ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2021
Loss of Slfn3 induces a sex-dependent repair vulnerability after 50% bowel resection.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 17 citations in OpenAlex.
- Vil-Cre specific Slfn3KO mice exhibit sex-specific differences in lung, stomach, cecum, kidney, and proximal colon differentiation markers and Slfn family members expression levels.Biochemistry and biophysics reports · 2023Article
- Article
- Muscle hypertrophy and neuroplasticity in the small bowel in short bowel syndrome.Histochemistry and cell biology · 2023Article
- Systematic review reveals sexually antagonistic knockouts in model organisms.Ecology and evolution · 2022Review
- Article
- Microbiome diversity declines while distinct expansions of Th17, iNKT, and dendritic cell subpopulations emerge after anastomosis surgery.Gut pathogens · 2021Article
- Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Bowel resection accelerates enterocyte proliferation in the remaining gut with suboptimal absorptive and digestive capacity because of a proliferation-associated decrease in functional differentiation markers. We hypothesized that although schlafen 3 (Slfn3) is an important regulator of enterocytic differentiation, Slfn3 would have less impact on bowel resection adaptation, where accelerated proliferation takes priority over differentiation. We assessed proliferation, cell shedding, and enterocyte differentiation markers from resected and postoperative bowel of wild-type (WT) and Slfn3-knockout (Slfn3KO) mice. Villus length and crypt depth were increased in WT mice and were even longer in Slfn3KO mice. Mitotic marker, Phh3+, and the proliferation markers Lgr5, FoxL1, and platelet-derived growth factor-α (PDGFRα) were increased after resection in male WT, but this was blunted in male Slfn3KO mice. Cell-shedding regulators Villin1 and TNFα were downregulated in female mice and male WT mice only, whereas Gelsolin and EGFR increased expression in all mice.
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Registered trials
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