Down-regulation of V1a vasopressin receptors in the cerebellum after myocardial infarction

2011 ◽  
Vol 499 (2) ◽  
pp. 119-123 ◽  
Author(s):  
Elwira Milik ◽  
Ewa Szczepanska-Sadowska ◽  
Agnieszka Cudnoch-Jedrzejewska ◽  
Jakub Dobruch
Keyword(s):  
Myocardial Infarction ◽  
Down Regulation ◽  
Vasopressin Receptors

Abstract 58: AT2 Receptor Agonism Regulates TIMP1/MMP9 Axis in the Heart Preventing Cardiac Fibrosis and Improving Heart Function After Experimental Myocardial Infarction

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Dilyara Lauer ◽  
Svetlana Slavic ◽  
Manuela Sommerfeld ◽  
Christa Thöne-Reineke ◽  
Yuliya Sharkovska ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Left Ventricle ◽  
Late Stage ◽  
Heart Function ◽  
Cardiac Fibroblasts ◽  
Collagen Content ◽  
Vehicle Group ◽  
At2 Receptor ◽  
Down Regulation ◽  
Tgf Β1

Aims: A selective nonpeptide agonist for the angiotensin AT2 receptor compound 21 (C21) improved cardiac functions 7 days after myocardial infarction (MI). Here, we aimed to investigate what are the cellular mechanisms underlying cardiac protection in the late stage after MI. Methods and Results: MI was induced in Wistar rats by permanent ligation of the left coronary artery. Treatment with C21 (0.03mg/kg i.p. daily) started 6h after MI and continued for 6 weeks. Hemodynamic parameters were measured via transthoracic Doppler echocardiography and intracardiac Samba catheter. The expression of MMP9, TIMP1, TGF-β1 and collagen content were determined in left ventricle. Anti-proteolytic effects were additionally studied in primary cardiac fibroblasts. C21 significantly improved systolic and diastolic function 6 weeks after MI in comparison with the vehicle group as shown by ejection fraction (71.2±4.7 % vs. 53.4±7.0%; p<0.001), fractional shortening (40.8±2.3% vs. 30.9±3.1%; p<0.05), LVIDs (4.4±0.5mm vs. 5.2±0.8mm; p<0.05), LV EDP (16.9±1.2mmHg vs. 22.1±1.4mmHg; p<0.05), E/A ratio, dP/dt max and dP/dt min (p<0.05). Moreover, C21 improved arterial stiffness parameter (AIx) (18±1.2% vs. 25%±1.8, p<0.05) and reduced collagen content (15%; p<0.05) in postinfarcted myocardium. TIMP1 protein expression in the left ventricle was strongly up-regulated (17.7-fold; p<0.05) whereas MMP9 and TGF-β1 were significantly down-regulated (1.5-fold, p<0.05; 3.4-fold p<0.001, respectively) in the treated group. In cardiac fibroblasts, C21 primarily induced TIMP1 expression followed by attenuated MMP9 secretion and TGF-β1 down-regulation. Conclusion: C21 improves heart function in the late stage after MI and prevents cardiac remodeling. Activation of TIMP1 and subsequent inhibition of MMP9-mediated proteolysis as well as down-regulation of TGF-β1 followed by decreased collagen accumulation may attenuate disintegration of the extracellular matrix and reduce fibrosis.

Down-regulation of miR-133a/b in patients with myocardial infarction correlates with the presence of ventricular fibrillation

2018 ◽  
Vol 99 ◽  
pp. 65-71 ◽  
Author(s):  
Emanuela Boštjančič ◽  
Tanisa Brandner ◽  
Nina Zidar ◽  
Damjan Glavač ◽  
Dušan Štajer
Keyword(s):  
Myocardial Infarction ◽  
Ventricular Fibrillation ◽  
Down Regulation

scholarly journals Upregulation of neutrophil integrins and down regulation of L-selectin by plasma from patients with myocardial infarction

1996 ◽  
Vol 27 (2) ◽  
pp. 183
Author(s):  
Tomasz Siminiak ◽  
Robin M. Egdell ◽  
Daniel J. O'Gorman ◽  
Julian F. Dye ◽  
Desmond J. Sheridan
Keyword(s):  
Myocardial Infarction ◽  
Down Regulation

scholarly journals Suppression of microRNA-16 protects against acute myocardial infarction by reversing beta2-adrenergic receptor down-regulation in rats

Oncotarget ◽  
2017 ◽  
Vol 8 (12) ◽  
pp. 20122-20132 ◽  
Author(s):  
Jiaqi Liu ◽  
Fei Sun ◽  
Yuying Wang ◽  
Wanqi Yang ◽  
Hongwen Xiao ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Adrenergic Receptor ◽  
Down Regulation

Abstract P274: Cardiac-Specific Knockout of Capn4 Attenuates Myocardial Remodeling and Improves Function After Myocardial Infarction in Mice

2011 ◽  
Vol 109 (suppl_1) ◽  
Author(s):  
Jian Ma ◽  
Meng Wei ◽  
Hao Wang ◽  
Weihua Liu ◽  
Wei Zhu ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Mouse Model ◽  
Coronary Artery Ligation ◽  
Down Regulation ◽  
Artery Ligation ◽  
Cardiac Apoptosis ◽  
Myocardial Remodelling ◽  
Calpain 2 ◽  
Specific Deletion

