Highlights:

Skills:Heart, Molecular Biology, Physiology, Immunology, Flow cytometry, Single cell analysis, PCR, Western blot, Histology, Animal surgery, Immunohistochemistry, Immune cells, Metabolism, Aging

Senior Postdoctoral Fellow 07/01/2022 - current
NYU, New York, New York United States
TO DISCOVER WHY DELETION OF MYELOID RAGE OR DIAPH IS PROTECTIVE.
MYELOID DELETION OF RAGE MICE IN DIABETIC AND NON-DIABETIC MICE--
Postdoctoral Fellow 11/14/2019 - 06/30/2022
NIH, Nottingham, Maryland United States
I investigated the mechanisms of adaptive changes in the heart induced by cardiac-specific overexpression of the Human adenylyl cyclase (AC) type VIII (ADCY8) gene.
The human heart accompanies hemodynamic stress with advancing age, leading to ventricular hypertrophy, hypertension, arrhythmia, atherosclerosis, and heart failure. It is thus essential to study a cardiac aging model that shows a similar phenotype to address these challenges in the aging heart. The incessant cAMP-PKA-Ca2+ signaling drives increased heart rate at three months in the ADCY8 overexpressed mice (TGAC8); these mice survive chronic stress up to 12 months of age and then develop accelerated adverse cardiac remodeling leading to heart failure and reduced life span. It is unclear how the TGAC8 mice heart adapts and survives chronic stress up to 12 months of age. I found that ADCY8-driven calcium signaling contributes to RelA activation and associated inflammation in the TGAC8 mice heart (manuscript under preparation). We are studying if immune cell infiltration, especially macrophages, contributes to these mice's increased heart rate.--

Kurukshetra University 05/01/2007 - 05/01/2011
Kurukshetra, Haryana, India
Degree: Bachelor's Degree
Major:Pharmaceutical Sciences
Learned the basic pharmaceutical science

Vikas Kumar_CV