Project description:We performed RNA sequencing (RNA-seq) of granulocyte-macrophage colony-stimulating factor (GM-CSF) cultured bone marrow cells (GM-BMCs) treated with hydroxychloroquine (HCQ) or cyclic guanosine monophosphate–adenosine monophosphate (cGAMP) to compare the gene expression profiles between HCQ and cGAMP treatments in GM-BMCs.
Project description:We performed single-cell RNA sequencing (scRNA-seq) of lung cells from hydroxychloroquine (HCQ)-treated mice to examine HCQ-induced IFN-I response in the lung.
Project description:We performed single-cell RNA sequencing (scRNA-seq) of granulocyte-macrophage colony-stimulating factor (GM-CSF) cultured bone marrow cells (GM-BMCs) treated with hydroxychloroquine (HCQ) or cyclic guanosine monophosphate–adenosine monophosphate (cGAMP) to reveal a divergence of the gene expression pattern in interferon β (IFNβ)-expressing cells between HCQ and cGAMP treatments.
Project description:Objectives: Natural Killer (NK) cell dysfunction contributes to systemic lupus erythematosus (SLE) pathogenesis, but its underlying mechanisms remain poorly understood. This study investigates immunometabolic alterations in NK cells from SLE patients and explores therapeutic strategies for their restoration. Methods: We characterized mitochondrial structure and function in NK cells from the peripheral blood of SLE patients and healthy controls using flow cytometry, electron microscopy, and proteomics. Key mitophagy-related gene expressions were quantified using qPCR. The therapeutic effects of hydroxychloroquine (HCQ) on mitochondrial recycling and NK cell function were assessed in vitro. Results: SLE NK cells were characterized by an accumulation of enlarged, hyperpolarized mitochondria with cristae disorganization, and reduced mitophagy. Impaired lysosomal acidification and mtDNA extrusion into the cytosol were also observed. Treatment with hydroxychloroquine restored lysosomal pH, mitochondrial recycling, and NK cell effector functions, including cytokine production and cytotoxicity. Conclusions: This study identifies mitochondrial recycling dysfunction as a driver of NK cell abnormalities in SLE and highlights the potential of HCQ to restore NK cell functionality. These findings provide new insights into the immunometabolic mechanisms underlying SLE and suggest avenues for targeted therapeutic interventions.
Project description:Several Human PDA Cell Lines (ASPC1, PANC1, KP4, HPAFII, PATU8988S, PK45H, S2013, CAPAN1, BXPC3, HPAC, SW1990, MIAPACA2) were cultured and treated with DMSO, Trametinib (TRAM), Hydroxychloroquine (HCQ) and the combination of them before being prepared for Single-Cell RNA Sequencing