Babinska Anna, Clement Cristina C, Li Yan, Wzorek Joanna, Przygodzki Tomasz, Talar Marcin, Braun Marcin, Swiatkowska Maria, Ehrlich Yigal H, Kornecki Elizabeth, Watala Cezary, Salifu Moro O
Department of Medicine, 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.
Data Brief. 2020 Apr 23;30:105516. doi: 10.1016/j.dib.2020.105516. eCollection 2020 Jun.
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 . Utilizing a nonhydrolyzable peptide derived from an amino acid sequence of F11R/JAM-A, peptide 4D, we have shown 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.
本文中的数据聚焦于F11受体（F11R/JAM-A；连接粘附分子A；JAM-A，F11R），这是一种在循环血小板膜表面组成性表达且定位于健康内皮细胞紧密连接处的细胞粘附蛋白。先前的报道表明，由于F11R/JAM-A在细胞因子炎症内皮的管腔表面病理性表达，它在血小板与炎症内皮的粘附中起关键作用。由于血小板与炎症内皮的粘附是动脉粥样硬化斑块形成发展的早期步骤，且随着时间推移会导致心脏病发作和中风，我们利用易患动脉粥样硬化的载脂蛋白E小鼠进行了一项长期研究，试图通过阻止血小板与炎症血管系统的粘附来阻断动脉粥样硬化斑块的形成。利用源自F11R/JAM-A氨基酸序列的不可水解肽——肽4D，我们已表明肽4D可阻断血小板与炎症内皮细胞间的粘附。目前的数据证明了对易患动脉粥样硬化的载脂蛋白E小鼠长期给予肽4D对健康有益，并为该源自F11R的肽在预防动脉粥样硬化方面的潜在应用提供了新信息。本文所呈现的数据为Babinska等人发表于《动脉粥样硬化》284卷（2019年）第92 - 101页的研究提供了进一步的实验支持。
