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Articles 1 - 4 of 4
Full-Text Articles in Other Biochemistry, Biophysics, and Structural Biology
Editorial: Mitochondria, Metabolism And Cardiovascular Diseases, Jun-Ichiro Koga, Xinghui Sun, Masuko Ushio-Fukai
Editorial: Mitochondria, Metabolism And Cardiovascular Diseases, Jun-Ichiro Koga, Xinghui Sun, Masuko Ushio-Fukai
Department of Biochemistry: Faculty Publications
No abstract provided.
Reduction Of Stabilin-2 Contributes To A Protection Against Atherosclerosis, Yukako Kayashima, Connor A. Clanton, Amanda M. Lewis, Xinghui Sun, Sylvia Hiller, Phillip Huynh, Jennifer Wilder, John Hagaman, Feng Li, Nobuyo Maeda-Smithies, Ed Harris
Reduction Of Stabilin-2 Contributes To A Protection Against Atherosclerosis, Yukako Kayashima, Connor A. Clanton, Amanda M. Lewis, Xinghui Sun, Sylvia Hiller, Phillip Huynh, Jennifer Wilder, John Hagaman, Feng Li, Nobuyo Maeda-Smithies, Ed Harris
Department of Biochemistry: Faculty Publications
We have previously identified a novel atherosclerosis quantitative trait locus (QTL), Arch atherosclerosis 5 (Aath5), on mouse chromosome 10 by three-way QTL analyses between Apoe−/− mice on a DBA/2J, 129S6 and C57BL/6J background. The DBA/2J haplotype at the Aath5 locus was associated with smaller plaque size. One of the candidate genes underlying Aath5 was Stabilin-2 (Stab2), which encodes a clearance receptor for hyaluronan (HA) predominantly expressed in liver sinusoidal endothelial cells (LSECs). However, the role of Stab2 in atherosclerosis is unknown. A congenic line of Apoe−/− mice carrying Aath5 covering the Stab2 …
Reduction Of Stabilin-2 Contributes To A Protection Against Atherosclerosisstabilin, Yukako Kayashima1*,, Conner A. Clanton, Amanda M. Lewis, Xinghui Sun, Sylvia Hiller, Phillip Huynh, Jennifer Wilder, John Hagaman, Feng Li, Nobuyo Maeda-Smithies, Edward N. Harris
Reduction Of Stabilin-2 Contributes To A Protection Against Atherosclerosisstabilin, Yukako Kayashima1*,, Conner A. Clanton, Amanda M. Lewis, Xinghui Sun, Sylvia Hiller, Phillip Huynh, Jennifer Wilder, John Hagaman, Feng Li, Nobuyo Maeda-Smithies, Edward N. Harris
Department of Biochemistry: Faculty Publications
We have previously identified a novel atherosclerosis quantitative trait locus (QTL), Arch atherosclerosis 5 (Aath5), on mouse chromosome 10 by three-way QTL analyses between Apoe−/− mice on a DBA/2J, 129S6 and C57BL/6J background. The DBA/2J haplotype at the Aath5 locus was associated with smaller plaque size. One of the candidate genes underlying Aath5 was Stabilin-2 (Stab2), which encodes a clearance receptor for hyaluronan (HA) predominantly expressed in liver sinusoidal endothelial cells (LSECs). However, the role of Stab2 in atherosclerosis is unknown. A congenic line of Apoe−/− mice carrying Aath5 covering the Stab2DBA allele …
Endothelial Cell-Specific Deletion Of A Microrna Accelerates Atherosclerosis, Dafeng Yang, Stefan Haemmig, Jingshu Chen, Michael Mccoy, Henry S. Cheng, Haoyang Zhou, Daniel Pérez-Cremades, Xiao Cheng, Xinghui Sun, Jorge Haneo-Mejia, Shamsudheen K. Vellarikkal, Rajat M. Gupta, Victor Barrera, Mark W. Feinberg
Endothelial Cell-Specific Deletion Of A Microrna Accelerates Atherosclerosis, Dafeng Yang, Stefan Haemmig, Jingshu Chen, Michael Mccoy, Henry S. Cheng, Haoyang Zhou, Daniel Pérez-Cremades, Xiao Cheng, Xinghui Sun, Jorge Haneo-Mejia, Shamsudheen K. Vellarikkal, Rajat M. Gupta, Victor Barrera, Mark W. Feinberg
Department of Biochemistry: Faculty Publications
Background and aims: Chronic vascular endothelial inflammation predisposes to atherosclerosis; however, the cell-autonomous roles for endothelial-expressing microRNAs (miRNAs) are poorly understood in this process. MiR-181b is expressed in several cellular constituents relevant to lesion formation. The aim of this study is to examine the role of genetic deficiency of the miR-181b locus in endothelial cells during atherogenesis.
Methods and Results: Using a proprotein convertase subtilisin/kexin type 9 (PCSK9)-induced atherosclerosis mouse model, we demonstrated that endothelial cell (EC)-specific deletion of miR-181a2b2 significantly promoted atherosclerotic lesion formation, cell adhesion molecule expression, and the influx of lesional macrophages in the vessel wall. Yet, …