Stroke outcome is determined by delayed neuronal cell death and edema formation. TWEAK, a cytokine of the TNF superfamily, and its membrane receptor Fn14 promote ischemia-induced neuronal apoptosis and leakage of the blood-brain barrier. Both TWEAK and Fn14 are upregulated in experimental stroke models. In this study, we investigated whether TWEAK and Fn14 are upregulated in stroke patients. We measured serum concentrations of TWEAK in stroke patients and matched control subjects by ELISA. Expression of Fn14 in the brain was evaluated by real-time RT-PCR and immunohistochemistry. TWEAK serum concentrations were elevated in stroke patients. In autopsy samples, we found elevated mRNA levels of the receptor Fn14 and a trend towards higher TWEAK mRNA levels. In the infarcted and peri-infarct tissue immunostaining for Fn14 was enhanced. These data show that the cytokine TWEAK and its membrane receptor Fn14 are upregulated in stroke and suggest that they contribute to stroke outcome.
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http://dx.doi.org/10.1016/j.jns.2008.08.005 | DOI Listing |
Clin Exp Rheumatol
December 2024
Department of Dermatology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Objectives: Systemic sclerosis (SSc), a chronic autoimmune disorder, characterised by local inflammation and progressive fibrosis. Tumour necrosis factor-like weak inducer of apoptosis (TWEAK) has been established as a key mediator in fibrotic processes across multiple organs, primarily through binding to its receptor, fibroblast growth factor-inducible 14 (Fn14). However, the precise role of the TWEAK/Fn14 signalling in SSc pathogenesis remains unclear.
View Article and Find Full Text PDFJCI Insight
December 2024
Division of Rheumatology, Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, United States of America.
In systemic lupus erythematosus (lupus), environmental effects acting within a permissive genetic background lead to autoimmune dysregulation. Dysfunction of CD4+ T cells contributes to pathology by providing help to autoreactive B and T cells, and CD4+ T cell dysfunction coincides with altered DNA methylation and histone modifications of select gene loci. However, chromatin accessibility states of distinct T cell subsets and mechanisms driving heterogeneous chromatin states across patients remain poorly understood.
View Article and Find Full Text PDFRev Gastroenterol Peru
November 2024
Department of Biochemistry, Faculty of Medicine, University of Cartagena, Cartagena de Indias, Colombia.
Background: One of the pathways involved in liver regeneration processes is TWEAK/Fn14 (tumor necrosis factor-related weak inducer of apoptosis/fibroblast growth factor-inducible 14), which has been proposed to act directly and selectively on hepatic progenitor cells; however, its role in the regeneration of steatotic liver metabolic dysfunction associated fatty liver disease has not been fully elucidated.
Objective: To evaluate the behavior of Fn14 and its ligand TWEAK, as well as cellular stress signals as biochemical cues for possible liver regeneration in MAFLD.
Materials And Methods: A prospective study was carried out where the behavior of Fn14 and its ligand TWEAK, as well as cellular stress signals were observed as biochemical indications of a possible liver regeneration in a condition of tissue damage caused by excessive lipid accumulation.
Int Immunopharmacol
December 2024
Organ Transplantation Centre, Tianjin First Central Hospital, Tianjin 300192, China. Electronic address:
Hepatic ischemia-reperfusion injury (IRI) represents a formidable complication commonly linked with hemorrhagic shock, liver resection, and transplantation. This study aims to elucidate the role of Tumor Necrosis Factor-like Weak Inducer of Apoptosis (TWEAK) in the pathogenesis of hepatic I/R injury and to delineate the underlying mechanisms involved. Utilizing a hypoxia-reoxygenation model in human liver organoids (HLOs) alongside a murine model of warm ischemia-reperfusion injury, we systematically investigated the interplay between TWEAK, its receptor Fn14, and the HIPPO signaling pathway.
View Article and Find Full Text PDFCNS Neurol Disord Drug Targets
October 2024
Chitkara College of Pharmacy, Chitkara University, Punjab, 140401, India.
Autism Spectrum Disorder (ASD) is a neurodevelopmental disorder with a complex, multiple etiology that is marked by impaired social interaction, communication, and repetitive behaviour. There is presently no pharmaceutical treatment for the core symptoms of ASD, even though the prevalence of ASD is increasing worldwide. Treatment of autism spectrum disorder involves the interaction of numerous signalling pathways, such as the Wnt/beta-catenin pathway, probiotics and kynurenine pathway, PPAR pathway, PI3K-AKT-mTOR pathway, Hedgehog signaling pathway, etc.
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