Sphingolipid de novo biosynthesis is essential for intestine cell survival and barrier function View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2018-02-07

AUTHORS

Zhiqiang Li, Inamul Kabir, Gladys Tietelman, Chongmin Huan, Jianglin Fan, Tilla Worgall, Xian-Cheng Jiang

ABSTRACT

Serine palmitoyltransferase (SPT) is the rate-limiting enzyme for sphingolipid biosynthesis. SPT has two major subunits, SPTLC1 and SPTLC2. We previously found that liver Sptlc2 deficiency in early life impairs the development of adherens junctions. Here, we investigated the role of Sptlc2 deficiency in intestine. We treated Sptlc2-Flox/villin-Cre-ERT2 mice with tamoxifen (days 1, 2, and 3) to ablate Sptlc2 specifically in the intestine. At day 6 after tamoxifen treatment, Sptlc2-deficient mice had significantly decreased body weight with concurrent diarrhea and rectal bleeding. The number of goblet cells was reduced in both large and small intestine of Sptlc2-deficient mice compared with controls. Sptlc2 deficiency suppressed the level of mucin2 in the colon and increased circulating lipopolysaccharides, suggesting that SPT activity has a housekeeping function in the intestine. All Sptlc2-deficient mice died 7–10 days after tamoxifen treatment. Notably, supplementation with antibiotics and dexamethasone reduced lethality by 70%. We also found that colon specimens from patients with inflammatory bowel diseases had significantly reduced Sptlc2 expression, SPTLC2 staining, and goblet cell numbers. SPT activity is crucial for intestinal cell survival and barrier function. More... »

PAGES

173

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/s41419-017-0214-1

DOI

http://dx.doi.org/10.1038/s41419-017-0214-1

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1100892755

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/29415989


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