To determine whether von Willebrand Factor (vWF) is a valid marker of liver endothelial cells, we determined vWF immunoreactivity in rat and guinea pig liver sections and in smears of elutriated nonparenchymal cells isolated from these two species. In frozen sections, positive staining for vWF was seen only in the endothelium lining large hepatic vessels in both species, and no immunoactivity was detected in the sinusoids. On the other hand, immunohistochemical staining for vimentin (a marker of mesenchymal cells) showed positive reaction throughout the vascular and sinusoidal endothelial cells in both the rat and guinea pig liver. In fractions of elutriated rat and guinea pig nonparenchymal liver cells, which included almost exclusively liver endothelial cells, only 25-40% of the cells displayed a positive reaction for vWF. However, when these same fractions were stained for vimentin, 70-95% of the cells exhibited immunoreactivity. Most of the vWF-negative cells were not red and white blood cells, biliary epithelial and Kupffer cells, and hepatocytes, and had ultrastructural features of sinusoidal endothelial cells. We conclude that in both the rat and guinea pig, liver sinusoidal endothelial cells do not exhibit vWF immunoreactivity. Thus, in routine immunohistochemical assays, vWF is not an accurate marker of rat and guinea pig liver endothelial cells. Vimentin is more appropriate for this purpose, provided that other mesenchymal cells are separated or independently identified.
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http://dx.doi.org/10.1111/j.1600-0676.1990.tb00483.x | DOI Listing |
Comput Methods Biomech Biomed Engin
January 2025
Department of Gastroenterolgy, The Second Affiliated Hospital of Chengdu Medical College, China National Nuclear Corporation 416 Hospital, Chengdu, China.
The global rise in Crohn's Disease (CD) incidence has intensified diagnostic challenges. This study identified circadian rhythm-related biomarkers for CD using datasets from the GEO database. Differentially expressed genes underwent Weighted Gene Co-Expression Network Analysis, with 49 hub genes intersected from GeneCards data.
View Article and Find Full Text PDFReceptors for the vasoactive adipokine apelin, termed APJ receptors, are G-protein-coupled receptors and are widely expressed throughout the cardiovascular system. APJ receptors can also signal via G-protein-independent pathways, including G-protein-coupled-receptor kinase 2 (GRK2), which inhibits nitric oxide synthase (eNOS) activity and nitric oxide (NO) production in endothelial cells. Apelin causes endothelium-dependent, NO-mediated relaxation of coronary arteries from normotensive animals, but the effects of activating APJ receptor signaling pathways in hypertensive coronary arteries are largely unknown.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
January 2025
Department of Pathology, University of California San Diego, La Jolla, CA 92093.
We hypothesized that a strategy employing tissue-specific endothelial cells (EC) might facilitate the identification of tissue- or organ-specific vascular functions of ubiquitous metabolites. An unbiased approach was employed to identify water-soluble small molecules with mitogenic activity on choroidal EC. We identified adenosine diphosphate (ADP) as a candidate, following biochemical purification from mouse EL4 lymphoma extracts.
View Article and Find Full Text PDFClin Transl Med
January 2025
Vascular Research Laboratory, IIS-Fundación Jiménez Díaz, Madrid, Spain.
Background: Atherosclerosis is a chronic inflammatory disease characterized by the accumulation of lipids and leukocytes within the arterial wall. By studying the aortic transcriptome of atherosclerosis-prone apolipoprotein E (ApoE) mice, we aimed to identify novel players in the progression of atherosclerosis.
Methods: RNA-Seq analysis was performed on aortas from ApoE and wild-type mice.
Front Cell Dev Biol
January 2025
Department of Pediatrics, Key Laboratory of Birth Defects and Related Diseases of Women and Children (Ministry of Education), NHC Key Laboratory of Chronobiology, West China Second University Hospital, Sichuan University, Chengdu, Sichuan, China.
Recent advancements in the mechanistic comprehension of vascular biology have concentrated on METTL3-mediated N-methyladenosine modification of RNA, which modulates a spectrum of RNA functionalities with precision. Despite extensive investigations into the roles and mechanisms of METTL3 within vascular biology, a holistic review elucidating their interconnections remains absent. This analysis endeavors to meticulously scrutinize the involvement of METTL3 in both the physiological and pathological paradigms of vascular biology.
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