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Recently, photothermal therapy (PTT) has been proved to have great potential in tumor therapy. In the last several years, MoS2, as one novel member of nanomaterials, has been applied into PTT due to its excellent photothermal conversion efficacy. In this work, we applied fluorescence lifetime imaging microscopy (FLIM) techniques into monitoring the PPT-triggered cell death under MoS2 nanosheet treatment. Two types of MoS2 nanosheets (single layer nanosheets and few layer nanosheets) were obtained, both of which exhibited presentable photothermal conversion efficacy, leading to high cell death rates of 4T1 cells (mouse breast cancer cells) under PTT. Next, live cell images of 4T1 cells were obtained via directly labeling the mitochondria with Rodamine123, which were then continuously observed with FLIM technique. FLIM data showed that the fluorescence lifetimes of mitochondria targeting dye in cells treated with each type of MoS2 nanosheets significantly increased during PTT treatment. By contrast, the fluorescence lifetime of the same dye in control cells (without nanomaterials) remained constant after laser irradiation. These findings suggest that FLIM can be of great value in monitoring cell death process during PTT of cancer cells, which could provide dynamic data of the cellular microenvironment at single cell level in multiple biomedical applications. [ABSTRACT FROM AUTHOR]

Aims: Lupus nephritis is a frequent and serious complication of systemic lupus erythematosus (SLE). Therefore, better understanding regarding the underlying mechanism of renal tubular injury induced by SLE, is beneficial to develop different therapeutic strategies for lupus nephritis. The study aimed to investigate the role of miR-130a against lipopolysaccharide-induced glomerular cell injury., Methods: HK-2 cells (human renal proximal tubule cells) were used for detecting miR-130a levels. Cells were divided into scramble, miR-130 mimic, siNC, si-miR-130a and si-Klotho groups apoptosis and CCK-8 assays were performed to investigate the cell apoptosis and proliferation rates. qRT-PCR, ELISA, and western blotting were performed to detect the proteins and their expressions., Results: LPS induced inflammatory injury in HK-2 cells by inducing cell apoptosis (P < 0.01) and by expressing the inflammatory factors such as IL-1β, IL-6, IL-8 and TNF-α in HK-2 cells. LPS increased the expression of miR-130a compared to control group of cells (P < 0.01). miR-130a was highly expressed in HK-2 cells (P < 0.001). Overexpression of miR-130a reversed LPS-induced apoptosis (P < 0.05), increased expression of inflammatory mediators and decreased cell viability (P < 0.05), and miR-130a knockdown in HK-2 cells revealed to just the opposite effects upon treatment with LPS. Western blotting results showed that overexpression of miR-130a promoted the expression of Klotho and activated the PI3K/AKT pathway but inhibited Wnt and NF-κB pathways., Conclusions: These findings demonstrated that miR-130a promoted PI3K/AKT pathway but inhibited Wnt and NF-κB pathways through upregulation of Klotho. Furthermore, miR-130a protects against lipopolysaccharide-induced glomerular cell injury by upregulating Klotho expression.