We submitted twelve dogs to aorto-superior vena cava by-pass with saphenous vein. Six months later, all dogs had developed areas of chondroid metaplasia in the tunica media of the aorta, near the area of anastomosis. Three dogs also had bony metaplasia. The Foci of metaplasia had no relation to sutures. This lesion begins with a build-up store of glycosaminoglycans in the tunica media. Later, elastic fibers show a fenestration and dissolution, while chondrocytes replace smooth muscle fibres. We suggest that the rupture of the vasa vasorum during operation and the traction and pulsation of the by-pass over the area of suture could be the cause of this direct metaplasia.
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Commun Biol
January 2025
Department of Biochemistry and Molecular Biology, Key Laboratory of Neural and Vascular Biology, Ministry of Education, Hebei Key Laboratory of Forensic Medicine, Hebei Medical University, Shijiazhuang, 050017, China.
Aberrant autophagy in vascular smooth muscle cells (VSMCs) is associated with the progression of vascular remodeling diseases caused by neointimal hyperplasia. Platelet-derived growth factor-BB (PDGF-BB)-induced vascular remodeling is accompanied by autophagy activation, however, the involvement of circular RNAs (circRNAs) remains unclear. Here, we show the role of PDGF-BB-regulated hsa_circ_0001304 (circ-1304) in neointimal hyperplasia and its potential involvement in VSMC autophagy, while also elucidating the potential mechanisms.
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December 2024
Department of Neurosurgery, Institute of Science Tokyo, Tokyo, Japan.
Moyamoya disease (MMD) is characterized by distinct histopathological changes in intracranial arteries, such as narrowing of the arterial lumen due to thickening of the tunica intima, waving of the internal elastic membranes, and thinning of the tunica media. Ring finger protein 213 is a susceptibility gene for MMD that affects clinical outcomes. However, little is known about its relationship with histopathology.
View Article and Find Full Text PDFJCI Insight
January 2025
Section of Vascular Surgery, Department of Surgery, and.
Abdominal aortic aneurysms (AAA) are a life-threatening cardiovascular disease for which there is a lack of effective therapy preventing aortic rupture. During AAA formation, pathological vascular remodeling is driven by vascular smooth muscle cell (VSMC) dysfunction and apoptosis, for which the mechanisms regulating loss of VSMCs within the aortic wall remain poorly defined. Using single-cell RNA-Seq of human AAA tissues, we identified increased activation of the endoplasmic reticulum stress response pathway, PERK/eIF2α/ATF4, in aortic VSMCs resulting in upregulation of an apoptotic cellular response.
View Article and Find Full Text PDFJ Physiol Sci
January 2025
Department of Frontier Health Sciences, Graduate School of Human Health Sciences, Tokyo Metropolitan University, 7-2-10 Higashiogu, Arakawa-Ku, 116-8551, Tokyo, Japan. Electronic address:
Actin linked regulatory mechanisms are known to contribute contraction/relaxation in smooth muscle. In order to clarify whether modulation of polymerization/depolymerization of actin filaments affects relaxation process, we examined the effects of cytochalasin D on relaxation process by Ca removal after Ca-induced contraction of β-escin skinned (cell membrane permeabilized) taenia cecum and carotid artery preparations from guinea pigs. Cytochalasin D, an inhibitor of actin polymerization, significantly suppressed the force during relaxation both in skinned taenia cecum and carotid artery.
View Article and Find Full Text PDFActa Neuropathol
January 2025
Department of Clinical Sciences, Lund Brain Injury Laboratory for Neurosurgical Research, Lund University, 222 20, Lund, Sweden.
Traumatic brain injury (TBI) often leads to impaired regulation of cerebral blood flow, which may be caused by pathological changes of the vascular smooth muscle cells (VSMCs) in the arterial wall. Moreover, these cerebrovascular changes may contribute to the development of various neurodegenerative disorders such as Alzheimer's-like pathologies that include amyloid beta aggregation. Despite its importance, the pathophysiological mechanisms responsible for VSMC dysfunction after TBI have rarely been evaluated.
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