Parietal cell hyperstimulation and autoimmune gastritis in cholera toxin transgenic mice

Lopez-Diaz, Lymari; Hinkle, Karen L.; Jain, Renu; Zavros, Yana; Brunkan, Cynthia S.; Keeley, Theresa M.; Eaton, Kathryn A.; Merchant, Juanita L.; Chew, Catherine S.; Samuelson, Linda C.

doi:10.1152/ajpgi.00461.2005

Cited by 42 publications

(55 citation statements)

References 41 publications

(52 reference statements)

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“…5A-C). We also observed increased expression of transcription factors that function downstream of Atoh1 to orchestrate secretory cell differentiation, including Gfi1 (Shroyer et al, 2005;Bjerknes and Cheng, 2010), Spdef (Gregorieff et al, 2009;Noah et al, 2010) and Neurog3 (Jenny et al, 2002;Bjerknes and Cheng, 2006;Lopez-Diaz et al, 2006) (Fig. 5D-F).…”

Section: Notch Regulation Of Olfm4 Expression Is Atoh1 Independentmentioning

confidence: 73%

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Notch signaling modulates proliferation and differentiation of intestinal crypt base columnar stem cells

et al. 2012

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SUMMARYNotch signaling is known to regulate the proliferation and differentiation of intestinal stem and progenitor cells; however, direct cellular targets and specific functions of Notch signals had not been identified. We show here in mice that Notch directly targets the crypt base columnar (CBC) cell to maintain stem cell activity. Notch inhibition induced rapid CBC cell loss, with reduced proliferation, apoptotic cell death and reduced efficiency of organoid initiation. Furthermore, expression of the CBC stem cellspecific marker Olfm4 was directly dependent on Notch signaling, with transcription activated through RBP-J binding sites in the promoter. Notch inhibition also led to precocious differentiation of epithelial progenitors into secretory cell types, including large numbers of cells that expressed both Paneth and goblet cell markers. Analysis of Notch function in Atoh1-deficient intestine demonstrated that the cellular changes were dependent on Atoh1, whereas Notch regulation of Olfm4 gene expression was Atoh1 independent. Our findings suggest that Notch targets distinct progenitor cell populations to maintain adult intestinal stem cells and to regulate cell fate choice to control epithelial cell homeostasis.

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Section: Notch Regulation Of Olfm4 Expression Is Atoh1 Independentmentioning

confidence: 73%

“…Immunostaining was performed as described (Lopez-Diaz et al, 2006). Primary antibodies were used as described (Keeley and Samuelson, 2010;VanDussen and Samuelson, 2010) For electron microscopy, jejunum and ileum from three mice from each treatment group were evaluated.…”

Section: Histological Analysismentioning

confidence: 99%

Notch signaling modulates proliferation and differentiation of intestinal crypt base columnar stem cells

et al. 2012

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“…Several studies have demonstrated that the PCs play an important role in the process of differentiation and development of other cell lineages in the gastric mucosa, as loss of mature PCs alters the normal differentiation program of the gastric epithelium and causes different types of mucosal cell remodeling (Li et al 1995(Li et al , 1996Canfield et al 1996;Lopez-Diaz et al 2006;Jain et al 2008). In our previous investigations we reported that inhibition of BMP signaling in the stomach leads to a marked decrease in the number of PCs and to the appearance of aberrant lineages that express markers of both zymogenic and mucus neck cell differentiation (Shinohara et al 2010;Takabayashi et al 2014).…”

Section: Discussionmentioning

confidence: 99%

“…Several studies have suggested that in mice, the ZCs differentiate from pluripotent stem cells through a multistep process that involves the progressive transition of mucus neck cells into fully differentiated ZCs (Nam et al 2010). It has been also shown that this process might be regulated by parietal-cell secreted factors as loss of PCs leads to alterations in the normal process of ZC maturation and differentiation (Li et al 1995(Li et al , 1996Canfield et al 1996;Lopez-Diaz et al 2006;Jain et al 2008;Shinohara et al 2010;Takabayashi et al 2014). It is therefore possible that the abnormalities in ZC differentiation that we observed in the NogTG;GasKO mice might be mostly secondary to the presence of aberrant, poorly differentiated PCs, although we cannot completely exclude that both gastrin and the BMPs might have cooperative, direct effects on the ZCs.…”

Section: Discussionmentioning

confidence: 99%

Regulation of Gastric Epithelial Cell Homeostasis by Gastrin and Bone Morphogenetic Protein Signaling

