Expression of urocortin peptides in canine myocardium and plasma

Veloso, Gemma Fraga; Ohad, Dan G.; Francis, Andrew; Vaughan, Joan; Brownstein, David G.; Culshaw, Geoff; Vale, Wylie; French, Anne; Jamieson, Pauline

doi:10.1016/j.tvjl.2010.05.019

Cited by 4 publications

(2 citation statements)

References 35 publications

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“…CRF and urocortins also have cardioprotective effects that are mediated by cardiac CRF 2 receptors [ 67 ]. Urocortins 1, 2, and 3 are present in the heart, with the abundant expression of urocortins 2 and 3 in myocardium [ 68 ]. Urocortins are cardioprotective when added to post-ischemic/hypoxic cardiomyocytes or to the isolated intact heart during reperfusion after regional ischemia [ 69 ].…”

Section: Psychiatric and Cardiometabolic Mediators That Could Be Umentioning

confidence: 99%

Epigenetic Programming of Synthesis, Release, and/or Receptor Expression of Common Mediators Participating in the Risk/Resilience for Comorbid Stress-Related Disorders and Coronary Artery Disease

Campo

Martínez-Rosas

Guarner-Lans

2018

IJMS

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Corticotrophin releasing factor, vasopressin, oxytocin, natriuretic hormones, angiotensin, neuregulins, some purinergic substances, and some cytokines contribute to the long-term modulation and restructuring of cardiovascular regulation networks and, at the same time, have relevance in situations of comorbid abnormal stress responses. The synthesis, release, and receptor expression of these mediators seem to be under epigenetic control since early stages of life, possibly underlying the comorbidity to coronary artery disease (CAD) and stress-related disorders (SRD). The exposure to environmental conditions, such as stress, during critical periods in early life may cause epigenetic programming modifying the development of pathways that lead to stable and long-lasting alterations in the functioning of these mediators during adulthood, determining the risk of or resilience to CAD and SRD. However, in contrast to genetic information, epigenetic marks may be dynamically altered throughout the lifespan. Therefore, epigenetics may be reprogrammed if the individual accepts the challenge to undertake changes in their lifestyle. Alternatively, epigenetics may remain fixed and/or even be inherited in the next generation. In this paper, we analyze some of the common neuroendocrine functions of these mediators in CAD and SRD and summarize the evidence indicating that they are under early programming to put forward the theoretical hypothesis that the comorbidity of these diseases might be epigenetically programmed and modified over the lifespan of the individual.

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Section: Psychiatric and Cardiometabolic Mediators That Could Be Umentioning

confidence: 99%

Epigenetic Programming of Synthesis, Release, and/or Receptor Expression of Common Mediators Participating in the Risk/Resilience for Comorbid Stress-Related Disorders and Coronary Artery Disease

Campo

Martínez-Rosas

Guarner-Lans

2018

IJMS

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“…[16][17][18][19][20][21][22][23][24] In the adult heart, CRF and/or its ligands have been found to be expressed in both animals and humans. More specifically, they were identified in the heart of rodents, 25 including rats 26,18 and mice, 21 dogs 27 and Tupaia belangeri. 28 In adult humans on the other hand, an immunohistochemical study revealed Ucn I immunoreactivity in myocytes of the normal heart, which was more intense in the diseased heart, indicating, together with evidence of its positive inotropic action, its possible role in the pathophysiology of cardiac hypertrophy or the failing heart.…”

mentioning

confidence: 99%

Corticotropin-releasing factor (CRF) system localization in human fetal heart

Chouridou

Lambropoulou

Koureta

et al. 2016

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oBJectIVe: the corticotropin-releasing factor (cRf) family consists of the neuropeptides cRf, ucn I, II and III and the binding sites cRfR1, cRfR2 and cRf-BP. It regulates stress response and the homeostasis of an organism. In this study, we examined the presence of the cRf system in the human hearts of normal and pathological fetuses. desIGn: Heart tissues from 40 archival human fetuses were divided into Group A (without pathology, 'normal'), Group B (with chromosomal abnormalities) and Group c (with congenital disorders). Immunohistochemistry was used to localize the cRf system. Results correlated to gestational trimester and pathology. ResuLts: Immunoreactivity for all antigens was found in cardiac myocytes of all groups, in almost all samples, except ucn III which was present in almost half of the fetuses of Groups B and c and was not detected at all in Group A. ucn III was more often present during the earlier stage of development (<21weeks) and in fetuses with congenital disorders. In a fetus diagnosed with heart pathology, all but ucn III antigens were also present. concLusIons: we localized a complete cRf system in the human fetal heart and correlated the presence of ucn III to development and pathology. More studies are needed to verify and clarify the exact role of the cRf system in the human fetal heart.

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