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Telomere shortening is associated with reduced duodenal HCO3−secretory but normal gastric acid secretory capacity in aging mice
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| Zeitschriftentitel: | American Journal of Physiology-Gastrointestinal and Liver Physiology |
|---|---|
| Personen und Körperschaften: | , , , , , , |
| In: | American Journal of Physiology-Gastrointestinal and Liver Physiology, 303, 2012, 12, S. G1312-G1321 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
American Physiological Society
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| Schlagwörter: |
| author_facet |
Tuo, Biguang Ju, Zhenyu Riederer, Brigitte Engelhardt, Regina Manns, Michael P. Rudolph, K. Lenhard Seidler, Ursula Tuo, Biguang Ju, Zhenyu Riederer, Brigitte Engelhardt, Regina Manns, Michael P. Rudolph, K. Lenhard Seidler, Ursula |
|---|---|
| author |
Tuo, Biguang Ju, Zhenyu Riederer, Brigitte Engelhardt, Regina Manns, Michael P. Rudolph, K. Lenhard Seidler, Ursula |
| spellingShingle |
Tuo, Biguang Ju, Zhenyu Riederer, Brigitte Engelhardt, Regina Manns, Michael P. Rudolph, K. Lenhard Seidler, Ursula American Journal of Physiology-Gastrointestinal and Liver Physiology Telomere shortening is associated with reduced duodenal HCO3−secretory but normal gastric acid secretory capacity in aging mice Physiology (medical) Gastroenterology Hepatology Physiology |
| author_sort |
tuo, biguang |
| spelling |
Tuo, Biguang Ju, Zhenyu Riederer, Brigitte Engelhardt, Regina Manns, Michael P. Rudolph, K. Lenhard Seidler, Ursula 0193-1857 1522-1547 American Physiological Society Physiology (medical) Gastroenterology Hepatology Physiology http://dx.doi.org/10.1152/ajpgi.00035.2012 <jats:p>The incidence of duodenal ulcer, especially Helicobacter pylori-negative duodenal ulcer, strongly increases with age. In humans, telomere length shortening is considered to be one critical factor in cellular senescence and organ survival. In this study, we compared basal and stimulated gastric acid and duodenal HCO<jats:sub>3</jats:sub><jats:sup>−</jats:sup>secretory rates in aged late-generation (G<jats:sub>3</jats:sub>) telomerase-deficient (mTERC<jats:sup>−/−</jats:sup>) mice, which are characterized by severe telomere dysfunction due to the inability to elongate telomeres during cell division. We found that basal and forskolin-stimulated HCO<jats:sub>3</jats:sub><jats:sup>−</jats:sup>secretion and short-circuit current ( I<jats:sub>sc</jats:sub>) in isolated duodenal mucosa of G<jats:sub>3</jats:sub>mTERC<jats:sup>−/−</jats:sup>mice were markedly reduced compared with age-matched wild-type mice. In contrast, basal and forskolin-stimulated acid secretory rates in isolated G<jats:sub>3</jats:sub>mTERC<jats:sup>−/−</jats:sup>gastric mucosa were not significantly altered. Correspondingly, duodenal mucosa of G<jats:sub>3</jats:sub>mTERC<jats:sup>−/−</jats:sup>mice showed slimming and shortening of villi, whereas gastric mucosal histology was not significantly altered. However, the ratios of cystic fibrosis transmembrane conductance regulator (CFTR) and solute-linked carrier 26 gene family (Slc26a6) mRNA expression in relation to cytokeratin-18 were not altered in duodenal mucosa. The further knockout of p21, which is a downstream effector of telomere shortening-induced senescence, rescued villus atrophy of duodenal mucosa, and basal and forskolin-stimulated duodenal HCO<jats:sub>3</jats:sub><jats:sup>−</jats:sup>secretion and I<jats:sub>sc</jats:sub>in mTERC<jats:sup>−/−</jats:sup>p21<jats:sup>−/−</jats:sup>double-knockout mice were not different from wild-type controls. In conclusion, genetic ablation of telomerase resulted in p21-dependent duodenal mucosal atrophy and reduced duodenal HCO<jats:sub>3</jats:sub><jats:sup>−</jats:sup>secretory capacity, whereas gastric morphology and acid secretory function were preserved. This suggests that telomere shortening during aging may result in an imbalance between aggressive and protective secretions against duodenal mucosa and thus predispose to ulcer formation.</jats:p> Telomere shortening is associated with reduced duodenal HCO<sub>3</sub><sup>−</sup>secretory but normal gastric acid secretory capacity in aging mice American Journal of Physiology-Gastrointestinal and Liver Physiology |
