In a subtractive differential screening, we identified a novel gene with interesting characteristics, termed Xenopus wounding induced gene 1 (Xwig1). Xwig1 encodes a novel protein of 912 amino acids containing 13 putative transmembrane segments and an evolutionarily conserved carboxy-terminal domain. Protein localization studies revealed that Xwig1 is anchored in cytoplasmic structures, presumably the endoplasmic reticulum. Expression is largely confined to epithelial cells in regions that undergo morphogenetic processes, such as blastopore closure, hindgut closure, dorsal closure and optic vesicle invagination. Interestingly, Xwig1 transcription is activated in response to embryonic epidermal wounding. The wounding-induced transcription occurs downstream of the transient phosphorylation of extracellular signal-regulated protein kinases and is in part mediated by Elk-1, but independent of dissection-induced FGF signalling. Thus, Xwig1 provides a molecular link between epithelial morphogenesis and wound healing.
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Kidney Int
February 2025
Department of Nephrology, Graduate School of Medicine, Kyoto University, Kyoto, Japan; Institute for the Advanced Study of Human Biology, Kyoto University, Kyoto, Japan. Electronic address:
Previous reports have suggested that both the endoplasmic reticulum (ER) stress and cyclic guanosine monophosphate-adenosine monophosphate synthase-stimulator of interferon genes pathways contribute to the progression of chronic kidney disease; however, the relationship between these 2 pathways in kidney injury has not been fully elucidated. Andrade-Silva et al. revealed that the cyclic guanosine monophosphate-adenosine monophosphate synthase-stimulator of interferon genes pathway can enhance ER stress through the protein kinase R-like ER kinase (PERK)-mediated signaling cascade in kidney tubular epithelial cells and sequentially augment fibrosis during kidney injury.
View Article and Find Full Text PDFProg Neuropsychopharmacol Biol Psychiatry
January 2025
Department of Pharmacology and Toxicology, Faculty of Pharmacy, Ain Shams University, Cairo 11566, Egypt. Electronic address:
Chemotherapy-induced cognitive impairment, referred to as "chemobrain", is widely acknowledged as a significant adverse effect of cancer therapy. Paclitaxel, a chemotherapeutic drug, has been reported to cause cognitive impairment clinically and in animal models. However, the precise mechanisms are not fully understood.
View Article and Find Full Text PDFFree Radic Biol Med
January 2025
Institute of Systems Biomedicine, School of Basic Medical Sciences, Department of Pathology, Beijing Key Laboratory of Tumor Systems Biology, Peking University Health Science Center, Beijing 100191, China. Electronic address:
Cuproptosis, a copper-dependent form of regulated cell death, has been implicated in the progression and treatment of various tumors. The copper ionophores, such as Disulfiram (DSF), an FDA-approved drug previously used to treat alcohol dependence, have been found to induce cuproptosis. However, the limited solubility and effectiveness of the combination of DSF and copper ion restrict its widespread application.
View Article and Find Full Text PDFJ Psychiatr Res
January 2025
Laboratory of Molecular Psychiatry. Rua Ramiro Barcelos, Centro de Pesquisa Experimental - Hospital de Clínicas de Porto Alegre (HCPA), Federal University of Rio Grande do Sul (UFRGS), Porto Alegre, 2350, Brazil; Postgraduate Program of Psychiatry and Behavioral Sciences. Rua Ramiro Barcelos, Department of Psychiatry, Federal University of Rio Grande do Sul (UFRGS), Porto Alegre, Rio Grande do Sul, 2400, Brazil.
Major depressive disorder (MDD) is a highly prevalent and debilitating disorder, yet its pathophysiology has not been fully elucidated. The aim of this study is to identify novel potential proteins and biological processes associated with MDD through a systems biology approach. Original articles involving the measurement of proteins in the blood of patients diagnosed with MDD were selected.
View Article and Find Full Text PDFJ Mol Cell Cardiol
January 2025
Department of Cardiology, Harbin Medical University Cancer Hospital, NHC Key Laboratory of Cell Transplantation, Department of Cardiology, Central Laboratory, The First Affiliated Hospital of Harbin Medical University, Institute of Metabolic Disease, Heilongjiang Academy of Medical Sciences, Heilongjiang Key Laboratory for Metabolic Disorder & Cancer Related Cardiovascular Diseases, Key Laboratories of Education Ministry for Myocardial Ischemia Mechanism and Treatment, State Key Laboratory of Frigid Zone Cardiovascular Diseases (SKLFZCD), Harbin, China. Electronic address:
Unlabelled: Treatment of cancer patients with tyrosine kinase inhibitors (TKIs) often results in hypertension, but the underlying mechanism remains unclear. This study aimed to examine the role of mitochondrial morphology and function, particularly mitochondria-associated endoplasmic reticulum membranes (MAMs), in sunitinib-induced hypertension.
Methods: Both in vitro and in vivo experiments performed to assesse reactive oxygen species (ROS), nitric oxide (NO), endothelium-dependent vasorelaxation, systemic blood pressure, and mitochondrial function in human umbilical vein endothelial cells (HUVECs) and C57BL/6 mouse aortic endothelial cells, under vehicle or sunitinib treatment condition.
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