Ji-Woo Lim

Neuroinflammation, a significant contributor to various neurodegenerative diseases, is strongly associated with the aging process; however, to date, no efficacious treatments for neuroinflammation have been developed. In aged mouse brains, the number of infiltrating immune cells increases, and the key transcription factor associated with increased chemokine levels is nuclear factor kappa B (NF-κB). Exosomes are potent therapeutics or drug delivery vehicles for various materials, including protei

Aging is a major risk factor for common neurodegenerative diseases. Although multiple molecular, cellular, structural, and functional changes occur in the brain during aging, the involvement of caveolin-2 (Cav-2) in brain ageing remains unknown. We investigated Cav-2 expression in brains of aged mice and its effects on endothelial cells. The human umbilical vein endothelial cells (HUVECs) showed decreased THP-1 adhesion and infiltration when treated with Cav-2 siRNA compared to control siRNA. In

BACKGROUND/AIMS: CD4+ T cells are a critical component of the adaptive immune response. While the mechanisms controlling the differentiation of the Th1, Th17, and regulatory T cell subsets from naïve CD4+ T cells are well described, the factors that induce Th2 differentiation are still largely unknown. METHODS: The effects of treatment with exogenous H2O2 on STAT-6 phosphorylation and activation in T cells were examined by immunoblotting, immunofluorescence and gel shift assay. Anti-CD3 antibody

BACKGROUND: Brain metastasis occurs in 40-50% of lung cancer patients and is associated with poor prognosis. This study aimed to identify potential exosomal biomarkers for the early detection of brain metastasis in lung cancer using a comprehensive multi-omics approach. METHODS: Using a lung cancer mouse model, which develops brain metastasis, we collected serum samples at different stages (control, 6 weeks for lung cancer, and 10 weeks for brain metastasis). We profiled the contents of serum-de

) gene, through alternative splicing of its C-terminal region, generates several PML isoforms that interact with specific partners and perform distinct functions. The PML protein is a tumor suppressor that plays an important role by interacting with various proteins. Herein, we investigated the effect of the PML isoforms on oncostatin M (OSM)-induced signal transducer and activator of transcription-3 (STAT-3) transcriptional activity. PML influenced OSM-induced STAT-3 activity in a cell type-spe

Intraventricular hemorrhage (IVH) is a cause of morbidity and mortality in preterm infants and is strongly associated with adverse neurological outcomes. The incidence of severe IVH (grade 3 or 4) has persisted despite the overall decline in IVH. IVH has been attributed to changes in cerebral blood flow to the immature germinal matrix microvasculature. The cascade of adverse events following IVH includes inflammation, white matter injury, and delayed oligodendrial maturation. In this study, we a

Abstract Glioblastoma multiform (GBM), a grade IV astrocytoma, is most lethal and common adult primary intracranial tumor. GBM is characterized by diffuse infiltration into normal brain parenchyma, rapid growth and the presence of necrosis and microglia/macrophage infiltration. Among these properties of GBM, necrosis has been implicated to be a strong predictor of poor prognosis; however, the effect of necrosis on GBM progression is poorly understood at present. In this study, we examined the ef

Necrosis is a characteristic feature of glioblastoma multiforme (GBM) and is closely associated with tumor-associated inflammation and poor clinical outcomes. However, the molecular consequences of necrotic cell death on endoplasmic reticulum (ER) stress signaling in GBM cells remain unclear. In this study, we examined the effects of necrotic cells on the ER stress signaling and unfolded protein response (UPR) in human glioblastoma cell lines. Exposure to necrotic cells reduced IRE1α phosphoryla