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Tissue nanotransfection-based endothelial PLCγ2-targeted epigenetic gene editing in vivo rescues perfusion and diabetic ischemic wound healing.
Mol Ther
January 2025
Department of Surgery, McGowan Institute for Regenerative Medicine, University of Pittsburgh, Pittsburgh, PA 15219, United States; Department of Surgery, Indiana Center for Regenerative Medicine and Engineering, Indiana University School of Medicine, Indianapolis, IN 46202, United States. Electronic address:
Diabetic wounds are complicated by underlying peripheral vasculopathy. Reliance on vascular endothelial growth factor (VEGF) therapy to improve perfusion makes logical sense, yet clinical study outcomes on rescuing diabetic wound vascularization have yielded disappointing results. Our previous work has identified that low endothelial phospholipase Cγ2 (PLCγ2) expression hinders the therapeutic effect of VEGF on the diabetic ischemic limb.
View Article and Find Full Text PDFNeutrophil-to-lymphocyte ratio and short-term mortality in patients having anti-MDA5-positive dermatomyositis with interstitial lung disease: a retrospective study.
BMC Pulm Med
January 2025
Department of Key Laboratory of Ningxia Stem Cell and Regenerative Medicine, Institute of Medical Sciences, Department of Pulmonary and Critical Care Medicine, General Hospital of Ningxia Medical University, Yinchuan, Ningxia, 750004, China.
Background: In this study, we aimed to explore the association between baseline and early changes in the neutrophil-to-lymphocyte ratio (NLR) and the 30-day mortality rate in patients having anti-melanoma differentiation-associated gene 5 (MDA5)-positive dermatomyositis with interstitial lung disease (DM-ILD).
Methods: Overall, 263 patients with anti-MDA5 DM-ILD from four centers in China were analyzed. Multivariate logistic regression analysis was used to evaluate the impact of baseline NLR on the 30-day mortality rate in patients with anti-MDA5-positive DM-ILD.
Differentiation of stem cells into chondrocytes and their potential clinical application in cartilage regeneration.
Histochem Cell Biol
January 2025
Department of Forensic Medicine and Forensic Toxicology, Medical University of Silesia, 18 Medyków Street, 40-752, Katowice, Poland.
Cartilage diseases and injuries are considered difficult to treat owing to the low regenerative capacity of this tissue. Using stem cells (SCs) is one of the potential methods of treating cartilage defects and creating functional cartilage models for transplants. Their ability to proliferate and to generate functional chondrocytes, a natural tissue environment, and extracellular cartilage matrix, makes SCs a new opportunity for patients with articular injuries or incurable diseases, such as osteoarthritis (OA).
View Article and Find Full Text PDFDevelopment and characterization of in vitro inducible immortalization of a murine microglia cell line for high throughput studies.
Sci Rep
January 2025
Department of Pharmacology and Experimental Therapeutics, Boston University School of Medicine, Boston, United States.
There are few in vitro models available to study microglial physiology in a homeostatic context. Recent approaches include the human induced pluripotent stem cell model, but these can be challenging for large-scale assays and may lead to batch variability. To advance our understanding of microglial biology while enabling scalability for high-throughput assays, we developed an inducible immortalized murine microglial cell line using a tetracycline expression system.
View Article and Find Full Text PDFMAPK4 inhibits the early aberrant activation of B cells in rheumatoid arthritis by promoting the IRF4-SHIP1 signaling pathway.
Cell Death Dis
January 2025
Department of Pediatrics, Affiliated Hospital of Zunyi Medical University, Zunyi, China.
The involvement of B lymphocytes in the pathogenesis of rheumatoid arthritis (RA) is well-established, with their early and aberrant activation being a crucial factor. However, the mechanisms underlying this abnormal activation in RA remain incompletely understood. In this study, we identified a significant reduction in MAPK4 expression in both RA patients and collagen-induced arthritis (CIA) mouse models, which correlates with disrupted B cell activation.
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