Achlorhydria by ezrin knockdown

• Atsushi Tamura

  1Department of Cell Biology, Faculty of Medicine, Kyoto University, Sakyo-ku, Kyoto 606-8501, Japan

• Shojiro Kikuchi

  1Department of Cell Biology, Faculty of Medicine, Kyoto University, Sakyo-ku, Kyoto 606-8501, Japan

• Masaki Hata

  3KAN Research Institute, Kyoto Research Park, Shimogyo-ku, Kyoto 606-8317, Japan

• Tatsuya Katsuno

  1Department of Cell Biology, Faculty of Medicine, Kyoto University, Sakyo-ku, Kyoto 606-8501, Japan

• Takeshi Matsui

  3KAN Research Institute, Kyoto Research Park, Shimogyo-ku, Kyoto 606-8317, Japan

• Hisayoshi Hayashi

  4Laboratory of Physiology, School of Food and Nutritional Sciences, University of Shizuoka, Shizuoka 422-8526, Japan

• Yuichi Suzuki

  4Laboratory of Physiology, School of Food and Nutritional Sciences, University of Shizuoka, Shizuoka 422-8526, Japan

• Tetsuo Noda

  5Department of Cell Biology, Cancer Institute of Japanese Foundation for Cancer Research, Koto-ku, Tokyo 135-8550, Japan

• Shoichiro Tsukita

  1Department of Cell Biology, Faculty of Medicine, Kyoto University, Sakyo-ku, Kyoto 606-8501, Japan

• Sachiko Tsukita

  1Department of Cell Biology, Faculty of Medicine, Kyoto University, Sakyo-ku, Kyoto 606-8501, Japan

抄録

Loss of gastric acid secretion is pathologically known as achlorhydria. Acid-secreting parietal cells are characterized by abundant expression of ezrin (Vil2), one of ezrin/radixin/moesin proteins, which generally cross-link actin filaments with plasma membrane proteins. Here, we show the direct in vivo involvement of ezrin in gastric acid secretion. Ezrin knockout (Vil2−/−) mice did not survive >1.5 wk after birth, making difficult to examine gastric acid secretion. We then generated ezrin knockdown (Vil2kd/kd) mice by introducing a neomycin resistance cassette between exons 2 and 3. Vil2kd/kd mice born at the expected Mendelian ratio exhibited growth retardation and a high mortality. Approximately 7% of Vil2kd/kd mice survived to adulthood. Ezrin protein levels in Vil2kd/kd stomachs decreased to <5% of the wild-type levels without compensatory up-regulation of radixin or moesin. Adult Vil2kd/kd mice suffered from severe achlorhydria. Immunofluorescence and electron microscopy revealed that this achlorhydria was caused by defects in the formation/expansion of canalicular apical membranes in gastric parietal cells.

収録刊行物

• The Journal of Cell Biology

  The Journal of Cell Biology 169 (1), 21-28, 2005-04-04

  Rockefeller University Press

キーワード

• Cell Biology

詳細情報

• CRID: 1363107369287775232
• NII論文ID: 80017277300
• DOI: 10.1083/jcb.200410083
• ISSN: 15408140
• ISSN: 00219525
• Web Site: https://rupress.org/jcb/article-pdf/169/1/21/1534088/jcb169121.pdf
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