期刊
AMERICAN JOURNAL OF PATHOLOGY
卷 185, 期 8, 页码 2219-2231出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.ajpath.2015.04.009
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资金
- Vanderbilt Digestive Disease Research Center Pilot Project [NIH P30 DK058404]
- Yonsei University College of Medicine [6-2013-0061, 2013-32-0031]
- Korea Mouse Phenotyping Center
- Brain Korea 21 PLUS Project for Medical Science, Yonsei University
- Bio and Medical Technology Development Program of the National Research Foundation (NRF) - Ministry of Science, ICT and Future Planning [NRF-2013M3A9D5072551]
- Basic Science Research Program through the NRF - Ministry of Education [2014R1A1A2058389]
- Department of Veterans Affairs Merit Review grant [1BX000930]
- NIH [RO1 DK071590, R01 DK101332, R24 DK096527]
- Vanderbilt Digestive Disease Center grant [P30 DK058404]
- Vanderbilt-Ingram Cancer Center through National Cancer Institute Cancer Center support grant [P30 CA068485]
- National Research Foundation of Korea [2014R1A1A2058389] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Doublecortin-like kinase 1 (Dclk1) is considered a reliable marker for tuft cells in the gastrointestinal tract. We investigated the dynamic changes of tuft cells associated with mouse models of oxyntic atrophy and metaplasia in the stomach. Increases in the numbers of Dclk1-positive tuft cells were observed in several models of parietal cell loss. However, the expanded population of Dclk1-expressing cells showed a morphologically distinct structure in apical microvilli and acetylated microtubules, which was not seen in the tuft cells present in the normal gastric mucosa. These microvillar sensory cells (MVSCs) showed no evidence of proliferation. The expansion of the MVSCs induced by oxyntic atrophy was reversible after the return of parietal cells. More important, expansion of MVSCs after induced parietal cell loss was not observed in Gast(-/-) mice. Although the Dclk1-expressing cells in the normal gastric mucosa were in part derived from Lrig1-expressing stem cells, the Lrig1-lineaged cells did not produce the expanded Dclk1-expressing cells associated with oxyntic atrophy. These studies indicate that loss of parietal cells leads to the reversible emergence of a novel Dclk1-expressing sensory cell population in the gastric mucosa.
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