The distribution of desmosomes and of gap-junctions was studied by morphometric means, at the electron microscopic level, in the following lesions of the uterine cervix: metaplasia, moderate and severe dysplasia, carcinoma in situ and invasive epidermoid carcinoma. The results were compared with normal exocervical epithelium. The proportion of the cell surface occupied by gap-junctions was decreased in all lesions; gap-junctions were statistically absent from moderate dysplasia and more advanced lesions. The number of desmosomes decreased gradually from metaplasia to invasive carcinoma, with each stage forming a discrete group. This gradual loss of intercellular structures with increasing degrees of malignancy might express dedifferentiation and could be associated with increasing cellular autonomy.
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Background: Patients with arrhythmogenic cardiomyopathy (ACM) due to pathogenic variants in , the gene for the desmosomal protein plakophilin-2, are being enrolled in gene therapy trials designed to replace the defective allele via adeno-associated viral (AAV) transduction of cardiac myocytes. Evidence from experimental systems and patients indicates that ventricular myocytes in ACM have greatly reduced electrical coupling at gap junctions and reduced Na current density. In previous AAV gene therapy trials, <50% of ventricular myocytes have generally been transduced.
View Article and Find Full Text PDFGenetic Mutations in Cell Junction Proteins Associated with Brain Calcification.
Mov Disord
December 2024
Department of Neurology, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Article Synopsis
- Intracerebral calcium deposition includes primary familial brain calcification (PFBC), which leads to motor decline, speech difficulties, and cognitive issues, with limited treatment options available.* -
- Recent findings link PFBC to blood-brain barrier dysfunction, influenced by genetic variants that affect the neurovascular unit (NVU), leading to brain calcification.* -
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Latrophilin-2 Deletion in Cardiomyocyte Disrupts Cell Junction, Leading to D-CMP.
Circ Res
November 2024
Department of Molecular Medicine and Biopharmaceutical Sciences, Graduate School of Convergence Science and Technology, College of Medicine or College of Pharmacy, Seoul National University, South Korea (M.K., C.-S.L., H.S., H.J.S., H.-S.K.).
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Methods: The embryonic lethality resulting from deletion necessitates the establishment of cardiomyocyte-specific, tamoxifen-inducible knockout mice, which was achieved by crossing mice with mice having MerCreMer (tamoxifen-inducible Cre [Cyclization recombinase] recombinase) under the α-myosin heavy chain promoter.
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Department of Pharmaceutical and Pharmacological Sciences, Vrije Universiteit Brussel, Brussels, Belgium.
Cell junctions, including anchoring, occluding and communicating junctions, play an indispensable role in the structural and functional organization of multicellular tissues, including in liver. Specifically, hepatic cell junctions mediate intercellular adhesion and communication between liver cells. The establishment of the hepatic cell junction network is a prerequisite for normal liver functioning.
View Article and Find Full Text PDFAnimal Models and Molecular Pathogenesis of Arrhythmogenic Cardiomyopathy Associated with Pathogenic Variants in Intercalated Disc Genes.
Int J Mol Sci
June 2024
Department of Biology, University of Padova, Via U. Bassi 58/B, 35121 Padova, Italy.
Arrhythmogenic cardiomyopathy (ACM) is a rare genetic cardiac disease characterized by the progressive substitution of myocardium with fibro-fatty tissue. Clinically, ACM shows wide variability among patients; symptoms can include syncope and ventricular tachycardia but also sudden death, with the latter often being its sole manifestation. Approximately half of ACM patients have been found with variations in one or more genes encoding cardiac intercalated discs proteins; the most involved genes are plakophilin 2 (), desmoglein 2 (), and desmoplakin ().
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