Microglial Phagocytosis & Brain Inflammation Are Controlled By Nitric Oxide & TRPV2 | FPS#7

In this episode, we discuss the mechanisms that regulate microglia phagocytosis (such as TRPV2 and other vanilloid receptors) - AKA eating apoptosis ready cells - and how the brain maintains healthy function in aging and after injury, such as traumatic brain injury (TBI).Because neurons get all the attention, you don't hear too much about glia. Although glia cells DO NOT carry nerve impulses (action potentials) they do have many important functions. In fact, without glia, the neurons would not work properly! Neuroscience PhD Candidates Matthew Maksoud and Viki Tellios join us to speak on their article - Nitric Oxide Upregulates microglia phagocytosis and increases transient receptor potential vanilloid type 2 channel expression on the plasma membrane - published in the journal Glia: https://onlinelibrary.wiley.com/doi/full/10.1002/glia.23685

Abstract
Microglia phagocytosis is critical for central nervous system development, and dysregulation of phagocytosis may contribute to a variety of neurological disorders. During initial stages of phagocytosis, microglia display increased nitric oxide (NO) production via inducible nitric oxide synthase (iNOS) activity and amplified calcium entry through transient receptor potential vanilloid type 2 (TRPV2) channels. The present study investigated the regulatory role of iNOS/NO signaling in microglial phagocytosis and TRPV2 channel activation using phagocytosis assay, calcium imaging, patch clamp electrophysiology, immunocytochemistry, and immunoblot assays. Results showed that primary microglia from iNOS‐knockout (iNOS−/−) mice exhibited substantial deficits in phagocytic capacity and TRPV2 channel activity relative to wild‐type (WT) controls. Specifically, iNOS−/− microglia displayed a lower level of TRPV2 protein localized on the plasma membrane (PM) without any significant change in the mRNA levels of Fc‐gamma receptors and TRPV2. In addition, iNOS−/− microglia, unlike their WT controls, failed to elicit a calcium influx in response to application of the TRPV2‐agonist 2‐aminoethoxydiphenyl borate (2APB). Importantly, the phagocytic capacity and the PM expression and activity of TRPV2 in iNOS−/− microglia were largely corrected by pretreatment with NO‐donors. Accordingly, the 2APB‐evoked calcium influx and the PM expression of TRPV2 in WT microglia were significantly decreased by selective inhibition of iNOS, protein kinase‐G (PKG), or phosphoinositide‐3‐kinase (PI3K), respectively. Together, results from this study indicated that iNOS/NO signaling upregulates microglial phagocytosis and increases TRPV2 trafficking to the PM via PKG/PI3K dependent pathway(s) and vanilloid receptors.

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