In vivo data: treatment with the F11R/JAM-A peptide 4D decreases mortality and reduces the generation of atherosclerotic plaques in ApoE-deficient mice
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 report...
| Main Authors: | , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Elsevier
2020-06-01
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| Series: | Data in Brief |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S2352340920304108 |
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| author | Anna Babinska Cristina C. Clement Yan Li Joanna Wzorek Tomasz Przygodzki Marcin Talar Marcin Braun Maria Swiatkowska Yigal H. Ehrlich Elizabeth Kornecki Cezary Watala Moro O. Salifu |
| author_facet | Anna Babinska Cristina C. Clement Yan Li Joanna Wzorek Tomasz Przygodzki Marcin Talar Marcin Braun Maria Swiatkowska Yigal H. Ehrlich Elizabeth Kornecki Cezary Watala Moro O. Salifu |
| author_sort | Anna Babinska |
| collection | DOAJ |
| description | 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. |
| first_indexed | 2024-12-13T12:01:48Z |
| format | Article |
| id | doaj.art-aa78a92e420442fda5e9b89fe5da3c9f |
| institution | Directory Open Access Journal |
| issn | 2352-3409 |
| language | English |
| last_indexed | 2024-12-13T12:01:48Z |
| publishDate | 2020-06-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Data in Brief |
| spelling | doaj.art-aa78a92e420442fda5e9b89fe5da3c9f2022-12-21T23:47:05ZengElsevierData in Brief2352-34092020-06-0130105516In vivo data: treatment with the F11R/JAM-A peptide 4D decreases mortality and reduces the generation of atherosclerotic plaques in ApoE-deficient miceAnna Babinska0Cristina C. Clement1Yan Li2Joanna Wzorek3Tomasz Przygodzki4Marcin Talar5Marcin Braun6Maria Swiatkowska7Yigal H. Ehrlich8Elizabeth Kornecki9Cezary Watala10Moro O. Salifu11Department of Medicine, State University of New York, Downstate Medical Center, Brooklyn, New York 11203, USA; Corresponding author.Department of Pathology, Albert Einstein College of Medicine, New York 10461, USADepartment of Neurology, State University of New York, Downstate Medical Center, Brooklyn, New York 11203, USADepartment of Haemostasis and Haemostatic Disorders, Biomedical Sciences, Medical University of Lodz, 92-215 Lodz, PolandDepartment of Haemostasis and Haemostatic Disorders, Biomedical Sciences, Medical University of Lodz, 92-215 Lodz, PolandDepartment of Haemostasis and Haemostatic Disorders, Biomedical Sciences, Medical University of Lodz, 92-215 Lodz, PolandDepartment of Pathology, Medical Univeristy of Lodz, 92-213 Lodz, PolandDepartment of Cytobiology and Proteomics, Biomedical Sciences, Medical University of Lodz, 92-215 Lodz, PolandProgram in Neuroscience, College of Staten Island of the City University of New York, Staten Island, New York 10314, USADepartment of Medicine, State University of New York, Downstate Medical Center, Brooklyn, New York 11203, USA; Department of Cell Biology, State University of New York, Downstate Medical Center, Brooklyn, New York, 11203, USADepartment of Haemostasis and Haemostatic Disorders, Biomedical Sciences, Medical University of Lodz, 92-215 Lodz, PolandDepartment of Medicine, State University of New York, Downstate Medical Center, Brooklyn, New York 11203, USAThe 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.http://www.sciencedirect.com/science/article/pii/S2352340920304108ApoE-/-miceAtherosclerosisEndotheliumF11RF11R/JAM-AInflammation |
| spellingShingle | Anna Babinska Cristina C. Clement Yan Li Joanna Wzorek Tomasz Przygodzki Marcin Talar Marcin Braun Maria Swiatkowska Yigal H. Ehrlich Elizabeth Kornecki Cezary Watala Moro O. Salifu 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 ApoE-/-mice Atherosclerosis Endothelium F11R F11R/JAM-A Inflammation |
| title | In vivo data: treatment with the F11R/JAM-A peptide 4D decreases mortality and reduces the generation of atherosclerotic plaques in ApoE-deficient mice |
| title_full | In vivo data: treatment with the F11R/JAM-A peptide 4D decreases mortality and reduces the generation of atherosclerotic plaques in ApoE-deficient mice |
| title_fullStr | In vivo data: treatment with the F11R/JAM-A peptide 4D decreases mortality and reduces the generation of atherosclerotic plaques in ApoE-deficient mice |
| title_full_unstemmed | In vivo data: treatment with the F11R/JAM-A peptide 4D decreases mortality and reduces the generation of atherosclerotic plaques in ApoE-deficient mice |
| title_short | In vivo data: treatment with the F11R/JAM-A peptide 4D decreases mortality and reduces the generation of atherosclerotic plaques in ApoE-deficient mice |
| title_sort | in vivo data treatment with the f11r jam a peptide 4d decreases mortality and reduces the generation of atherosclerotic plaques in apoe deficient mice |
| topic | ApoE-/-mice Atherosclerosis Endothelium F11R F11R/JAM-A Inflammation |
| url | http://www.sciencedirect.com/science/article/pii/S2352340920304108 |
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