, Irene Peral-Sanchez, Suchitra Muenthaisong, Melinda Zana, Sandrine Willaime-Morawek, and András Dinnyés. "Environmental Alterations during Embryonic Development: Studying the Impact of Stressors on Pluripotent Stem Cell-Derived Cardiomyocytes." Genes 12, no. 10 (September 30, 2021): 1564. http://dx.doi.org/10.3390/genes12101564.
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Non-communicable diseases (NCDs) sauch as diabetes, obesity and cardiovascular diseases are rising rapidly in all countries world-wide. Environmental maternal factors (e.g., diet, oxidative stress, drugs and many others), maternal illnesses and other stressors can predispose the newborn to develop diseases during different stages of life. The connection between environmental factors and NCDs was formulated by David Barker and colleagues as the Developmental Origins of Health and Disease (DOHaD) hypothesis. In this review, we describe the DOHaD concept and the effects of several environmental stressors on the health of the progeny, providing both animal and human evidence. We focus on cardiovascular diseases which represent the leading cause of death worldwide. The purpose of this review is to discuss how in vitro studies with pluripotent stem cells (PSCs), such as embryonic and induced pluripotent stem cells (ESC, iPSC), can underpin the research on non-genetic heart conditions. The PSCs could provide a tool to recapitulate aspects of embryonic development “in a dish”, studying the effects of environmental exposure during cardiomyocyte (CM) differentiation and maturation, establishing a link to molecular mechanism and epigenetics.
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Stenvers, Kaye L., Melinda L. Tursky, Kenneth W. Harder, Nicole Kountouri, Supavadee Amatayakul-Chantler, Dianne Grail, Clayton Small, Robert A. Weinberg, Andrew M. Sizeland, and Hong-Jian Zhu. "Heart and Liver Defects and Reduced Transforming Growth Factor β2 Sensitivity in Transforming Growth Factor β Type III Receptor-Deficient Embryos." Molecular and Cellular Biology 23, no. 12 (June 15, 2003): 4371–85. http://dx.doi.org/10.1128/mcb.23.12.4371-4385.2003.
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ABSTRACT The type III transforming growth factor β (TGFβ) receptor (TβRIII) binds both TGFβ and inhibin with high affinity and modulates the association of these ligands with their signaling receptors. However, the significance of TβRIII signaling in vivo is not known. In this study, we have sought to determine the role of TβRIII during development. We identified the predominant expression sites of ΤβRIII mRNA as liver and heart during midgestation and have disrupted the murine TβRIII gene by homologous recombination. Beginning at embryonic day 13.5, mice with mutations in ΤβRIII developed lethal proliferative defects in heart and apoptosis in liver, indicating that TβRIII is required during murine somatic development. To assess the effects of the absence of TβRIII on the function of its ligands, primary fibroblasts were generated from TβRIII-null and wild-type embryos. Our results indicate that TβRIII deficiency differentially affects the activities of TGFβ ligands. Notably, TβRIII-null cells exhibited significantly reduced sensitivity to TGFβ2 in terms of growth inhibition, reporter gene activation, and Smad2 nuclear localization, effects not observed with other ligands. These data indicate that TβRIII is an important modulator of TGFβ2 function in embryonic fibroblasts and that reduced sensitivity to TGFβ2 may underlie aspects of the TβRIII mutant phenotype.
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Vacante, Fernanda, Pamela Senesi, Anna Montesano, Alice Frigerio, Livio Luzi, and Ileana Terruzzi. "L-Carnitine: An Antioxidant Remedy for the Survival of Cardiomyocytes under Hyperglycemic Condition." Journal of Diabetes Research 2018 (December 9, 2018): 1–12. http://dx.doi.org/10.1155/2018/4028297.