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10.1152/ajpgi.00035.2012 |
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Biologie Medizin |
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American Journal of Physiology-Gastrointestinal and Liver Physiology |
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| title |
Telomere shortening is associated with reduced duodenal HCO3−secretory but normal gastric acid secretory capacity in aging mice |
| title_unstemmed |
Telomere shortening is associated with reduced duodenal HCO3−secretory but normal gastric acid secretory capacity in aging mice |
| title_full |
Telomere shortening is associated with reduced duodenal HCO3−secretory but normal gastric acid secretory capacity in aging mice |
| title_fullStr |
Telomere shortening is associated with reduced duodenal HCO3−secretory but normal gastric acid secretory capacity in aging mice |
| title_full_unstemmed |
Telomere shortening is associated with reduced duodenal HCO3−secretory but normal gastric acid secretory capacity in aging mice |
| title_short |
Telomere shortening is associated with reduced duodenal HCO3−secretory but normal gastric acid secretory capacity in aging mice |
| title_sort |
telomere shortening is associated with reduced duodenal hco<sub>3</sub><sup>−</sup>secretory but normal gastric acid secretory capacity in aging mice |
| topic |
Physiology (medical) Gastroenterology Hepatology Physiology |
| url |
http://dx.doi.org/10.1152/ajpgi.00035.2012 |
| publishDate |
2012 |
| physical |
G1312-G1321 |
| description |
<jats:p>The incidence of duodenal ulcer, especially Helicobacter pylori-negative duodenal ulcer, strongly increases with age. In humans, telomere length shortening is considered to be one critical factor in cellular senescence and organ survival. In this study, we compared basal and stimulated gastric acid and duodenal HCO<jats:sub>3</jats:sub><jats:sup>−</jats:sup>secretory rates in aged late-generation (G<jats:sub>3</jats:sub>) telomerase-deficient (mTERC<jats:sup>−/−</jats:sup>) mice, which are characterized by severe telomere dysfunction due to the inability to elongate telomeres during cell division. We found that basal and forskolin-stimulated HCO<jats:sub>3</jats:sub><jats:sup>−</jats:sup>secretion and short-circuit current ( I<jats:sub>sc</jats:sub>) in isolated duodenal mucosa of G<jats:sub>3</jats:sub>mTERC<jats:sup>−/−</jats:sup>mice were markedly reduced compared with age-matched wild-type mice. In contrast, basal and forskolin-stimulated acid secretory rates in isolated G<jats:sub>3</jats:sub>mTERC<jats:sup>−/−</jats:sup>gastric mucosa were not significantly altered. Correspondingly, duodenal mucosa of G<jats:sub>3</jats:sub>mTERC<jats:sup>−/−</jats:sup>mice showed slimming and shortening of villi, whereas gastric mucosal histology was not significantly altered. However, the ratios of cystic fibrosis transmembrane conductance regulator (CFTR) and solute-linked carrier 26 gene family (Slc26a6) mRNA expression in relation to cytokeratin-18 were not altered in duodenal mucosa. The further knockout of p21, which is a downstream effector of telomere shortening-induced senescence, rescued villus atrophy of duodenal mucosa, and basal and forskolin-stimulated duodenal HCO<jats:sub>3</jats:sub><jats:sup>−</jats:sup>secretion and I<jats:sub>sc</jats:sub>in mTERC<jats:sup>−/−</jats:sup>p21<jats:sup>−/−</jats:sup>double-knockout mice were not different from wild-type controls. In conclusion, genetic ablation of telomerase resulted in p21-dependent duodenal mucosal atrophy and reduced duodenal HCO<jats:sub>3</jats:sub><jats:sup>−</jats:sup>secretory capacity, whereas gastric morphology and acid secretory function were preserved. This suggests that telomere shortening during aging may result in an imbalance between aggressive and protective secretions against duodenal mucosa and thus predispose to ulcer formation.</jats:p> |
