altered expression of a putative progenitor cell marker dcamkl1 in the rat gastric mucosa in regeneration, metaplasia and dysplasia改变表达式的一个假定的祖细胞标记dcamkl1在大鼠胃粘膜再生,化生和发育不良.pdfVIP

altered expression of a putative progenitor cell marker dcamkl1 in the rat gastric mucosa in regeneration, metaplasia and dysplasia改变表达式的一个假定的祖细胞标记dcamkl1在大鼠胃粘膜再生,化生和发育不良.pdf

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altered expression of a putative progenitor cell marker dcamkl1 in the rat gastric mucosa in regeneration, metaplasia and dysplasia改变表达式的一个假定的祖细胞标记dcamkl1在大鼠胃粘膜再生,化生和发育不良

Kikuchi et al. BMC Gastroenterology 2010, 10:65 /1471-230X/10/65 R E S E A R C H A R T I C L E Open Access Research article Altered expression of a putative progenitor cell marker DCAMKL1 in the rat gastric mucosa in regeneration, metaplasia and dysplasia 1 2 3 4 5 1 Miho Kikuchi , Hiroshi Nagata* , Norihito Watanabe , Hiromitsu Watanabe , Masayuki Tatemichi and Toshifumi Hibi Abstract Background: Doublecortin and calcium/calmodulin-dependent protein kinase-like-1 (DCAMKL1) is a candidate marker for progenitor cells in the gastrointestinal mucosa. Lineage cells in the gastric mucosa are derived from progenitor cells, but this process can be altered after injury. Therefore, we explored DCAMKL1 expression under pathological conditions. Methods: An immunohistochemical analysis was performed in rat stomach with acute superficial injury, chronic ulcer, intestinal metaplasia and dysplasia. Results: DCAMKL1 was exclusively expressed in immature quiescent ce lls in the isthmus of normal fundic glands, where putative progenitor cells are thought to reside. DCAMKL1-positive cells and proliferating cells shed into the lumen after superficial injury and re-appeared during the regenerative process, mainly in the superficial mucosa. In the marginal mucosa around the active ulcer, parietal and chief cells diminished, foveolar hyperplasia was evident, and trefoil factor family 2 (TFF2)/spasmolytic polypeptide-expressing metaplasia (SPEM) emerged at the gland base. DCAMKL1 cells re-emerged in the deep mucosa juxtaposed with SPEM and proliferating cells. In the healing ulcer, the TFF2 cell population expanded and seemed to redifferentiate to chief cells, while proliferating cells and DCAMKL1 cells appe

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