Additional file 1: Figure S1 . (A-B) PM induces dose-dependent reduction in transendothelial resistance (TER). (C) PM induces dosedependent (6 hr) reduction of ZO-1 protein levels. Figure S2 . PM induced FITC-dextran leakage across EC monolayer. Figure S3 . PM (100 μg/ml, 1-16 hr) does not induce LDH release from human ECs. Figure  S4 . NAC or PEG-CAT attenuates PM-induced ROS in ECs. Figure S5 . NAC (5 mM, 1-24 hr) does not change ZO-1 protein levels in human ECs. Figure S6 . EUK-134 (5 μM, 1 hr pre-treatment) attenuates PM (100 μg/ml, 6 hr)-induced ZO-1 degradation and TER reduction. Figure S7 . We hypothesize that PM induces EC barrier disruption in delayed phase (via ZO-1 degradation) and acute phase (via stress fiber formation). The expression of nicotinic receptor alpha7 during cochlear development Nicotinic acetylcholine receptor alpha7 expression was examined in the developing and adult auditory system using mice that were modified through homologous recombination to coexpress either GFP (alpha7GFP) or Cre (alpha7Cre), respectively. The expression of alpha7GFP is first detected at embryonic (E) day E13.5 in cells of the spiral prominence. By E14.5, sensory regions including the putative outer hair cells and Deiters' cells express alpha7GFP as do solitary efferent fibers. This pattern diminishes after E16.5 in a basal to apex progression, as Hensen's cells and cells of the spiral ligament acquire alpha7GFP expression. At birth and thereafter alpha7GFP also identifies a subset of spiral ganglion cells whose processes terminate on inner hair cells. Efferent fibers identified by peripherin or calcitonin gene-related protein do not coexpress alpha7GFP. In addition to cochlear structures, there is strong expression of alpha7GFP by cells of the central auditory pathways including the ventral posterior cochlear nucleus, lateral lemniscus, central inferior colliculus, and the medial geniculate nucleus. Our findings suggest that alpha7 expression by both neuronal and non-neuronal cells has the potential to impact multiple auditory functions through mechanisms that are not traditionally attributed to this receptor. Numerous neurotransmitter systems contribute to the normal development and function of the auditory sensory (cochlear) apparatus and the circuitry of the central nervous system. This includes members of the excitatory ligand-activated nicotinic acetylcholine receptor family (nAChR; Albuquerque et al. 2009 ). The nAChR subunit family consists of 16 distinct subunits that in various pentameric combinations form ligand-activated ion channels that each exhibit uniquely specialized pharmacological and functional properties (Albuquerque et al. 2009 ). One of these is the homomeric alpha7 nAChR (a7) whose functional uniqueness is in part due to its expression by both neuronal and non-neuronal cells in many tissues throughout the body and because it is responsive to multiple agonists (including acetylcholine and choline as well as nicotine). This results in its ability to modulate a diverse range of cellular functions including cell growth, cell survival, neurotransmission, and inflammation (Gahring and Rogers 2005; Levin et al. 2006; Albuquerque et al. 2009 ).