Genomes and Genes


Bysani Chandrasekar


Affiliation: University of Missouri
Country: USA


  1. Higashi Y, Mummidi S, Sukhanov S, Yoshida T, Noda M, Delafontaine P, et al. Minocycline inhibits PDGF-BB-induced human aortic smooth muscle cell proliferation and migration by reversing miR-221- and -222-mediated RECK suppression. Cell Signal. 2019;57:10-20 pubmed publisher
    ..These results indicate that the induction of RECK is one of the mechanisms by which minocycline exerts vasculoprotective effects. ..
  2. Wörner P, Schächtele D, Barabadi Z, Srivastav S, Chandrasekar B, Izadpanah R, et al. Breast Tumor Microenvironment Can Transform Naïve Mesenchymal Stem Cells into Tumor Forming Cells in Nude Mice. Stem Cells Dev. 2018;: pubmed publisher
    ..Understanding the crosstalk between MSCs and tumor cells, and identifying the players involved in their interaction, will help us develop novel therapeutics for breast cancer regression and elimination. ..
  3. Das N, Carpenter A, Yoshida T, Kumar S, Gautam S, Mostany R, et al. TRAF3IP2 mediates TWEAK/TWEAKR-induced pro-fibrotic responses in cultured cardiac fibroblasts and the heart. J Mol Cell Cardiol. 2018;121:107-123 pubmed publisher
  4. Mummidi S, Das N, Carpenter A, Kandikattu H, Krenz M, Siebenlist U, et al. Metformin inhibits aldosterone-induced cardiac fibroblast activation, migration and proliferation in vitro, and reverses aldosterone+salt-induced cardiac fibrosis in vivo. J Mol Cell Cardiol. 2016;98:95-102 pubmed publisher
    ..These in vitro and in vivo data indicate that metformin has the potential to reduce adverse cardiac remodeling in hypertensive heart disease. ..
  5. Sakamuri S, Higashi Y, Sukhanov S, Siddesha J, Delafontaine P, Siebenlist U, et al. TRAF3IP2 mediates atherosclerotic plaque development and vulnerability in ApoE(-/-) mice. Atherosclerosis. 2016;252:153-160 pubmed publisher
    ..TRAF3IP2 could be a potential therapeutic target in atherosclerotic vascular diseases. ..
  6. Yariswamy M, Yoshida T, Valente A, Kandikattu H, Sakamuri S, Siddesha J, et al. Cardiac-restricted Overexpression of TRAF3 Interacting Protein 2 (TRAF3IP2) Results in Spontaneous Development of Myocardial Hypertrophy, Fibrosis, and Dysfunction. J Biol Chem. 2016;291:19425-36 pubmed publisher
    ..In summary, these results demonstrate that overexpression of TRAF3IP2 in male mice is sufficient to induce myocardial hypertrophy, cardiac fibrosis, and contractile dysfunction. ..
  7. Erikson J, Valente A, Mummidi S, Kandikattu H, Demarco V, Bender S, et al. Targeting TRAF3IP2 by Genetic and Interventional Approaches Inhibits Ischemia/Reperfusion-induced Myocardial Injury and Adverse Remodeling. J Biol Chem. 2017;292:2345-2358 pubmed publisher
    ..Therefore, TRAF3IP2 could be a potential therapeutic target in ischemic heart disease. ..
  8. Padilla J, Carpenter A, Das N, Kandikattu H, López Ongil S, Martinez Lemus L, et al. TRAF3IP2 mediates high glucose-induced endothelin-1 production as well as endothelin-1-induced inflammation in endothelial cells. Am J Physiol Heart Circ Physiol. 2018;314:H52-H64 pubmed publisher
    ..The findings presented herein suggest that TRAF3 interacting protein 2 may be an important therapeutic target in diabetic vasculopathy characterized by excess endothelin-1 production. ..
  9. Sakamuri S, Valente A, Siddesha J, Delafontaine P, Siebenlist U, Gardner J, et al. TRAF3IP2 mediates aldosterone/salt-induced cardiac hypertrophy and fibrosis. Mol Cell Endocrinol. 2016;429:84-92 pubmed publisher
    ..These results indicate that TRAF3IP2 is a critical signaling intermediate in aldosterone/salt-induced myocardial hypertrophy and fibrosis, and thus a potential therapeutic target in hypertensive heart disease...