Erdosteine salvages cardiac necrosis: Novel effect through modulation of MAPK and Nrf‐2/HO‐1 pathway

2020 ◽  
Vol 34 (12) ◽  
Author(s):  
Ekta Mutneja ◽  
Vipin K. Verma ◽  
Salma Malik ◽  
Anil K. Sahu ◽  
Ruma Ray ◽  
...  
Keyword(s):  
Cardiac Necrosis

scholarly journals Ivabradine Induces Cardiac Protection against Myocardial Infarction by Preventing Cyclophilin-A Secretion in Pigs under Coronary Ischemia/Reperfusion

2021 ◽  
Vol 22 (6) ◽  
pp. 2902
Author(s):  
Ignacio Hernandez ◽  
Laura Tesoro ◽  
Rafael Ramirez-Carracedo ◽  
Javier Diez-Mata ◽  
Sandra Sanchez ◽  
...  
Keyword(s):  
Matrix Metalloproteinase ◽  
Ischemia Reperfusion ◽  
Cardiac Injury ◽  
Cyclophilin A ◽  
Cardiac Ischemia ◽  
Cardiac Protection ◽  
Cardiac Inflammation ◽  
Risk Areas ◽  
Lysosome Degradation ◽  
Cardiac Necrosis

In response to cardiac ischemia/reperfusion, proteolysis mediated by extracellular matrix metalloproteinase inducer (EMMPRIN) and its secreted ligand cyclophilin-A (CyPA) significantly contributes to cardiac injury and necrosis. Here, we aimed to investigate if, in addition to the effect on the funny current (I(f)), Ivabradine may also play a role against cardiac necrosis by reducing EMMPRIN/CyPA-mediated cardiac inflammation. In a porcine model of cardiac ischemia/reperfusion (IR), we found that administration of 0.3 mg/kg Ivabradine significantly improved cardiac function and reduced cardiac necrosis by day 7 after IR, detecting a significant increase in cardiac CyPA in the necrotic compared to the risk areas, which was inversely correlated with the levels of circulating CyPA detected in plasma samples from the same subjects. In testing whether Ivabradine may regulate the levels of CyPA, no changes in tissue CyPA were found in healthy pigs treated with 0.3 mg/kg Ivabradine, but interestingly, when analyzing the complex EMMPRIN/CyPA, rather high glycosylated EMMPRIN, which is required for EMMPRIN-mediated matrix metalloproteinase (MMP) activation and increased CyPA bonding to low-glycosylated forms of EMMPRIN were detected by day 7 after IR in pigs treated with Ivabradine. To study the mechanism by which Ivabradine may prevent secretion of CyPA, we first found that Ivabradine was time-dependent in inhibiting co-localization of CyPA with the granule exocytosis marker vesicle-associated membrane protein 1 (VAMP1). However, Ivabradine had no effect on mRNA expression nor in the proteasome and lysosome degradation of CyPA. In conclusion, our results point toward CyPA, its ligand EMMPRIN, and the complex CyPA/EMMPRIN as important targets of Ivabradine in cardiac protection against IR.

Strategic Use of Immunoprecipitation and LC/MS/MS for Trace-Level Protein Quantification:  Myosin Light Chain 1, a Biomarker of Cardiac Necrosis

2007 ◽  
Vol 79 (11) ◽  
pp. 4199-4205 ◽  
Author(s):  
Michael J. Berna ◽  
Yuejun Zhen ◽  
David E. Watson ◽  
John E. Hale ◽  
Bradley L. Ackermann
Keyword(s):  
Light Chain ◽  
Myosin Light Chain ◽  
Protein Quantification ◽  
Trace Level ◽  
Cardiac Necrosis

scholarly journals Description of the pathology of a gazelle that died during a major outbreak of foot-and-mouth disease in Israel : clinical communication