Todisco¹,

Eaton²,

Samuelson³

et al. 2011

Gastroenterology

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We reported that transgenic expression of the bone morphogenetic protein (BMP) signaling inhibitor noggin in the mouse stomach, leads to parietal-cell (PC) loss, expansion of transitional cells expressing markers of both mucus neck and zymogenic lineages, and to activation of proliferative mechanisms. Because these cellular changes were associated with increased levels of the hormone gastrin, we investigated if gastrin mediates the expression of the phenotypic changes of the noggin transgenic mice (NogTG mice). Three-month-old NogTG mice were crossed to gastrin-deficient (GasKO mice) to generate NogTG;GasKO mice. Morphology of the corpus of wild type, NogTG, GasKO, and NogTG;GasKO mice was analyzed by H&E staining. Distribution of PCs and zymogenic cells (ZCs) was analyzed by immunostaining for the H + /K + -ATPase and intrinsic factor (IF). Expression of the H + /K + -ATPase and IF genes and proteins were measured by QRT-PCR and western blots. Cell proliferation was assessed by immunostaining for proliferating cell nuclear antigen. The corpus of the NogTG;GasKO mice displayed a marked reduction in the number of PCs and ZCs in comparison to NogTG mice. Further, cellular proliferation was significantly lower in NogTG;GasKO mice, than in the NogTG mice. Thus, gastrin mediates the increase in gastric epithelial cell proliferation induced by inhibition of BMP signaling in vivo. Moreover, gastrin and BMP signaling exert cooperative effects on the maturation and differentiation of both the zymogenic and PC lineages. These findings contribute to a better understanding of the factors involved in the control of gastric epithelial cell homeostasis.

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“…Research, with the aid of canine and rodent models, has shown that histamine is able to induce a species specific secretion of pepsinogen by the gastric chief cells (Wiederanders et al, 1960;Lopez-Diaz et al, 2006;Tani & Tanaka, 1990). In the case of rat chief cells, Lopez-Diaz et al have shown that histamine, possibly working through the chief cells H2 receptors, induces a dose-dependent pepsinogen secretion.…”

Section: Cellular Atrophymentioning

confidence: 99%

The Morphological Effects of Asthma, As Well As Conventional and Alternative Asthma Therapies on Parietal and Chief Cells in the Stomach of BALB/c Mice

2011

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VIEIRA, W. A.; OBERHOLZER, H. M. & PRETORIUS, E.The morphological effects of asthma, as well as conventional and alternative asthma therapies on parietal and chief cells in the stomach of BALB/c mice. Int. J. Morphol., 29(4):1341-1350, 2011. SUMMARY:Scientific literature, although limited in this area, supports the hypothesis that asthma, by means of selective leukocyte trafficking between the various mucosal and glandular sites of the body, can have the same pathophysiological effects on the stomach as the airways. This study aimed to determine if asthma, in the absence and presence of various asthma therapies (Hydrocortisone and Modul8 TM ), imparted any morphological alteration on the stomach parietal and chief cells. The BALB/c murine asthmatic mouse model was the model of choice in this study. The asthma induction protocol as well as the asthma therapies were proved to be effective with the aid of bronchial lavage fluid leukocyte quantification. Fundic and pyloric biopsies were extracted at termination and assessed by means of transmission electron, scanning electron and light microscopy. The extracted fundic and pyloric biopsies revealed asthma alone induced parietal cell hypertrophy (increase in parietal cell size P < 0.000100 in both stomach regions) and chief cell hyper functioning. The use of Hydrocortisone and Modul8 TM , as a therapy to correct the perceived gastric alterations were dismal; only in the case of fundic parietal cells were both treatments able to compensate for the hypertrophic effect caused by asthma, while in the pylorus parietal cell asthma-induced hypertrophy was only compensated for by Modul8 TM .

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Parietal cell hyperstimulation and autoimmune gastritis in cholera toxin transgenic mice

Cited by 42 publications

References 41 publications

Notch signaling modulates proliferation and differentiation of intestinal crypt base columnar stem cells

Notch signaling modulates proliferation and differentiation of intestinal crypt base columnar stem cells

Regulation of Gastric Epithelial Cell Homeostasis by Gastrin and Bone Morphogenetic Protein Signaling

The Morphological Effects of Asthma, As Well As Conventional and Alternative Asthma Therapies on Parietal and Chief Cells in the Stomach of BALB/c Mice

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