cIAP1 may be involved in survival of the olfactory system

Abstract

Maintenance of neurons is regulated by various factors from in the molecular manner to the systemic manner. And external and internal environmental cues also modulate the maintenance of neurons. In this process, neurons are exposed to the stimuli and can easily get stressed, and which leads to neuronal death and impairs to establishment of their connections and activities. As a representative sensory system, the peripheral olfactory system is directly exposed to the environment to detect the external stimuli. Volatile molecules or natural gas in the air are detected by the olfactory sensory neurons (OSNs) in the olfactory epithelium (OE), and the OSNs are connected to the central nervous system (CNS) via the olfactory bulb (OB). Constant exposure to external stimuli may cause damages to the OSNs, and which in turn afflicts to acute or chronic diseases like olfactory impairment, chronic rhinitis, etc. Inhibitor of apoptosis proteins (IAPs) interact with caspases and inhibit apoptosis. In particular, cIAP1 is one of the regulators of NF-κB (nuclear factor kappa-light-chain-enhancer of B cells) activation and TNF (tumor necrosis factor) signals, which is crucial for inflammatory responses. Although there were several studies related to the cell death of the olfactory system caused by external stimuli, the mechanisms and the role of cIAP1 in the olfactory system has not been fully understood. To this end, cIAP1 KO mice were studied to identify the critical roles of cIAP1 in the olfactory system. Behavioral assay demonstrated that cIAP1 deprivation caused smell dysfunction. Moreover, the numbers of OSNs in the OE was decreased and the thickness of the OE was observed thinner compared to WT animals. In summary, cIAP1 may play important roles for OSN survival.