METHODS: Reverse transcription-quantitative PCR (RT-qPCR) was used to detect miR-455-5p expression in breast cancer tissues and cell lines. CCK8 and Transwell assays were conducted to assess the effects of miR-455-5p on breast cancer line proliferation, migration, and invasion. SOCS3 expression level in breast cancer tissues and cell lines was determined by qPCR and western blotting. The targeting relationship between miR-455-5p and SOCS3 was determined by dual luciferase reporter gene assay in different breast cancer cell lines. Finally, the upstream and downstream regulatory association between miR-455-5p and SOCS3 was confirmed in breast cancer cells by CCK8, western blot, and Transwell assays.
RESULTS: MiR-455-5p expression was up-regulated in breast cancer tissues; miR-455-5p regulates TNBC proliferation, migration, and invasion of TNBC. SOCS3 was the direct target of miR-455-5p and was down-regulated in breast cancer. Interference with SOCS3 reversed the inhibitory effect of the miR-455-5p inhibitor on breast cancer cells' malignant potential.
CONCLUSION: MiR-455-5p promotes breast cancer progression by targeting the SOCS3 pathway and may be a potential therapeutic target for breast cancer.
Methods: The animals were allotted into control dimethyl sulfoxide (DMSO), saline + harmaline [30 mg/kg, intraperitoneally, (i.p.)], harmaline + FTY720 (1 mg/kg, i.p, 1 h and 24 h before harmaline injection) groups (n = 10). The cerebellum and inferior olive nucleus (ION) were studied for neuronal degeneration using immunohistochemistry (IHC) and ultrastructural study by transmission electron microscopy (TEM) techniques.
Results: Harmaline caused neuronal cell loss, caspase-3 mediated apoptosis, astrocytosis and ultrastructural changes in cerebellar Purkinje cells and inferior olive neurons. FTY720 exhibited neuroprotective effects on cerebellar Purkinje cells and inferior olivary neurons.
Conclusion: These results suggest that FTY720 has potential efficacy for prevention of ET neurodegeneration and astrocytosis induced by harmaline in male rats.
Methods: Using a pilocarpine-induced epileptic mouse model, sensory-motor and visual cortical slices were prepared, and the whole-cell patch clamp technique was used to record spontaneous inhibitory post-synaptic currents (sIPSCs).
Results: The primary finding was that the mean amplitude of sIPSC from the sensory-motor cortex increased significantly in epileptic mice when the recording pipette contained MK-801 compared to control mice, whereas the mean sIPSC frequency was not significantly different, indicating that post-synaptic mechanisms are involved. However, there was no significant pre-synaptic inhibition through preNMDARs in the acute brain slices from pilocarpine-induced epileptic mice.
Conclusion: In the acute case of epilepsy, a compensatory mechanism of post-synaptic inhibition, possibly from ambient GABA, was observed through changes in the amplitude without significant changes in the frequency of sIPSC compared to control mice. The role of preNMDAR-mediated inhibition in epileptogenesis during the chronic condition or in the juvenile stage warrants further investigation.
METHODS: The harvested stem cells from adipose tissues were isolated, cultured, and then starved. The centrifugation of cell cultures medium yielded the human adipose-derived stem cells conditional medium (HADSCs-CM). Collagen secretion and fibroblast viability of human fibroblasts (Hs68) were measured in the presence of HADSCs-CM. The dermal layer, vascular endothelial growth factor (VEGF), and collagen levels were evaluated on the mice animal models between the treatments with and without HADSCs-CM.
RESULTS: Western blotting, transmission electron microscopy (TEM), and dynamic light scattering (DLS) confirmed that the functional particles in HADSCs-CM were exosomes. When Hs68 fibroblasts were treated with HADSCs-CM, both cell viability and collagen secretion increased in a dose-dependent manner. Following the post-ultraviolet A (post-UVA) exposure, the mice exposed to the HADSCs-CM have decreased dermal thickness and VEGF expression and increased collagen volume compared to the non-HADSCs-CM exposed mice (control group).
CONCLUSION: HADSCs-CM significantly alleviated signs of skin senescence, including reduced dermal thickness, decreased VEGF expression, and enhanced collagen production. Exosomes, identified in the HADSCs-CM, are the functional component of these regenerative effects. This study highlights that the exosomal nanomedicine found in HADSCs-CM could regenerate skin, boost collagen production, improve fibroblast cell viability, and contain functional exosomes.