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Background. Metabolic alterations as hyperglycemia and inflammation induce myocardial molecular events enhancing oxidative stress and mitochondrial dysfunction. Those alterations are responsible for a progressive loss of cardiomyocytes, cardiac stem cells, and consequent cardiovascular complications. Currently, there are no effective pharmacological measures to protect the heart from these metabolic modifications, and the development of new therapeutic approaches, focused on improvement of the oxidative stress condition, is pivotal. The protective effects of levocarnitine (LC) in patients with ischemic heart disease are related to the attenuation of oxidative stress, but LC mechanisms have yet to be fully understood. Objective. The aim of this work was to investigate LC’s role in oxidative stress condition, on ROS production and mitochondrial detoxifying function in H9c2 rat cardiomyocytes during hyperglycemia. Methods. H9c2 cells in the hyperglycemic state (25 mmol/L glucose) were exposed to 0.5 or 5 mM LC for 48 and 72 h: LC effects on signaling pathways involved in oxidative stress condition were studied by Western blot and immunofluorescence analysis. To evaluate ROS production, H9c2 cells were exposed to H2O2 after LC pretreatment. Results. Our in vitro study indicates how LC supplementation might protect cardiomyocytes from oxidative stress-related damage, preventing ROS formation and activating antioxidant signaling pathways in hyperglycemic conditions. In particular, LC promotes STAT3 activation and significantly increases the expression of antioxidant protein SOD2. Hyperglycemic cardiac cells are characterized by impairment in mitochondrial dysfunction and the CaMKII signal: LC promotes CaMKII expression and activation and enhancement of AMPK protein synthesis. Our results suggest that LC might ameliorate metabolic aspects of hyperglycemic cardiac cells. Finally, LC doses herein used did not modify H9c2 growth rate and viability. Conclusions. Our novel study demonstrates that LC improves the microenvironment damaged by oxidative stress (induced by hyperglycemia), thus proposing this nutraceutical compound as an adjuvant in diabetic cardiac regenerative medicine.
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Li, Zhe, Tuan T. Nguyen, and Alan Valaperti. "Human cardiac fibroblasts produce pro-inflammatory cytokines upon TLRs and RLRs stimulation." Molecular and Cellular Biochemistry 476, no. 9 (April 21, 2021): 3241–52. http://dx.doi.org/10.1007/s11010-021-04157-7.
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AbstractHeart inflammation is one of the major causes of heart damage that leads to dilated cardiomyopathy and often progresses to end-stage heart failure. In the present study, we aimed to assess whether human cardiac cells could release immune mediators upon stimulation of Toll-like receptors (TLRs) and Retinoic acid-inducible gene (RIG)-I-like receptors (RLRs).Commercially available human cardiac fibroblasts and an immortalized human cardiomyocyte cell line were stimulated in vitro with TLR2, TLR3, and TLR4 agonists. In addition, cytosolic RLRs were activated in cardiac cells after transfection of polyinosinic-polycytidylic acid (PolyIC). Upon stimulation of TLR3, TLR4, MDA5, and RIG-I, but not upon stimulation of TLR2, human cardiac fibroblasts produced high amounts of the pro-inflammatory cytokines IL-6 and IL-8. On the contrary, the immortalized human cardiomyocyte cell line was unresponsive to the tested TLRs agonists. Upon RLRs stimulation, cardiac fibroblasts, and to a lesser extent the cardiomyocyte cell line, induced anti-viral IFN-β expression.These data demonstrate that human cardiac fibroblasts and an immortalized human cardiomyocyte cell line differently respond to various TLRs and RLRs ligands. In particular, human cardiac fibroblasts were able to induce pro-inflammatory and anti-viral cytokines on their own. These aspects will contribute to better understand the immunological function of the different cell populations that make up the cardiac tissue.
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Bollati, Martina, Chiara Lopez, Fabio Bioletto, Federico Ponzetto, Ezio Ghigo, Mauro Maccario, and Mirko Parasiliti-Caprino. "Atrial Fibrillation and Aortic Ectasia as Complications of Primary Aldosteronism: Focus on Pathophysiological Aspects." International Journal of Molecular Sciences 23, no. 4 (February 14, 2022): 2111. http://dx.doi.org/10.3390/ijms23042111.
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Primary aldosteronism (PA) is the most common cause of secondary hypertension. A growing body of evidence has suggested that, beyond its well-known effects on blood pressure and electrolyte balance, aldosterone excess can exert pro-inflammatory, pro-oxidant and pro-fibrotic effects on the kidney, blood vessels and heart, leading to potentially harmful pathophysiological consequences. In clinical studies, PA has been associated with an increased risk of cardiovascular, cerebrovascular, renal and metabolic complication compared to essential hypertension, including atrial fibrillation (AF) and aortic ectasia. An increased prevalence of AF in patients with PA has been demonstrated in several clinical studies. Aldosterone excess seems to be involved in the pathogenesis of AF by inducing cardiac structural and electrical remodeling that in turn predisposes to arrhythmogenicity. The association between PA and aortic ectasia is less established, but several studies have demonstrated an effect of aldosterone on aortic stiffness, vascular smooth muscle cells and media composition that, in turn, might lead to an increased risk of aortic dilation and dissection. In this review, we focus on the current evidence regarding the potential role of aldosterone excess in the pathogenesis of AF and aortic ectasia.