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| author | Tuo, Biguang, Ju, Zhenyu, Riederer, Brigitte, Engelhardt, Regina, Manns, Michael P., Rudolph, K. Lenhard, Seidler, Ursula |
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| description | <jats:p>The incidence of duodenal ulcer, especially Helicobacter pylori-negative duodenal ulcer, strongly increases with age. In humans, telomere length shortening is considered to be one critical factor in cellular senescence and organ survival. In this study, we compared basal and stimulated gastric acid and duodenal HCO<jats:sub>3</jats:sub><jats:sup>−</jats:sup>secretory rates in aged late-generation (G<jats:sub>3</jats:sub>) telomerase-deficient (mTERC<jats:sup>−/−</jats:sup>) mice, which are characterized by severe telomere dysfunction due to the inability to elongate telomeres during cell division. We found that basal and forskolin-stimulated HCO<jats:sub>3</jats:sub><jats:sup>−</jats:sup>secretion and short-circuit current ( I<jats:sub>sc</jats:sub>) in isolated duodenal mucosa of G<jats:sub>3</jats:sub>mTERC<jats:sup>−/−</jats:sup>mice were markedly reduced compared with age-matched wild-type mice. In contrast, basal and forskolin-stimulated acid secretory rates in isolated G<jats:sub>3</jats:sub>mTERC<jats:sup>−/−</jats:sup>gastric mucosa were not significantly altered. Correspondingly, duodenal mucosa of G<jats:sub>3</jats:sub>mTERC<jats:sup>−/−</jats:sup>mice showed slimming and shortening of villi, whereas gastric mucosal histology was not significantly altered. However, the ratios of cystic fibrosis transmembrane conductance regulator (CFTR) and solute-linked carrier 26 gene family (Slc26a6) mRNA expression in relation to cytokeratin-18 were not altered in duodenal mucosa. The further knockout of p21, which is a downstream effector of telomere shortening-induced senescence, rescued villus atrophy of duodenal mucosa, and basal and forskolin-stimulated duodenal HCO<jats:sub>3</jats:sub><jats:sup>−</jats:sup>secretion and I<jats:sub>sc</jats:sub>in mTERC<jats:sup>−/−</jats:sup>p21<jats:sup>−/−</jats:sup>double-knockout mice were not different from wild-type controls. In conclusion, genetic ablation of telomerase resulted in p21-dependent duodenal mucosal atrophy and reduced duodenal HCO<jats:sub>3</jats:sub><jats:sup>−</jats:sup>secretory capacity, whereas gastric morphology and acid secretory function were preserved. This suggests that telomere shortening during aging may result in an imbalance between aggressive and protective secretions against duodenal mucosa and thus predispose to ulcer formation.</jats:p> |
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| spelling | Tuo, Biguang Ju, Zhenyu Riederer, Brigitte Engelhardt, Regina Manns, Michael P. Rudolph, K. Lenhard Seidler, Ursula 0193-1857 1522-1547 American Physiological Society Physiology (medical) Gastroenterology Hepatology Physiology http://dx.doi.org/10.1152/ajpgi.00035.2012 <jats:p>The incidence of duodenal ulcer, especially Helicobacter pylori-negative duodenal ulcer, strongly increases with age. In humans, telomere length shortening is considered to be one critical factor in cellular senescence and organ survival. In this study, we compared basal and stimulated gastric acid and duodenal