Inflammatory stimuli prompt autophagic events in cortical astrocytes.

An impaired inflammatory response represents the initial starting point for many neurodegenerative diseases. For their capability of releasing and being target as well of pro-inflammatory molecules and growth factors, astrocytes can be considered key players participating in the development of these neu-rodegenerative processes. Moreover, astroglial cells cover unique functions in the adult brain parenchyma by regulating synaptic transmission and, therefore, contributing to the maintenance of neuronal homeostasis. To investigate how astrocytes react to the initial phases of inflammation, we cultured rat cortical astrocytes and exposed them to pro-inflammatory molecules such as lipopolysaccharide (LPS) and interferon-gamma (IFN-gamma). We observed that stimulated cells rapidly (8-24h) acquire typical features of reactive atrocytes, by increasing the expression of markers such as glial fibrillary acidic pro-tein (GFAP) and inducible nitric oxide synthase (iNOS) evaluated by immunocytochemistry and im-munoblotting, respectively. Surprisingly, LPS/IFN-gamma treatment did not influence cell viability, meas-ured by MTT test, even at later time-points, but inflammation altered astrocyte morphology inducing the formation of vacuoles characteristic of autophagic processes. We analyzed the expression of the au-tophagic marker Microtubule Associated Protein 1 Light Chain (LC3B) over time and correlated it with an altered morphology of mitochondria in these cells by time-lapse microscopy. Our data demonstrate that astrocytes rapidly respond to inflammation by undergoing autophagy. Further experiments will reveal the molecular pathways involved in this reaction and what role these events have in controlling the inflammatory response.