Anti-CCL2 (aa 24-99) polyclonal antibody

Extremely low-frequency electromagnetic fields (ELF-EMFs) (1-300 Hz) have been found to have practical applications in biological research. A case in point is the effect of ELF-EMF on the regulation of cell fate. In this study, we investigated the correlation between ELF-EMF stimulation of PPAR gamma to the stemness, tumorigenicity, and invasiveness of breast cancer stem cellsin vitro.The CD44(+)/CD24(-) subpopulation of the breast CSCs was isolated from the MDA-MB-231 breast cancer cell line. The CSCs were then exposed to ELF-EMF and further assays were carried out. ELF-EMF increased the expression of PPAR gamma and other critical proteins leading to cell cycle arrest and reduced stemness as evidenced by decreased expression of stemness genes and reduced proliferation rate in ELF-EMF-exposed CSCs compared to that in nonexposed CSCs. There was a decrease in the tumor-forming and invasion ability of CSCs that were exposed to ELF-EMFs.

In the CNS, chemokines and chemokine receptors are involved in pleiotropic physiological and pathological activities. Several evidences demonstrated that chemokine signaling in the CNS plays key homeostatic roles and, being expressed on neurons, glia and endothelial cells, chemokines mediate the bidirectional cross-talk among parenchymal cells. An efficient communication between neurons and glia is crucial to establish and maintain a healthy brain environment which ensures normal functionality. Glial cells behave as active sensors of environmental changes induced by neuronal activity or detrimental insults, supporting and exerting neuroprotective activities. In this review we summarize the evidence that chemokines (CXCL12, CX3CL1, CXCL16 and CCL2) modulate neuroprotective processes upon different noxious stimuli and participate to orchestrate neurons-microglia-astrocytes action to preserve and limit brain damage. This article is part of a Special Issue entitled: Honoring Ricardo Miledi - outstanding neuroscientist of XX-XXI centuries. (c) 2019 IBRO. Published by Elsevier Ltd. All rights reserved.