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Tain, You-Lin, and Chien-Ning Hsu. "Oxidative Stress-Induced Hypertension of Developmental Origins: Preventive Aspects of Antioxidant Therapy." Antioxidants 11, no. 3 (March 7, 2022): 511. http://dx.doi.org/10.3390/antiox11030511.
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Hypertension remains the leading cause of disease burden worldwide. Hypertension can originate in the early stages of life. A growing body of evidence suggests that oxidative stress, which is characterized as a reactive oxygen species (ROS)/nitric oxide (NO) disequilibrium, has a pivotal role in the hypertension of developmental origins. Results from animal studies support the idea that early-life oxidative stress causes developmental programming in prime blood pressure (BP)-controlled organs such as the brain, kidneys, heart, and blood vessels, leading to hypertension in adult offspring. Conversely, perinatal use of antioxidants can counteract oxidative stress and therefore lower BP. This review discusses the interaction between oxidative stress and developmental programming in hypertension. It will also discuss evidence from animal models, how oxidative stress connects with other core mechanisms, and the potential of antioxidant therapy as a novel preventive strategy to prevent the hypertension of developmental origins.
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Forssmann, W. G., Rudolf Richter, and Markus Meyer. "The endocrine heart and natriuretic peptides: histochemistry, cell biology, and functional aspects of the renal urodilatin system." Histochemistry and Cell Biology 110, no. 4 (September 14, 1998): 335–57. http://dx.doi.org/10.1007/s004180050295.
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Zhao, J. J., and G. Lemke. "Selective disruption of neuregulin-1 function in vertebrate embryos using ribozyme-tRNA transgenes." Development 125, no. 10 (May 15, 1998): 1899–907. http://dx.doi.org/10.1242/dev.125.10.1899.
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The products of the neuregulin-1 gene constitute a set of polypeptide growth factors whose signalling through the ErbB receptors is essential to the growth and differentiation of many cell types in culture. Although studies with neuregulin-1 mutant mice have demonstrated that these growth factors are also essential regulators of cellular differentiation in vivo, the mid-embryonic death of these mutants precludes an analysis of hypothesized neuregulin-1 roles in later aspects of development. To circumvent this early lethality, we have pursued a ribozyme-based strategy for the perturbation of neuregulin-1 function in developing chick embryos. Early administration of a retrovirus carrying neuregulin-1 hammerhead-type ribozymes to blastoderm-stage embryos leads to an embryonic lethal phenotype that results from the failure of ventricular trabeculation in the developing heart, a faithful phenocopy of the mouse neuregulin-1 mutations. Later, more localized delivery of the ribozyme to the developing retina inhibits both the differentiation of retinal ganglion cell neurons and the proliferation of the neuroepithelial cells from which they derive. These results suggest that neuregulin-1 promotes both muscle cell differentiation in the heart and neuronal differentiation in the central nervous system. In addition, they demonstrate the utility of hammerhead ribozymes as a simple, effective and easily adaptable method of conditional gene inactivation in vertebrates.
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Saint-Jeannet, J. P., G. Levi, J. M. Girault, V. Koteliansky, and J. P. Thiery. "Ventrolateral regionalization of Xenopus laevis mesoderm is characterized by the expression of alpha-smooth muscle actin." Development 115, no. 4 (August 1, 1992): 1165–73. http://dx.doi.org/10.1242/dev.115.4.1165.
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Mesodermal patterning in the amphibian embryo has been extensively studied in its dorsal aspects, whereas little is known regarding its ventrolateral regionalization due to a lack of specific molecular markers for derivatives of this type of mesoderm. Since smooth muscles (SM) are thought to arise from lateral plate mesoderm, we have analyzed the expression of an alpha-actin isoform specific for SM with regard to mesoderm patterning. Using an antibody directed against alpha-SM actin that recognized specifically this actin isoform in Xenopus, we have found that the expression of alpha-SM actin is restricted to visceral and vascular SM with a transient expression in the heart. The overall expression of the alpha-SM actin appears restricted to the ventral aspects of the differentiating embryo. alpha-SM actin expression appears to be activated following mesoderm induction in animal cap derivatives. Moreover, at the gastrula stage, SM precursor cells are regionalized since they will only differentiate from ventrolateral marginal zone explants. Using the animal cap assay, we have found that alpha-SM actin expression is specifically induced in treated animal cap with bFGF or a low concentration of XTC-MIF, which induce ventral structures, but not with a high concentration of XTC-MIF, which induces dorsal structures. Altogether, these results establish that alpha-SM actin is a reliable marker for ventrolateral mesoderm. We discuss the importance of this novel marker in studying mesoderm regionalization.