Background - Calpain has been implicated in myocardial injury after myocardial infarction (MI). However, no direct evidence is available on the role of calpain in post-MI myocardial remodelling and dysfunction. The present study investigated the effects of cardiomyocyte-specific deletion of Capn4 , essential for calpain-1 and calpain-2 activities on myocardial remodelling and dysfunction following MI. Methods and Results - A novel mouse model with cardiomyocyte-specific deletion of Capn4 ( Capn4-ko ) was generated. MI was induced by left coronary artery ligation. Deficiency of Capn4 significantly reduced the protein levels and activities of calpain-1 and calpain-2 in the Capn4-ko heart. In vivo cardiac function was relatively improved in Capn4-ko mice at 7 and 30 days after MI compared with their wild-type littermates. Deletion of Capn4 reduced cardiac apoptosis, limited infarct expansion and infarct zone thinning, and prevented left ventricle dilation in Capn4-ko mice. Furthermore, myocardial collagen deposition and cardiomyocyte cross-sectional areas were significantly attenuated in Capn4-ko mice, which were accompanied by down-regulation of pro-fibrotic genes and hypertrophic genes. These effects of Capn4 knockout correlated with down-regulation of inflammatory mediators and normalization of matrix metalloproteinase (MMP)-9 activity in the non-infarct area of Capn4-ko mice after MI. In vivo mouse model of endotoxemia confirmed that calpain activation resulted in inflammatory gene expression and MMP-9 activity in the heart. Conclusions - Cardiomyocyte-specific knockout of calpain attenuates myocardial adverse remodelling and improves myocardial function after MI. These beneficial effects of calpain disruption may result from inhibition of cardiac apoptosis, inflammation and MMP-9 activity.

scholarly journals AKAP150 participates in calcineurin/NFAT activation during the down-regulation of voltage-gated K+ currents in ventricular myocytes following myocardial infarction

2016 ◽  
Vol 28 (7) ◽  
pp. 733-740 ◽  
Author(s):  
Madeline Nieves-Cintrón ◽  
Dinesh Hirenallur-Shanthappa ◽  
Patrick J. Nygren ◽  
Simon A. Hinke ◽  
Mark L. Dell'Acqua ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Ventricular Myocytes ◽  
Down Regulation ◽  
Voltage Gated ◽  
Nfat Activation ◽  
K Currents

scholarly journals Acute endotoxemia in rats induces down-regulation of V2 vasopressin receptors and aquaporin-2 content in the kidney medulla

2004 ◽  
Vol 65 (1) ◽  
pp. 54-62 ◽  
Author(s):  
Valery Grinevich ◽  
Mark A. Knepper ◽  
Joseph Verbalis ◽  
Ivan Reyes ◽  
Greti Aguilera
Keyword(s):  
Down Regulation ◽  
Kidney Medulla ◽  
Aquaporin 2 ◽  
Vasopressin Receptors ◽  
V2 Vasopressin Receptors

Abstract 414: Putative Role of MicroRNA-143 in Modulating Natriuretic Peptide Signaling via Down-regulation of the Expression of Natriuretic Peptide Receptor 3

2016 ◽  
Vol 119 (suppl_1) ◽  
Author(s):  
Juan Wang ◽  
Lee L Wong ◽  
Arthur M Richards ◽  
Yei-Tsung Chen
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Natriuretic Peptide ◽  
Therapeutic Potential ◽  
Cardiac Cells ◽  
Luciferase Reporter ◽  
Natriuretic Peptide Receptor ◽  
Down Regulation ◽  
Peptide Receptor

Cardiac natriuretic peptides (NPs) play important roles in the regulation of intravascular blood volume and vascular tone. Among other clearance mechanisms, bio-active circulating NPs are removed by the clearance receptor, Natriuretic Peptide Receptor 3 (NPR3). We hypothesized that the level of NPR3 could be modulated by microRNAs (miRNAs) resulting in changes in the bioactivity of NPs. We have previously reported a cluster of miRNAs potentially regulating NPR3 expression. To extend these findings, expression of the microRNAs concerned was examined in multiple platforms, including plasma from a clinical heart failure cohort, in the rat myocardial infarction model, and in a human cardiac derived cell line subjected to hypoxic challenge. Results: miR-143 was up-regulated in peripheral blood in heart failure patients compared with controls. The binding of miR-143 to the 3’UTR of NPR3 m RNA was verified by luciferase reporter assay. Antagomir-based silencing of miR-143 enhanced NPR3 expression in human derived cardiac cells. Elevation of miR-143 and down-regulation of NPR3 levels were observed in hypoxia treated cells and in the myocardium from the rat myocardial infarction model. Taken together, these findings suggest miR-143 may be involved in the down-regulation of NPR3 which in turn may provide more cardiac protective bioactivity from NPs in heart failure, myocardial hypoxic stress and in myocardial infarction. In summary, NPR3 is negatively regulated by miR-143, pointing to the therapeutic potential of miR-143 to beneficially enhance NP responses.

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