Intracardiac/Epicardial injection of Erythropoietin/Hematopoietin  may attenuate pathogenesis-associated with Myocardial infarction: Erythropoietin/Hematopoietin decreases GM-CSF (Granulocyte-macrophage colony-stimulating factor) expression, inhibits undue leucocyte activation and invasion, suppresses recruitment of inflammatory cells, inhibits left ventricular rupture, and promotes heart healing via up regulation of its target gene, 30/March/2019, 12.04 am

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Introduction: What they say:

A recent study from Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; and Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston, MA shows thatThe infarcted myocardium solicits GM-CSF for the detrimental oversupply of inflammatory leukocytes.” This study was published, in the 4 October 2017 issue of Journal of Experimental Medicine, by Prof Swirski FK, Anzai A and others.


What we say:

On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that: Intracardiac/Epicardial injection of Erythropoietin/Hematopoietin  may attenuate pathogenesis-associated with Myocardial infarction: Erythropoietin/Hematopoietin decreases GM-CSF (Granulocyte-macrophage colony-stimulating factor) expression, inhibits undue leucocyte activation and invasion, suppresses recruitment of inflammatory cells, inhibits left ventricular rupture, and promotes heart healing via up regulation of its target gene

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From Significance of the study to Public Health relevance:

Given that: (1)  cardiovascular disease is the leading cause of death worldwide; (2) out of 55 million deaths that occur every year, nearly 18.33 million deaths are due to cardiovascular causes; (3) the raise of death rate, due to cardiovascular disease, has increased from  123 lakhs in 1990 to 173 lakhs in 2013; (4) 85% of people over 80 years are susceptible to cardiovascular diseases;(5) in India, in 2004, 14.6 lakhs deaths (14% of total deaths) were due to ischemic heart disease; (6) the death due to cardiovascular disease is higher in low-to-middle income countries compared to developed countries; (7) the global economic cost spent in the treatment of cardiovascular disease in 2011 was little more than 10 billion US dollars;  and (8) an alarming number of people, such as 230 lakhs people, will die from cardiovascular diseases each year from 2030 onwards, there is an urgent need to find: (i) a way to induce regeneration of cardiomyocytes that were lost in Myocardial patients; (ii) a cheaper alternative to the existing expensive drugs; and (iv) a side-effect-free natural product-based drug.


What is known?

It is known for years that myocardial infarction results in excessive recruitment of leukocytes near the damaged myocardium. However, the mechanistic basis of which is far from clear.

Prof Swirski FK’s research team has shown recently that after the onset of Ischemia: (1) cardiac fibroblasts release excessive amount of GM-CSF; (2) GM-CSF promotes recruitment of inflammatory and proteolytic cells; (3) GM-CSF stimulates myeloid cells to attract neutrophils and monocytes, to the site of damaged myocardium; and (4) GM-CSF promotes left ventricular rupture. Evidently, mice null for GM-CSF do not recruit leukocytes near the damaged myocardium and they function well, suggesting that inhibition of GM-CSF or its receptor expression may attenuate pathogenesis-associated with myocardial infarction.


From Research Findings to Therapeutic Opportunity:

This study provides mechanistic insights into how erythropoietin may attenuate pathogenesis-associated with Myocardial infarction. Intracardiac/Epicardial injection of Erythropoietin/Hematopoietin, by increasing the expression of its target genes, it may decrease the expression of GM-CSF (fig.1). Thereby, it may: (i) stall recruitment of inflammatory and proteolytic cells; (ii) inhibit accumulation of excessive amount of neutrophils and monocytes near the damaged myocardium; (iii) inhibit left ventricular rupture; (iv) suppress leukocyte supply chain; (v) control excessive inflammatory reaction; and (vi) improve myocardial function (fig 1).

Figure 1. Intracardiac/Epicardial injection of Erythropoietin/Hematopoietin functions as a Cardioprotective agent. Mechanistic insights into how Erythropoietin/Hematopoietin decreases the expression of GM-CSF and other genes that promote pathogenesis-associated with myocardial infarction.

Figure 2. Intracardiac/Epicardial injection of Erythropoietin/Hematopoietin  attenuates pathogenesis-associated with Myocardial infarction through down regulation of GM-CSF.

Together, this study suggests that intracardiac/Epicardial injection of Erythropoietin/Hematopoietin, either alone or in combination with other compounds,” may be used to heal damaged cardiac tissue after myocardial infarction (fig. 1).


Details of the research findings:

Idea Proposed/Formulated (with experimental evidence) by:

Dr L Boominathan Ph.D.

Terms & Conditions apply http://genomediscovery.org/registration/terms-and-conditions/

Undisclosed mechanistic information: How intracardiac/Epicardial injection of Erythropoietin/Hematopoietin  decreases the expression of GM-CSF, inhibits inflammatory leukocyte recruitment, and attenuates the pathogenesis-associated with myocardial infarction

Amount: $ 750 #

# Research cooperation

For purchase and payment details, you may reach us at admin@genomediscovery.org


References:

Web:http://genomediscovery.org or http://newbioideas.com/

Citation: Boominathan, L., Intracardiac/Epicardial injection of Erythropoietin/Hematopoietin  may attenuate pathogenesis-associated with Myocardial infarction: Erythropoietin/Hematopoietin decreases GM-CSF (Granulocyte-macrophage colony-stimulating factor) expression, inhibits undue leucocyte activation and invasion, suppresses recruitment of inflammatory cells, inhibits left ventricular rupture, and promotes heart healing via up regulation of its target gene, 30/March/2019, 12.03 am, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

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