出版社:Universita degli Studi di Modena e Reggio Emilia
摘要:LPS stimulation provokes serious cellular stress with an increase of cytoplasmic reactive oxygenspecies (ROS). We have investigated, among the different cellular defenses, amyloidogenesis ascommon physiological response to attenuate oxidative stress. Optical and electron microscopicobservations of the following LPS activated cell lines [insect (larval hemocytes, IPLB-LdFB andDrosophila Schneider’s S2 cells); mouse (NIH3T3 embryonic fibroblasts); Human (Human Umbilical Vein Endothelial Cells (HUVEC), neutrophils, and mesenchymal stem cells] reveal that, all are characterized by irregular profiles, cytoplasmic empty vacuoles or by cisternae containing fibrillar material. The compartmentalized fibrillar material shows staining properties typical of amyloid fibrils. LPS activation leads to ROS generation, resulting in pH acidification. Stimulated cells show pink cytoplasm in May-Grünwald Giemsa differential staining, giving a gross indication of a lower intracellular pH. Moreover the activation of amyloidogenesis is also linked with an extensive production of ACTH and α-MSH in all cultured cell types. We suggest that amyloidogenesis is a common, physiological cellular response to weak ROS, starting when other anti-stress cellular systems failed to restore homeostasis. The morphological evidence and/or functional characterization of synthesized amyloid fibrils could be an early indicator of oxidative stress that may lead to a general inflammatory process.