Efficacy and safety of current means to prevent cerebrovascular thrombosis in patients at high risk of stroke are suboptimal. In theory, anchoring fibrinolytic plasminogen activators to the luminal surface of the cerebral endothelium might arrest formation of occlusive clots in this setting. We tested this approach using the recombinant construct antiplatelet-endothelial cell adhesion molecule (PECAM) single-chain variable fragment (scFv)-urokinase-type plasminogen activator (uPA), fusing low-molecular-weight single-chain urokinase-type plasminogen activator with a scFv of an antibody directed to the stably expressed endothelial surface determinant PECAM-1, implicated in inflammation and thrombosis. Studies in mice showed that scFv-uPA, but not unconjugated uPA 1) accumulates in the brain after intravascular injection, 2) lyses clots lodged in the cerebral arterial vasculature without hemorrhagic complications, 3) provides rapid and stable cerebral reperfusion, and 4) alleviates post-thrombotic brain edema. Effective and safe thromboprophylaxis in the cerebral arterial circulation by anti-PECAM scFv-uPA represents a prototype of a new paradigm to prevent recurrent cerebrovascular thrombosis.
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http://dx.doi.org/10.1124/jpet.107.120535 | DOI Listing |
Environ Toxicol
January 2025
Department of Medical Research, Chung Shan Medical University Hospital, Taichung, Taiwan.
The epithelial-mesenchymal transition (EMT) assists in the acquisition of invasiveness, relapse, and resistance in non-small cell lung cancer (NSCLC) and can be caused by the signaling of transforming growth factor-β1 (TGF-β1) through Smad-mediated or Smad-independent pathways. (-)-Epigallocatechin-3-gallate (EGCG), a multifunctional cancer-preventing bioconstituent found in tea polyphenols, has been shown to repress TGF-β1-triggered EMT in the human NSCLC A549 cell line by inhibiting the activation of Smad2 and Erk1/2 or reducing the acetylation of Smad2 and Smad3. However, its impact on the Smad-independent pathway remains unclear.
View Article and Find Full Text PDFBiotechnol J
January 2025
Cancer Hospital of Dalian University of Technology, Dalian R&D Center for Stem Cell and Tissue Engineering, Dalian University of Technology, Dalian, China.
Osteochondral damage, caused by trauma, tumors, or degenerative diseases, presents a major challenge due to the limited self-repair capacity of the tissue. Traditional treatments often result in significant trauma and unpredictable outcomes. Recent advances in bone/cartilage tissue engineering, particularly in scaffold materials and fabrication technologies, offer promising solutions for osteochondral regeneration.
View Article and Find Full Text PDFBiochem Biophys Res Commun
January 2025
Key Laboratory of Industrial Fermentation Microbiology of the Ministry of Education, College of Biotechnology, Tianjin University of Science and Technology, Tianjin, 300457, China. Electronic address:
In previous reports, we highlighted the significant involvement of SMYD3, a histone methyltransferase (HMT), in various aspects of cancer progression, including cell adhesion, migration, and invasion. In this study, we delved deeper into understanding the relationship between SMYD3 and epithelial-mesenchymal transition (EMT) both in cell lines and clinical samples. Our investigation uncovered a notable correlation between heightened SMYD3 expression and the presence of EMT markers in human breast cancer tissues.
View Article and Find Full Text PDFBMC Med Genomics
January 2025
Department of Surgery, Faculty of General of Medicine, Koya University, Koya, Kurdistan Region - F.R., KOY45, Iraq.
Background: During mammalian spermatogenesis, the cytoskeleton system plays a significant role in morphological changes. Male infertility such as non-obstructive azoospermia (NOA) might be explained by studies of the cytoskeletal system during spermatogenesis.
Methods: The cytoskeleton, scaffold, and actin-binding genes were analyzed by microarray and bioinformatics (771 spermatogenic cellsgenes and 774 Sertoli cell genes).
Sci Rep
January 2025
Department of Biomedical Engineering, University of Rochester, Rochester, NY, USA.
The aberrant vascular response associated with tendon injury results in circulating immune cell infiltration and a chronic inflammatory feedback loop leading to poor healing outcomes. Studying this dysregulated tendon repair response in human pathophysiology has been historically challenging due to the reliance on animal models. To address this, our group developed the human tendon-on-a-chip (hToC) to model cellular interactions in the injured tendon microenvironment; however, this model lacked the key element of physiological flow in the vascular compartment.
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