| First Author | Tamura A | Year | 2005 |
| Journal | J Cell Biol | Volume | 169 |
| Issue | 1 | Pages | 21-8 |
| PubMed ID | 15809309 | Mgi Jnum | J:200366 |
| Mgi Id | MGI:5508375 | Doi | 10.1083/jcb.200410083 |
| Citation | Tamura A, et al. (2005) Achlorhydria by ezrin knockdown: defects in the formation/expansion of apical canaliculi in gastric parietal cells. J Cell Biol 169(1):21-8 |
| abstractText | 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 (Vil2(kd/kd)) mice by introducing a neomycin resistance cassette between exons 2 and 3. Vil2(kd/kd) mice born at the expected Mendelian ratio exhibited growth retardation and a high mortality. Approximately 7% of Vil2(kd/kd) mice survived to adulthood. Ezrin protein levels in Vil2(kd/kd) stomachs decreased to <5% of the wild-type levels without compensatory up-regulation of radixin or moesin. Adult Vil2(kd/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. |
