Brief accomplished from my lab:

1)    The strength of my lab includes cardiovascular remodeling. Remodeling by its very nature implies synthesis and degradation of extracellular matrix (ECM). Our lab is one of the original in Cardiac Remodeling (i.e., we discovered MMP/ADAMTS in the heart early in 1992). For example, we demonstrated the cardiac fibrosis and MMP activation coexist because during reconstitute remodeling ECM, collagen and elastin all are degraded by MMPs but because turnover of elastin is 1000x slower than collagen therefore degraded elastin is also replaced by rapidly synthesized collagen by myofibroblasts. The cardiac ECM remodeling, and reactive and reparative fibrosis terms led to the ideas of resident cardiac precursor/regenerative stem cells.

2)    It is our belief that endocardial endothelial-myocyte coupling contributes to cardiac synchronous relaxation and contraction cycle. This is primarily based on our research. Though the role of vascular (including coronary) endothelial in underlying smooth muscle contraction relaxation is studied very well, there is not many studies revealing the contribution of endocardial endothelium in myocyte regulation during systole and diastole.  

3)    The epigenetic methylation of any DNA/RNA/Protein, promoter or repressor of genes on chromatin and/or histones generates homocysteine, unequivocally. The strength of our laboratory programs relating to folate 1-carbon metabolism (FOCM) and homocystinuria in cardiovascular system is unique in the sense that it is triggered by epigenetic rhythmic methylation/de-methylation control of gene expression or suppression. The epigenetics by its very nature implies modifications of the genes prior to imprinting and off printing during the development, health, and disease. We are few of the leaders in the field of epigenetic control of cardiovascular development and disease, especially by folate-dependent mechanism. The epigenetic regulation of FOCM in DNA/RNA and histone methylation and acetylation by gene writer and erasers are studied in Dr. Tyagi’s laboratory. Based on our findings, the role of nutrition (folate) in “genetics and epigenetics of preventive medicine” are addressed.

Technological innovation: Our laboratory is one of the few laboratories in creating the chronic congestive cardiopulmonary heart failure (CHF) by creating aorta-vena cava fistula (AVF) in C57 wild type mice. There are basically four ways to create experimental CHF. 1) acute myocardial infarction (MI) model which is ligating the coronary by instrumenting and injuring the heart; 2) Although trans-aortic constriction (TAC) mimics the systematic hypertension, TAC is constricting the aorta on the top of the heart and pressing the heart. 3) there are some acquired models of CHF such as by dietary factors, diabetes/salt diets etc., but these are “single-hit to multiple-hits” models. 4) AVF is the one where AVF is created below the kidney ~1cm, where aorta and vena cava share common middle wall. By creating fistula red blood enters vena cava without an injury to the heart. This model mimics the CHF such as during aging where with age preload keeps increasing than the heart can pump out due to the weaken cardiac myocytes. This also involves right ventricle, lung then to left ventricle, creating congestion. The heart by AVF goes transition from compensatory (HFpEF) to de-compensatory (HFrEF) without multiple hits. There are more models of volume overload, such pacing-induced and mitral valve regurgitation. But these are also injurious models. Our lab is one of the original labs in creating AVF.