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Abca4, mutated in Stargardt Disease, is required for cone outer segment structural integrity.
Dis Model Mech
November 2024
Biology Department, University of Massachusetts, Amherst, USA.
Stargardt Disease (STGD), the leading cause of inherited childhood blindness, is primarily caused by mutations in the ABCA4 gene, yet the underlying mechanisms of photoreceptor degeneration remain elusive, partly due to limitations in existing animal disease models. To expand our understanding, we mutated the ABCA4 paralogues, abca4a and abca4b, in zebrafish, which has a cone-rich retina. Our study unveiled striking dysmorphology and elongation of cone outer segments in abca4a;abca4b double mutants, alongside reduced phagocytosis by the retinal pigmented epithelium.
View Article and Find Full Text PDFCritical role for platelet Ral GTPases in regulating venous thrombosis in mice.
J Thromb Haemost
October 2024
School of Physiology, Pharmacology & Neuroscience, University of Bristol, Bristol, United Kingdom. Electronic address:
Background: Deep vein thrombosis is a major cause of morbidity and mortality globally. While its pathophysiology is complex, increasing evidence suggests a more prominent role for platelets than previously suspected. Genetic deletion of Ral GTPases, RalA and RalB, conditionally in mouse platelets (RalAB double knockout [DKO]), results in a near complete defect in P-selectin externalization upon activation, while other platelet activation responses and arterial thrombosis are preserved.
View Article and Find Full Text PDFMicroglia Gravitate toward Amyloid Plaques Surrounded by Externalized Phosphatidylserine via TREM2.
Adv Sci (Weinh)
September 2024
Department of Biochemistry and Biomedical Sciences, College of Medicine, Seoul National University, Seoul, 03080, Republic of Korea.
Microglia play a crucial role in synaptic elimination by engulfing dystrophic neurons via triggering receptors expressed on myeloid cells 2 (TREM2). They are also involved in the clearance of beta-amyloid (Aβ) plaques in Alzheimer's disease (AD); nonetheless, the driving force behind TREM2-mediated phagocytosis of beta-amyloid (Aβ) plaques remains unknown. Here, using advanced 2D/3D/4D co-culture systems with loss-of-function mutations in TREM2 (a frameshift mutation engineered in exon 2) brain organoids/microglia/assembloids, it is identified that the clearance of Aβ via TREM2 is accelerated by externalized phosphatidylserine (ePtdSer) generated from dystrophic neurons surrounding the Aβ plaques.
View Article and Find Full Text PDFAntifungal activity of human antimicrobial peptides targeting apoptosis in .
J Med Microbiol
May 2024
Department of Clinical Microbiology and Infectious Diseases, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, 2193, South Africa.
Innovative antifungal therapies are of crucial importance to combat the potentially life-threatening infections linked to the multidrug-resistant fungal pathogen . Induction of regulated cell death, apoptosis, could provide an outline for future therapeutics. Human antimicrobial peptides (AMPs), well-known antifungal compounds, have shown the ability to induce apoptosis in pathogenic fungi.
View Article and Find Full Text PDFZAGA Double Pedicle Palatal Flap for Soft Tissue Management in Zygomatic Surgery.
Int J Periodontics Restorative Dent
February 2024
Oral rehabilitation of the atrophic maxilla using prostheses anchored on zygomatic implants is a well-documented process. To prevent the risk of sinusitis and or oro-antral communications, the placement of zygomatic implants with an externalized path has been proposed. In these cases where the sealing of the implant neck depends exclusively on a hemidesmosomal junction, there is a risk of dehiscence of the soft tissue.
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