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- Title
Achlorhydria by ezrin knockdown: defects in the formation/expansion of apical canaliculi in gastric parietal cells.
- Authors
Tamura, Atsushi; Kikuchi, Shojiro; Hata, Masaki; Katsuno, Tatsuyo; Matsui, Takeshi; Hayashi, Hisayoshi; Suzuki, Yuichi; Noda, Tetsuo; Tsukita, Shoicniro; Tsukita, Sachiko
- Abstract
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 mortalily. 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.
- Subjects
METABOLIC disorders; GASTRIC acid; ACHLORHYDRIA; CELL membranes; NEOMYCIN; ELECTRON microscopy
- Publication
Journal of Cell Biology, 2005, Vol 169, Issue 1, p21
- ISSN
0021-9525
- Publication type
Article
- DOI
10.1083/jcb.200410083