Posts Tagged: arteries

Stroke Caused by Atherosclerosis of the Major Intracranial Arteries

Stroke Caused by Atherosclerosis of the Major Intracranial Arteries

Chirantan Banerjee, Marc I. Chimowitz

Histological cross-section of intracranial atherosclerosis in basilar artery. Image courtesy Dr Tanya Turan. Red arrow—fibrous tissue, blue arrow—vessel wall, and green arrow—lipid [Powerpoint File]

Molecular Controls of Arterial Morphogenesis

Molecular Controls of Arterial Morphogenesis

Michael Simons, Anne Eichmann

Inhibition-dependent regulation of vascular endothelial growth factor receptor 2 (VEGFR2)–driven extracellular receptor kinase (ERK) activation. A, A schematic of rapidly accelerating fibrosarcoma (Raf1) phosphorylation control. Dephosphorylation of Ser259 allows phosphorylation of Ser338 and activation of Raf1 kinase activity. B, Raf1 regulation of ERK, AKT, and MST2 pathways cross-talk. VEGFR2–induced activation of Akt leads to MST2 phosphorylation and promotes formation of Raf1–MST2 complex that maintains Raf1 in an inactive (Ser259-phosphorylated) state. Dephosphorylation of Raf1S259 site shifts MST2 to the RASSF1A (Ras association [RalGDS/AF-6] domain family member 1) complex thereby activating large tumor suppressor kinase 1 (LATS1) that subsequently acts on YAP (Yes-associated protein 1). At the same time this allows phosphorylation of Raf1Ser338 thereby activating mitogen extracellular kinase (MEK)/extracellular receptor kinase (ERK) signaling. C, Increase dorsal aorta (DA) diameter in Raf1S29A (bottom) compared with wild type (WT; top) mice. D, Extraembryonic vasculature in control (WT) and Raf1SA259 mouse embryos. Note a marked increase in arterial size. For panel B, data derived from Romano et al.104 Panels C and D adapted from Deng et al78 with permission of the publisher (American Society of Hematology, 2013). Cx40 indicates Connexin-40. [Powerpoint File]

Molecular Controls of Arterial Morphogenesis

Molecular Controls of Arterial Morphogenesis

Michael Simons, Anne Eichmann

Arteriogenic defects associated with delayed intracellular vascular endothelial growth factor (VEGF) receptor 2 (VEGFR2) trafficking. A, Micro-computed tomographic (CT) images of mouse coronary arteries from wild-type (WT; top) and Synectin null (bottom) mice. B, Micro-CT of mouse renal arterial circulation from WT (top) and myosin-VI null (bottom) mice. C, Micro-CT images of mouse heart (top), hindlimb (middle), and renal (bottom) arterial circulations from mice carrying a deletion of the neuropilin-1 (Nrp1) cytoplasmic domain. Adapted from Lanahan et al67,68 with permission of Cell Press (2013 and 2010). [Powerpoint File]