Download full-text PDF |
Source |
|---|
Publication Analysis
Top Keywords
Similar Publications
Activation of S1PR2 on macrophages and the hepatocyte S1PR2/RhoA/ROCK1/MLC2 pathway in vanishing bile duct syndrome.
PLoS One
January 2025
Department of Surgical Pathology, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Immunologic bile duct destruction is a pathogenic condition associated with vanishing bile duct syndrome (VBDS) after liver transplantation and hematopoietic stem-cell transplantation. As the bile acid receptor sphingosine 1-phosphate receptor 2 (S1PR2) plays a critical role in recruitment of bone marrow-derived monocytes/macrophages to sites of cholestatic liver injury, S1PR2 expression was examined using cultured macrophages and patient tissues. Bile canaliculi destruction precedes intrahepatic ductopenia; therefore, we focused on hepatocyte S1PR2 and the downstream RhoA/Rho kinase 1 (ROCK1) signaling pathway and bile canaliculi alterations using three-dimensional hepatocyte culture models that form obvious bile canaliculus-like networks.
View Article and Find Full Text PDFLipid-induced condensate formation from the Alzheimer's Aβ peptide triggers amyloid aggregation.
Proc Natl Acad Sci U S A
January 2025
Yusuf Hamied Department of Chemistry, Centre for Misfolding Diseases, University of Cambridge, Cambridge CB2 1EW, United Kingdom.
The onset and development of Alzheimer's disease is linked to the accumulation of pathological aggregates formed from the normally monomeric amyloid-β peptide within the central nervous system. These Aβ aggregates are increasingly successfully targeted with clinical therapies at later stages of the disease, but the fundamental molecular steps in early stage disease that trigger the initial nucleation event leading to the conversion of monomeric Aβ peptide into pathological aggregates remain unknown. Here, we show that the Aβ peptide can form biomolecular condensates on lipid bilayers both in molecular assays and in living cells.
View Article and Find Full Text PDFEstablishment of an Ex Vivo Human Corneal Endothelium Wound Model.
Transl Vis Sci Technol
January 2025
UCL Institute of Ophthalmology, University College London, London, UK.
Purpose: A human model able to simulate the manifestation of corneal endothelium decompensation could be advantageous for wound healing and future cell therapy assessment. The study aimed to establish an ex vivo human cornea endothelium wound model where endothelium function can be evaluated by measuring corneal thickness changes.
Methods: The human cornea was maintained in an artificial anterior chamber, with a continuous culture medium infusion system designed to sustain corneal endothelium and epithelium simultaneously.
rDNA Copy Number Variation and Methylation During Normal and Premature Aging.
Aging Cell
January 2025
Institute of Human Genetics, Julius Maximilians University, Würzburg, Germany.
Ribosomal RNA is the main component of the ribosome, which is essential for protein synthesis. The diploid human genome contains several hundred copies of the rDNA transcription unit (TU). Droplet digital PCR and deep bisulfite sequencing were used to determine the absolute copy number (CN) and the methylation status of individual rDNA TU in blood samples of healthy individuals.
View Article and Find Full Text PDFCongenital Titinopathy: Comprehensive Characterization of the Most Severe End of the Disease Spectrum.
Ann Neurol
January 2025
School of Biotechnology and Biomolecular Sciences, University of New South Wales, Sydney, New South Wales, Australia.
Unlabelled: Congenital titinopathy has recently emerged as one of the most common congenital muscle disorders.
Objective: To better understand the presentation and clinical needs of the under-characterized extreme end of the congenital titinopathy severity spectrum.
Methods: We comprehensively analyzed the clinical, imaging, pathology, autopsy, and genetic findings in 15 severely affected individuals from 11 families.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!