HYBRID EVENT: You can participate in person at Madrid, Spain or Virtually from your home or work.

5th Edition of Cardiology World Conference

September 5-7, 2024 | Madrid, Spain

September 05 -07, 2024 | Madrid, Spain
Cardio 2023

Corina Rosales

Corina Rosales, Speaker at Cardiology Conference
Houston Methodist Research Institute, United States
Title : Normalizing effects of bacterial serum opacity factor on plasma lipids, tissues, and atherosclerosis


Although plasma HDL-C levels negatively correlate with atherosclerotic cardiovascular disease (ACVD), attempts to reduce ACVD risk by raising plasma HDL have disappointed. Thus, hypotheses about salutary HDL effects have shifted from higher-is-better to function-is-more-important. The SRB1-/- mouse is an extreme model of HDL dsyfunctionality; compared to WT mice, SRB1-/- mice have higher plasma HDL levels and an HDL surface that is free cholesterol (FC)-rich (60 vs. 15 mol%).  Superposition of high plasma HDL levels and a high mol% FC in SRB1-/- mice is expected to increase HDL-FC bioavailablity that contributes to whole-body FC-toxicity and the observed metabolic abnormalities—impaired red blood cells and platelets and increased atherosusceptibility, despite having high plasma HDL-C levels; moreover, female SRB1-/- mice are infertile.  Dietary probucol, an HDL-lowering drug, partially reverses infertility in SR-B1-/- mice. The mechanisms underlying ovaritoxicity are unknown and interventions that fully reverse this state have not been identified.  We have previously shown that bacterial protein, serum opacity factor (SOF), which acts on HDL and lowers cholesterol in WT mice by ~43% in 3 hours, normalized HDL and rescued infertility in SRBI -/- female mice.  SOF catalyzes the disproportionation of HDL into three products: a cholesteryl ester-rich micro emulsion (CERM) with abundant apo E, small neo-HDL, and lipid-free apo AI. Decrease in plasma cholesterol in SOF treated mice is attributed to diverting the CERM particle to hepatic LDL Receptor. We hypothesized that SOF treatment in SRBI1-/- mice would also rescue the dysfunctional phenotype in erythrocytes and lead to atheroprevention in high-fat fed mice. AAVSOF was used to constitutively express SOF in mice for these studies. Erythrocytes from SRBI-/- mice treated with SOF had significantly fewer reticulocytes and abnormal cells compared to non-treated mice. There was no significant difference in the total average plaque area of the treated mice vs. controls.  However, when grouped by gender, males had less plaque burden than female mice in the atheroprevention study.


Dr. Corina Rosales received her undergraduate degree at Michigan State University.  She continued her graduate studies in Molecular Pathology at the University of Texas-Houston where she earned her PhD in 2007.  She joined the lab of Henry J. Pownall at Baylor College of Medicine as a postdoctoral fellow.  She advanced through her career stages under Dr. Pownall’s mentorship and is now an Assistant Professor at the Houston Methodist Research Institute.  Dr. Rosales’ research focuses on metabolism of lipids and lipoproteins.