HCO<jats:sub>3</jats:sub><jats:sup>−</jats:sup>secretory rates in aged late-generation (G<jats:sub>3</jats:sub>) telomerase-deficient (mTERC<jats:sup>−/−</jats:sup>) mice, which are characterized by severe telomere dysfunction due to the inability to elongate telomeres during cell division. We found that basal and forskolin-stimulated HCO<jats:sub>3</jats:sub><jats:sup>−</jats:sup>secretion and short-circuit current ( I<jats:sub>sc</jats:sub>) in isolated duodenal mucosa of G<jats:sub>3</jats:sub>mTERC<jats:sup>−/−</jats:sup>mice were markedly reduced compared with age-matched wild-type mice. In contrast, basal and forskolin-stimulated acid secretory rates in isolated G<jats:sub>3</jats:sub>mTERC<jats:sup>−/−</jats:sup>gastric mucosa were not significantly altered. Correspondingly, duodenal mucosa of G<jats:sub>3</jats:sub>mTERC<jats:sup>−/−</jats:sup>mice showed slimming and shortening of villi, whereas gastric mucosal histology was not significantly altered. However, the ratios of cystic fibrosis transmembrane conductance regulator (CFTR) and solute-linked carrier 26 gene family (Slc26a6) mRNA expression in relation to cytokeratin-18 were not altered in duodenal mucosa. The further knockout of p21, which is a downstream effector of telomere shortening-induced senescence, rescued villus atrophy of duodenal mucosa, and basal and forskolin-stimulated duodenal HCO<jats:sub>3</jats:sub><jats:sup>−</jats:sup>secretion and I<jats:sub>sc</jats:sub>in mTERC<jats:sup>−/−</jats:sup>p21<jats:sup>−/−</jats:sup>double-knockout mice were not different from wild-type controls. In conclusion, genetic ablation of telomerase resulted in p21-dependent duodenal mucosal atrophy and reduced duodenal HCO<jats:sub>3</jats:sub><jats:sup>−</jats:sup>secretory capacity, whereas gastric morphology and acid secretory function were preserved. This suggests that telomere shortening during aging may result in an imbalance between aggressive and protective secretions against duodenal mucosa and thus predispose to ulcer formation.</jats:p> Telomere shortening is associated with reduced duodenal HCO<sub>3</sub><sup>−</sup>secretory but normal gastric acid secretory capacity in aging mice American Journal of Physiology-Gastrointestinal and Liver Physiology |
| spellingShingle | Tuo, Biguang, Ju, Zhenyu, Riederer, Brigitte, Engelhardt, Regina, Manns, Michael P., Rudolph, K. Lenhard, Seidler, Ursula, American Journal of Physiology-Gastrointestinal and Liver Physiology, Telomere shortening is associated with reduced duodenal HCO3−secretory but normal gastric acid secretory capacity in aging mice, Physiology (medical), Gastroenterology, Hepatology, Physiology |
| title | Telomere shortening is associated with reduced duodenal HCO3−secretory but normal gastric acid secretory capacity in aging mice |
| title_full | Telomere shortening is associated with reduced duodenal HCO3−secretory but normal gastric acid secretory capacity in aging mice |
| title_fullStr | Telomere shortening is associated with reduced duodenal HCO3−secretory but normal gastric acid secretory capacity in aging mice |
| title_full_unstemmed | Telomere shortening is associated with reduced duodenal HCO3−secretory but normal gastric acid secretory capacity in aging mice |
| title_short | Telomere shortening is associated with reduced duodenal HCO3−secretory but normal gastric acid secretory capacity in aging mice |
| title_sort | telomere shortening is associated with reduced duodenal hco<sub>3</sub><sup>−</sup>secretory but normal gastric acid secretory capacity in aging mice |
| title_unstemmed | Telomere shortening is associated with reduced duodenal HCO3−secretory but normal gastric acid secretory capacity in aging mice |
| topic | Physiology (medical), Gastroenterology, Hepatology, Physiology |
| url | http://dx.doi.org/10.1152/ajpgi.00035.2012 |