β-Adrenergic inhibition of exocytotic surface deposition of MHCII molecules in reactive astrocytes is mediated by amisyn

Authors

Vrsnik, J., Bozic, M., Bunc, Z., Potokar, M., Sugiyama, K., Dolinar, K., Pirkmajer, S., Anderluh, G., Kreft, M., Milosevic, I., Jorgacevski, J., Zorec, R., Stenovec, M.

Abstract

Degeneration of the locus coeruleus, a noradrenergic nucleus, reduces noradrenaline bioavailability in the central nervous system and promotes neuroinflammation via reactive astrocytes, although the underlying mechanisms remain unclear. We investigated whether interferon-{gamma}-induced expression of major histocompatibility complex class II (MHCII), a marker of pro-inflammatory reactive astrocytes, is regulated by adrenergic receptors and amisyn. {beta}-Adrenergic, but not -adrenergic, stimulation increased cyclic adenosine monophosphate (cAMP) and reduced MHCII expression, as detected immunocytochemically, in human and rat astrocytes. {beta}-Adrenergic treatment altered transient exocytosis of lysosome-like vesicles, increasing event frequency and reducing fusion-pore conductance and dwell time, thereby limiting MHCII surface expression. Overexpression of wild-type amisyn inhibited surface expression of MHCII and the lysosomal marker CD63 and reduced fusion-pore conductance and dwell time. Conversely, amisyn knockdown enhanced full fusion exocytosis of larger vesicles and abolished {beta}-adrenergic effects, indicating that amisyn mediates {beta}-adrenergic inhibition of exocytosis and MHCII surface deposition.

Preprint server: bioRxiv
The authors list and abstract were imported from bioRxiv on 25 Aug 2026.

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