Unlabelled: The aim of the present study was to investigate stage-specific changes in medial edge epithelium during in vivo fusion of embryonic palatal shelves in 25 Russian rabbits.
Material And Methods: The embryos were dissected following Caesarian section at day 18. Palatal shelves of specific developmental steps (approximation, contact, fusion) were examined by light microscopy, immunohistochemistry and transmission electron microscopy.
Results: Light microscopy revealed that the superfical peridermal cells underwent apoptosis prior to contact of the basal epithelial cells. Following contact, an epithelial monolayer was left on each shelf with an intact basement membrane. Apoptosis of the epithelial cells was followed by discontinuity of the basement membrane. Islands of epithelial cells remained.
Conclusion: This paper presents new data on palatal development in vivo. The results support our theory that apoptotic medial edge epithelial cell death is a precondition for palatal fusion. There were no indications of epithelial mesenchymal transformation or migration.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1054/jcms.2002.0323 | DOI Listing |
Sci Adv
January 2025
College of Chemistry, Fuzhou University, Fuzhou 350116, China.
The angiopoietin (Ang)-Tie axis, critical for endothelial cell function and vascular development, is a promising therapeutic target for treating vascular disorders and inflammatory conditions like sepsis. This study aimed to enhance the binding affinity of recombinant Ang1 variants to the Tie2 and explore their therapeutic potential. Structural insights from the Ang1-Tie2 complex enabled the identification of key residues within the Ang1 receptor binding domain (RBD) critical for Tie2 interaction.
View Article and Find Full Text PDFSci Transl Med
January 2025
Department of Medicine 1, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU) and Universitätsklinikum Erlangen, 91052 Erlangen, Germany.
Dysregulation at the intestinal epithelial barrier is a driver of inflammatory bowel disease (IBD). However, the molecular mechanisms of barrier failure are not well understood. Here, we demonstrate dysregulated mitochondrial fusion in intestinal epithelial cells (IECs) of patients with IBD and show that impaired fusion is sufficient to drive chronic intestinal inflammation.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
January 2025
Key Laboratory of Breeding Biotechnology and Sustainable Aquaculture, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan 430070, People's Republic of China.
Interferon regulatory factor 3 (IRF3) is the key transcription factor in the type I IFN signaling pathway, whose activation is regulated by multiple posttranslational modifications. Here, we identify SMYD3, a lysine methyltransferase, as a negative regulator of IRF3. SMYD3 interacts with IRF3 and catalyzes the dimethylation of IRF3 at lysine 39.
View Article and Find Full Text PDFPLoS One
January 2025
Department of Pharmaceutics, College of Pharmacy, King Khalid University, Abha, Saudi Arabia.
Multidrug resistant bacteria are causing health problems and economic burden worldwide; alternative treatment options such as natural products and nanoparticles have attained great attention recently. Therefore, we aimed to determine the phytochemicals, antibacterial potential, and anticancer activity of W. unigemmata.
View Article and Find Full Text PDFMol Biol Cell
January 2025
Department of Biology, The Catholic University of America, Washington, DC, 20064.
MAL2 (myelin and lymphocyte protein 2) and rab17 have been identified as hepatocellular carcinoma tumor suppressors. However, little is known how their functions in hepatic polarized protein sorting/trafficking translates into how they function in the epithelial to mesenchymal transition and/or the mesenchymal to epithelial transition in metastases. To investigate this, we expressed MAL2 and rab17 alone or together in hepatoma-derived Clone 9 cells (that lack endogenous MAL2 and rab17).
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!