In-vitro anticancer activity against Caco-2 cell line of colloidal nano silver synthesized using aqueous extract of Eucalyptus Camaldulensis leaves

In the current study, we investigated the anticancer potential against human colon cells (Caco-2) of colloidal nanosilver (CN–Ag) produced in Syria using bioactive compounds in the aqueous extract of Eucalyptus camaldulensis leaves (AEECL). The formation of AgNPs was confirmed by UV-visible spectroscopy analysis with surface plasmon peak at 449 nm and their average size was found to be 12, 10, 23 nm by SEM, DLS and NTA respectively. This small size has confirmed the effective role of AEECL as capping agent. Further morphological characterization was done by EDS showed the presence of metallic silver. Zeta potential value (-23 mV) indicated the repulsion among the particles and stability of the formulation nanosilver. The anticancer effect of synthesized CN–Ag against Caco-2 has been tested. The cytotoxicity assay showed a dose-dependent and a time-dependent effect of CN–Ag. The high cytotoxicity of CN–Ag at low concentration (5μ/mL) open new prospects for the development of novel therapeutic approaches against human colon cancer Caco-2

OPA1 functions in mitochondria and dysfunctions in optic nerve

OPA1 is the major gene responsible for Dominant Optic Atrophy (DOA), a blinding disease that affects specifically the retinal ganglion cells (RGCs), which function consists in connecting the neuro-retina to the brain. OPA1 encodes an intra-mitochondrial dynamin, involved in inner membrane structures and ubiquitously expressed, raising the critical question of the origin of the disease pathophysiology. Here, we review the fundamental knowledge on OPA1 functions and regulations, highlighting their involvements in mitochondrial respiration, membrane dynamic and apoptosis. In light of these functions, we then describe the remarkable RGC mitochondrial network physiology and analyse data collected from animal models expressing OPA1 mutations. If, to date RGC mitochondria does not present any peculiarity at the molecular level, they represent possible targets of numerous assaults, like light, pressure, oxidative stress and energetic impairment, which jeopardize their function and survival, as observed in OPA1 mouse models. Although fascinating fields of investigation are still to be addressed on OPA1 functions and on DOA pathophysiology, we have reached a conspicuous state of knowledge with pertinent cell and animal models, from which therapeutic trials can be initiated and deeply evaluated

Onset of Spinal Cord Astrocyte Precursor Emigration from the Ventricular Zone Involves the Zeb1 Transcription Factor

During spinal cord development, astrocyte precursors arise from neuroepithelial progenitors, delaminate from the ventricular zone, and migrate toward their final locations where they differentiate. Although the mechanisms underlying their early specification and late differentiation are being deciphered, less is known about the temporal control of their migration. Here, we show that the epithelial-mesenchymal transition regulator Zeb1 is expressed in glial precursors and report that loss of Zeb1 function specifically delays the onset of astrocyte precursor delamination from the ventricular zone, correlating with transient deregulation of the adhesion protein Cadherin-1. Consequently, astrocyte precursor invasion into the Zeb1−/− mutant white matter is delayed, and induction of their differentiation is postponed. These findings illustrate how fine regulation of adhesive properties influences the onset of neural precursor migration and further support the notion that duration of exposure of migrating astrocyte precursors to environmental cues and/or their correct positioning influence the timing of their differentiation