Hematological abnormalities and altered vascular permeability are frequently encountered in Dengue virus infected patients, but the mechanisms that alter platelet-endothelium interactions remain incompletely understood. The DENV NS1 protein has been implicated in adverse disease outcomes. In the present study the role of NS1 protein in affecting the expression of vWF and platelet adhesion properties of endothelial cells was studied in vitro. The results suggest that vWF is down regulated in cultured endothelial cells 6 and 24 h after exposure with increase in vWF levels in culture supernatants at corresponding time points. Ultrastructural studies showed distinct evidence of endothelial cell activation morphology and degranulation of Weibel-Palade bodies in NS1 exposed cells that also showed increased platelet activation physiology. The findings suggest that changes in vWF production and secretion may be induced in endothelial cells exposed to DENV NS1 protein; and play a role in bleeding complications of severe DENV disease.
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http://dx.doi.org/10.1007/s12288-018-1058-2 | DOI Listing |
J Immunol
February 2025
Herman B Wells Center for Pediatric Research, Department of Pediatrics, Indiana University School of Medicine, Indianapolis, IN, United States.
Food allergy has had a rapid rise in prevalence, and thus it is important to identify approaches to limit the development of food allergy early in life. Because maternal dietary supplementation with α-tocopherol (α-T), an isoform of vitamin E, during pregnancy and nursing increases neonate plasma levels of α-T and can limit neonate development of other allergies, we hypothesized that α-T can limit development of food allergy. To assess this, male mice with mutations in their skin barrier genes (FT-/- mice) were mated with wild-type females that received a diet supplemented with α-tocopherol or a control diet.
View Article and Find Full Text PDFACS Nano
March 2025
Department of Ophthalmology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, No. 100 Haining Road, Shanghai 200080, China.
Small interfering RNA (siRNA) has garnered tremendous interest as a potential therapeutic tool because of its intriguing gene-silencing ability. Toward the success in the manufacture of siRNA therapeutics for the potential treatment of choroidal neovascularization (CNV), siRNA conjugated with dual functional units of membrane-penetrating heptafluoropropyl and age-related macular degeneration-targeting cyclic Arg-Gly-Asp (RGD) peptide was attempted for transcellular transportation into the cell interiors. Of note, cyclic RGD allowed selective affinities toward the angiogenic endothelial cells in the pathological CNV.
View Article and Find Full Text PDFDiabetologia
March 2025
Department of Ophthalmology, Eye & ENT Hospital of Fudan University, Shanghai, China.
Aims/hypothesis: Signalling pathways that regulate endothelial cell (EC) dysfunction, ischaemia and inflammation play a crucial role in retinal microangiopathy such as diabetic retinopathy. MAP4K4 is highly expressed in ECs. However, the involvement of MAP4K4 in retinal vasculopathy of diabetic retinopathy remains unclear.
View Article and Find Full Text PDFCells
March 2025
Renal Division, Department of Medicine IV, Ludwig-Maximilians-University (LMU) Hospital, Ludwig-Maximilians-University (LMU), 80336 Munich, Germany.
A20/Tnfaip3, an early NF-κB response gene and key negative regulator of NF-κB signaling, suppresses proinflammatory responses. Its ubiquitinase and deubiquitinase activities mediate proteasomal degradation within the NF-κB pathway. This study investigated the involvement of A20 signaling alterations in podocytes in the development of kidney injury.
View Article and Find Full Text PDFCells
March 2025
School of Cardiovascular and Metabolic Medicine & Sciences, British Heart Foundation Centre of Research Excellence, Faculty of Life Sciences & Medicine, King's College London, London SE5 9NU, UK.
Endothelial dysfunction is the main initiating factor in atherosclerosis. Through mechanotransduction, shear stress regulates endothelial cell function in both homeostatic and diseased states. Accumulating evidence reveals that epigenetic changes play critical roles in the etiology of cardiovascular diseases, including atherosclerosis.
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