The purpose of this study was to evaluate transforming growth factor beta (TGFβ) isoform localization in rabbit corneas with spontaneous persistent epithelial defects (PEDs) after photorefractive keratectomy (PRK). Four cryofixed corneas from a previously reported series of PEDs in rabbits that had PRK were evaluated with triplex immunohistochemistry (IHC) for TGFβ3, myofibroblast marker alpha-smooth muscle actin (α-SMA) and mesenchymal marker vimentin. One cornea had sufficient remaining tissue for triplex IHC for TGFβ1, TGFβ2, or TGFβ3 (each with α-SMA and vimentin) using isoform-specific antibodies. All three TGFβ isoforms were detected in the subepithelial stroma at and surrounding the PED. Some of each TGFβ isoform co-localized with α-SMA of myofibroblasts, which could be TGFβ isoform autocrine production by myofibroblasts or TGFβ-1, -2, and -3 binding to these myofibroblasts.
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http://dx.doi.org/10.1016/j.exer.2024.109794 | DOI Listing |
Fish Physiol Biochem
January 2025
Institute of Agrifood Research and Technology (IRTA), Centre de La Ràpita, Crta. Poble Nou del Delta Km 5.5, 43540, la Ràpita, Spain.
The effect of different feeding habits on gut morphology and digestive function has been intensively studied during the last decades but sympatric closely related fishes are relatively rare objects of such studies. In the present study, we have identified both morphological and physiological changes in the digestive system of a sympatric pair of whitefish represented by "normal" Coregonus lavaretus pidschian (benthivorous) and "dwarf" C. l.
View Article and Find Full Text PDFCell Death Dis
January 2025
In vitro Toxicology and Biomedicine, Dept. inaugurated by the Doerenkamp-Zbinden foundation, University of Konstanz, 78457, Konstanz, Germany.
Neurite degeneration (ND) precedes cell death in many neurodegenerative diseases. However, it remains unclear how this compartmentalized cell death process is orchestrated in the central nervous system (CNS). The establishment of a CNS axotomy model (using modified 3D LUHMES cultures) allowed us to study metabolic control of ND in human midbrain-derived neurons without the use of toxicants or other direct disturbance of cellular metabolism.
View Article and Find Full Text PDFNeuromuscul Disord
January 2025
John Walton Muscular Dystrophy Research Centre, Newcastle University, Newcastle upon Tyne, UK; Newcastle Hospitals NHS Foundation Trusts, Newcastle upon Tyne, UK. Electronic address:
Cardiomyopathy is a common co-morbidity in individuals with Duchenne muscular dystrophy (DMD). This retrospective single centre study investigated the relationship between age at loss of ambulation (LOA) and late stage left ventricular ejection fraction (LVEF) in 84 individuals (> 16 years old) with DMD taking glucocorticoid and ACE inhibitors treatment. Regression analyses showed a positive correlation between later age at LOA and higher LVEF in adulthood (linear regression estimate 1.
View Article and Find Full Text PDFEur J Med Chem
December 2024
SynBioC Research Group, Department of Green Chemistry and Technology, Faculty of Bioscience Engineering, Ghent University, Ghent, Belgium; Cancer Research Institute Ghent (CRIG), Ghent, Belgium. Electronic address:
Histone deacetylase 6 (HDAC6) is a promising target for treating neurodegenerative disorders, several cancer types and viral infections. Unique among HDACs, the HDAC6 isoform possesses a zinc finger ubiquitin-binding domain (UBD) crucial for managing misfolded protein aggregates and facilitating viral infection. HDAC6 binds aggregated polyubiquitinated proteins through its UBD, mediating their transport to the aggresome and subsequent removal via autophagy.
View Article and Find Full Text PDFBiomed Pharmacother
January 2025
Jiangsu Key Laboratory for High Technology Research of TCM Formulae, Nanjing University of Chinese Medicine, 138 Xianlin Rd., Nanjing 210023, China; Jiangsu Collaborative Innovation Center of Chinese Medicinal Resources Industrialization, Nanjing University of Chinese Medicine, 138 Xianlin Rd., Nanjing 210023, China. Electronic address:
Neuroinflammation mediated by microglia is considered the primary cause and pathological process of anxiety. Abnormal glycolysis of microglia is observed during microglia activation. However, whether regulating the Warburg effect in microglia can effectively intervene anxiety and its potential mechanisms have not been elucidated.
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