Sphingomyelin synthase 2 deficiency suppresses airway mucus accumulation by altering sphingolipid flux and mucin glycosylation.

Authors

Harumi Sakae, Kento Sonoda, Hikari Nishisaka, Yuri Ogiso, Ryoma Miyazaki, Masaya Matsuda, Takeshi Nabe, Ken Watanabe, Toshiro Okazaki, Tomoyuki Furubayashi, Makoto Taniguchi, Kazuyuki Kitatani

Published in

Molecular and cellular biochemistry. Oct 05, 2026. Epub Oct 05, 2026.

Abstract

Sphingomyelin synthase 2 (SMS2) produces sphingomyelin from ceramide. In this study, SMS2 deficiency reduced airway accumulation of glycosylated mucins, such as MUC5AC, in a murine model of asthma, prompting investigation of the molecular mechanisms in mucin-forming epithelial cells. In the cell model, SMS2 silencing promoted the conversion of ceramide to glucosylceramide, a precursor of complex glycosphingolipids. This alteration reduced MUC5AC glycosylation, suggesting the potential for biochemical competition between sphingolipids and MUC5AC for glycosylation. Supplying C₆-ceramide, which increases biochemical glycosylation for sphingolipids, reduced glycosylated MUC5AC, but this effect was absent in glucosylceramide synthase-silenced cells. These findings indicate that SMS2 deficiency alters sphingolipid metabolism, reducing MUC5AC glycosylation and maturation, underscoring the role of sphingolipid dynamics in modulating mucus production.

PMID:
42832154
Bibliographic data and abstract were imported from PubMed on 06 Oct 2026.

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