Pancreas-specific aquaporin 12 null mice showed increased susceptibility to caerulein-induced acute pancreatitis

Eriko Ohta, Tomohiro Itoh, Tomomi Nemoto, Jiro Kumagai, Shigeru Ko, Kenichi Ishibashi, Mayuko Ohno, Keiko Uchida, Akihito Ohta, Eisei Sohara, Shinichi Uchida, Sei Sasaki, Tatemitsu Rai

Research output: Contribution to journalArticle

29 Citations (Scopus)

Abstract

Aquaporin 12 (AQP12) is the most recently identified member of the mammalian AQP family and is specifically expressed in pancreatic acinar cells. In vitro expression studies have revealed that AQP12 is localized at intracellular sites. To determine the physiological roles of AQP12 in the pancreas, we generated knockout mice for this gene (AQP12-KO). No obvious differences were observed under normal conditions between wild-type (WT) and AQP12-KO mice in terms of growth, blood chemistry, pancreatic fluid content, or histology. However, when we induced pancreatitis through the administration of a cholecystokinin-8 (CCK-8) analog, the AQP12-KO mice showed more severe pathological damage to this organ than WT mice. Furthermore, when we analyzed exocytosis in the pancreatic acini using a two-photon excitation imaging method, the results revealed larger exocytotic vesicles (vacuoles) in the acini of AQP12-KO mice at a high CCK-8 dose (100 nM). From these results, we conclude that AQP12 may function in the mechanisms that control the proper secretion of pancreatic fluid following rapid and intense stimulation.

Original languageEnglish
JournalAmerican Journal of Physiology - Cell Physiology
Volume297
Issue number6
DOIs
Publication statusPublished - 2009
Externally publishedYes

Fingerprint

Ceruletide
Aquaporins
Pancreatitis
Pancreas
Fluids and Secretions
Acinar Cells
Exocytosis
Vacuoles
Photons
Knockout Mice
Histology
mouse AQP12 protein
Growth
Genes
cholecystokinin 8

Keywords

  • Cholecystokinin
  • Exocytosis
  • Knockout mouse
  • Pancreatic acinar cell
  • Pancreatic exocrine function

ASJC Scopus subject areas

  • Cell Biology
  • Physiology
  • Medicine(all)

Cite this

Pancreas-specific aquaporin 12 null mice showed increased susceptibility to caerulein-induced acute pancreatitis. / Ohta, Eriko; Itoh, Tomohiro; Nemoto, Tomomi; Kumagai, Jiro; Ko, Shigeru; Ishibashi, Kenichi; Ohno, Mayuko; Uchida, Keiko; Ohta, Akihito; Sohara, Eisei; Uchida, Shinichi; Sasaki, Sei; Rai, Tatemitsu.

In: American Journal of Physiology - Cell Physiology, Vol. 297, No. 6, 2009.

Research output: Contribution to journalArticle

Ohta, E, Itoh, T, Nemoto, T, Kumagai, J, Ko, S, Ishibashi, K, Ohno, M, Uchida, K, Ohta, A, Sohara, E, Uchida, S, Sasaki, S & Rai, T 2009, 'Pancreas-specific aquaporin 12 null mice showed increased susceptibility to caerulein-induced acute pancreatitis', American Journal of Physiology - Cell Physiology, vol. 297, no. 6. https://doi.org/10.1152/ajpcell.00117.2009
Ohta, Eriko ; Itoh, Tomohiro ; Nemoto, Tomomi ; Kumagai, Jiro ; Ko, Shigeru ; Ishibashi, Kenichi ; Ohno, Mayuko ; Uchida, Keiko ; Ohta, Akihito ; Sohara, Eisei ; Uchida, Shinichi ; Sasaki, Sei ; Rai, Tatemitsu. / Pancreas-specific aquaporin 12 null mice showed increased susceptibility to caerulein-induced acute pancreatitis. In: American Journal of Physiology - Cell Physiology. 2009 ; Vol. 297, No. 6.
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