Open Access. Powered by Scholars. Published by Universities.®
- Publication
- Publication Type
Articles 1 - 2 of 2
Full-Text Articles in Medicine and Health Sciences
Trypanosoma Cruzi Modulates Piwi-Interacting Rna Expression In Primary Human Cardiac Myocytes During The Early Phase Of Infection, Kayla J. Rayford, Ayorinde Cooley, Ashutosh Arun, Girish Rachakonda, Yulia Kleschenko, Fernando Villalta, Siddharth Pratap, Maria F. Lima, Pius N. Nde
Trypanosoma Cruzi Modulates Piwi-Interacting Rna Expression In Primary Human Cardiac Myocytes During The Early Phase Of Infection, Kayla J. Rayford, Ayorinde Cooley, Ashutosh Arun, Girish Rachakonda, Yulia Kleschenko, Fernando Villalta, Siddharth Pratap, Maria F. Lima, Pius N. Nde
Publications and Research
Trypanosoma cruzi dysregulates the gene expression profile of primary human cardiomyocytes (PHCM) during the early phase of infection through a mechanism which remains to be elucidated. The role that small non-coding RNAs (sncRNA) including PIWI-interacting RNA (piRNA) play in regulating gene expression during the early phase of infection is unknown. To understand how T. cruzi dysregulate gene expression in the heart, we challenged PHCM with T. cruzi trypomastigotes and analyzed sncRNA, especially piRNA, by RNA-sequencing. The parasite induced significant differential expression of host piRNAs, which can target and regulate the genes which are important during the early infection phase. An …
The Role Of Neutrophils In Chronic Heart Failure, Sergey Antipenko
The Role Of Neutrophils In Chronic Heart Failure, Sergey Antipenko
All ETDs from UAB
Acute myocardial infarction (MI) produces massive, sudden cardiomyocyte death, triggering an inflammatory and healing response that initially leads to scar formation and ultimately may induce progressive ischemic cardiomyopathy and heart failure (HF). Scar formation and left ventricular (LV) hypertrophy occur in response to MI to stabilize injury compensating for lost myocardial function. Over time, heart function can become decompensated due to neuroendocrine dysfunction and adverse LV remodeling, ultimately leading to HF. Adverse remodeling is characterized by continued dysregulated collagen deposition, cardiomyocyte hypertrophy, and increased inflammation. Studies have documented a resurgence in inflammatory cytokines and infiltrating leukocytes after resolution of the …