In vivo data: treatment with the F11R/JAM-A peptide 4D decreases mortality and reduces the generation of atherosclerotic plaques in ApoE-deficient mice

Data in Brief

Cristina C. Clement¹  Moro O. Salifu²  Yigal H. Ehrlich³  Marcin Talar⁴  Marcin Braun⁴  Tomasz Przygodzki⁴  Anna Babinska⁵  Cezary Watala⁵  Joanna Wzorek⁶  Yan Li⁷  Maria Swiatkowska⁸  Elizabeth Kornecki⁹ 

[1] Corresponding author.;Department of Cell Biology, State University of New York, Downstate Medical Center, Brooklyn, New York, 11203, USA;Department of Cytobiology and Proteomics, Biomedical Sciences, Medical University of Lodz, 92-215 Lodz, Poland;Department of Haemostasis and Haemostatic Disorders, Biomedical Sciences, Medical University of Lodz, 92-215 Lodz, Poland;Department of Medicine, State University of New York, Downstate Medical Center, Brooklyn, New York 11203, USA;Department of Neurology, State University of New York, Downstate Medical Center, Brooklyn, New York 11203, USA;Department of Pathology, Albert Einstein College of Medicine, New York 10461, USA;Department of Pathology, Medical Univeristy of Lodz, 92-213 Lodz, Poland;Program in Neuroscience, College of Staten Island of the City University of New York, Staten Island, New York 10314, USA;

关键词: ApoE-/-mice;    Atherosclerosis;    Endothelium;    F11R;    F11R/JAM-A;    Inflammation;   

DOI  :  

来源: DOAJ

【 摘 要 】

The data in this article focus on the F11 Receptor (F11R/JAM-A; Junctional Adhesion Molecule-A; JAM-A, F11R), a cell adhesion protein constitutively expressed on the membrane surface of circulating platelets and localized within the tight junctions of healthy endothelial cells (ECs). Previous reports have shown that F11R/JAM-A plays a critical role in the adhesion of platelets to an inflamed endothelium due to its’ pathological expression on the luminal surface of the cytokine-inflamed endothelium. Since platelet adhesion to an inflamed endothelium is an early step in the development of atherosclerotic plaque formation, and with time, resulting in heart attacks and stroke, we conducted a long-term, study utilizing the atherosclerosis-prone ApoE-/- mice to attempt a blockade of the formation of atherosclerotic plaques by preventing the adhesion of platelets to the inflamed vasculature in vivo. Utilizing a nonhydrolyzable peptide derived from an amino acid sequence of F11R/JAM-A, peptide 4D, we have shown in culture that the adhesion of platelets to the inflamed endothelial cells could be blocked by peptide 4D. The present data demonstrate the positive health benefits of chronic peptide 4D administration to the atherosclerosis-prone ApoE-/- mice, and provides new information for potential use of this F11R derived peptide in the prevention of atherosclerosis. The data presented in this article provide further experimental support for the study presented in Babinska et al., Atherosclerosis 284 (2019) 92-101.

【 授权许可】

Unknown