2010 ◽  
Vol 81 (1) ◽  
Author(s):  
A. Berkowitz ◽  
T. Waner ◽  
R. King ◽  
H. Yadin ◽  
S. Perl
Keyword(s):  
Pancreatic Necrosis ◽  
Nature Reserve ◽  
Incidental Finding ◽  
Foot And Mouth Disease ◽  
Mouth Disease ◽  
Clinical Communication ◽  
Naturally Occurring ◽  
Foot And Mouth ◽  
Major Outbreak ◽  
Cardiac Necrosis

Naturally occurring foot-and-mouth disease (FMD) in wildlife is a relatively mild condition but occasionally it can be devastating as has been documented in impala in South Africa and in mountain gazelles in Israel. This report describes pathological changes in an adult male gazelle with FMD from an outbreak in the Nature Reserve of Ramot-Issachar region and the lower Galilee in Israel. The outbreak was characterised by the malignant form of the disease, which is uncommon among domestic animals. Lesions observed included, ulceration in the oral cavity, oesophagus and ruminal pillars, coronitis, multifocal cardiac necrosis and pancreatic necrosis and inflammation. Pneumonia, caused by Muellerius capillaries was an incidental finding.

Isoproterenol-induced acute experimental cardiac necrosis in the turtle (Testudo Horsfieldi)

1968 ◽  
Vol 76 (5) ◽  
pp. 645-649 ◽  
Author(s):  
Bohuslav Ošťádal ◽  
Vlasta Rychterová ◽  
Otakar Poupa
Keyword(s):  
Cardiac Necrosis

scholarly journals ERDOSTEINE SALVAGES CARDIAC NECROSIS: NOVEL EFFECT THROUGH MODULATION OF MAPK AND NRF-2/HO-1 PATHWAY

2021 ◽  
Vol 39 (Supplement 1) ◽  
pp. e201
Author(s):  
Ekta Mutneja ◽  
Vipin Verma ◽  
Salma Malik ◽  
D.S. Arya
Keyword(s):  
Cardiac Necrosis

Thiamine Deficiency and Experimental Cardiac Necrosis

1970 ◽  
Vol 135 (3) ◽  
pp. 735-738 ◽  
Author(s):  
M. L. Brown ◽  
J. J. McGrath
Keyword(s):  
Thiamine Deficiency ◽  
Cardiac Necrosis

Experimental cardiac necrosis in hypobaric and anemic hypoxia

1975 ◽  
Vol 39 (2) ◽  
pp. 205-208 ◽  
Author(s):  
J. J. McGrath ◽  
B. Ostadal ◽  
J. Prochazka ◽  
M. Wachtlova ◽  
V. Rychterova
Keyword(s):  
White Male ◽  
Male Rats ◽  
Standard Laboratory ◽  
Simulated Altitude ◽  
Subcutaneous Injections ◽  
The Third ◽  
Infant Rats ◽  
Significant Difference ◽  
Standard Laboratory Diet ◽  
Cardiac Necrosis

Resistance to isoproterenol-induced cardiac necrosis (IPRO) was compared in rats exposed to two types of hypoxia (i.e., hypobaric and anemic). IPRO was induced by two consecutive, subcutaneous injections of isoproterenol (80 mg/kg) at 24-h intervals. The animals were killed on the third day and the severity of the lesion was evaluated on a 0 (no damage) to 4 (severely damaged) scale. White male rats (HA) were exposed in a barometric chamber to a simulated altitude of 7,000 m (307 mmHg) for 4 h/day for 24 days. Two groups of control rats were kept at sea level; one group (SLA) was the same age and one group (SLW) was the same weight as the altitude-exposed rats. The HA rats were significantly more resistant to IPRO with a mean necrogenic rating of 1.8 compared to 3.3 for the SLA and SLW rats. Infant rats (AA) were made anemic by feeding full-cream milk and glucose for 100 days after weaning. Two groups of control animals were fed a standard laboratory diet; one group (AC) was the same age and one group (AW) was the same weight as the AA rats. There was no significant difference in the necrogenic ratings of the AA (3.3), AC (3.5), or WC (3.7) hearts. Thus, hypobaric hypoxia affords some protection against IPRO which is not afforded by anemic hypoxia. Similarities and differences in the two hypoxias are discussed.

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