title: Autophagy regulation in pancreatic acinar cells is independent of epidermal growth factor receptor signaling.
abstract: Autophagy is an intracellular degradation system in eukaryotic cells that occurs at a basal level. It can also be induced in response to environmental signals including nutrients, hormones, microbial pathogens, and growth factors, although the mechanism is not known in detail. We previously demonstrated that excessive autophagy is induced within pancreatic acinar cells deficient in Spink3, which is a trypsin inhibitor. SPINK1, the human homolog of murine Spink3, has structural similarity to epidermal growth factor (EGF), and can bind and stimulate the EGF receptor (EGFR). To analyze the role of the EGFR in pancreatic development, in the regulation of autophagy in pancreatic acinar cells, and in cerulein-induced pancreatitis, we generated and examined acinar cell-specific Egfr-deficient (Egfr(-/-)) mice. Egfr(-/-) mice showed no abnormalities in pancreatic development, induction of autophagy, or cerulein-induced pancreatitis, suggesting that Egfr is dispensable for autophagy regulation in pancreatic acinar cells.
authors.affiliation: Institute of Resource Development and Analysis, Kumamoto University, Kumamoto, Japan; Department of Gastroenterological Surgery, Kumamoto University, Kumamoto, Japan.
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Ozaki
authors.affiliation: Institute of Resource Development and Analysis, Kumamoto University, Kumamoto, Japan.
authors.forename: Yuko
authors.initials: Y
authors.lastname: Fukuchi
authors.affiliation: Institute of Resource Development and Analysis, Kumamoto University, Kumamoto, Japan.
authors.forename: Syun-rou
authors.initials: SR
authors.lastname: Tomiyoshi
authors.affiliation: Institute of Resource Development and Analysis, Kumamoto University, Kumamoto, Japan.
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Uehara
authors.affiliation: Institute of Resource Development and Analysis, Kumamoto University, Kumamoto, Japan; Department of Gastroenterological Surgery, Kumamoto University, Kumamoto, Japan.
authors.forename: Satoshi
authors.initials: S
authors.lastname: Ida
authors.affiliation: Department of Pathophysiology, College of Basic Medical Sciences, Dalian Medical University, Dalian, China.
authors.forename: Jung
authors.initials: J
authors.lastname: Wang
authors.affiliation: Institute of Resource Development and Analysis, Kumamoto University, Kumamoto, Japan.
authors.forename: Kimi
authors.initials: K
authors.lastname: Araki
authors.affiliation: Department of Medicine I, Medical University of Vienna, Austria.
authors.forename: Maria
authors.initials: M
authors.lastname: Sibilia
authors.affiliation: Department of Gastroenterological Surgery, Kumamoto University, Kumamoto, Japan.
authors.forename: Hideo
authors.initials: H
authors.lastname: Baba
authors.affiliation: Institute of Resource Development and Analysis, Kumamoto University, Kumamoto, Japan.
authors.forename: Ken-ichi
authors.initials: K
authors.lastname: Yamamura
authors.affiliation: Institute of Resource Development and Analysis, Kumamoto University, Kumamoto, Japan. Electronic address: ohmuraya@kumamoto-u.ac.jp.
authors.forename: Masaki
authors.initials: M
authors.lastname: Ohmuraya
mesh_terms: D061354:Acinar Cells / Q000166:cytology / Q000378:metabolism; D000818:Animals; D001343:Autophagy / Q000502:physiology*; D002352:Carrier Proteins / Q000378:metabolism; D002108:Ceruletide / Q000633:toxicity; D066246:ErbB Receptors / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D005260:Female; D006023:Glycoproteins / Q000172:deficiency / Q000235:genetics / Q000378:metabolism; D006801:Humans; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D046790:Pancreas, Exocrine / Q000166:cytology* / Q000378:metabolism*; D010195:Pancreatitis / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology; D029584:Prostatic Secretory Proteins / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction; D014359:Trypsin Inhibitor, Kazal Pancreatic
chemical_list: D002352:Carrier Proteins; D006023:Glycoproteins; D029584:Prostatic Secretory Proteins; C486642:SPINK1 protein, human; C487134:Spink1 protein, mouse; D014359:Trypsin Inhibitor, Kazal Pancreatic; D002108:Ceruletide; C541485:EGFR protein, mouse; D066246:ErbB Receptors
keywords: Acute pancreatitis; Autophagy; EGFR; SPINK1/Spink3