Regulation of acinar cell function in the pancreas

被引:54
作者
Williams, John A. [1 ,2 ]
机构
[1] Univ Michigan, Dept Mol & Integrat Physiol, Ann Arbor, MI 48109 USA
[2] Univ Michigan, Dept Internal Med, Ann Arbor, MI 48109 USA
关键词
calcium signaling; exocytosis; growth; receptors; secretion; HYDROGEN-SULFIDE; CALCIUM; PROTEIN; CHOLECYSTOKININ-58; TRANSLOCATION; EXPRESSION; SECRETION; MECHANISM; RELEASE; DELTA;
D O I
10.1097/MOG.0b013e32833d11c6
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Purpose of review This review identifies and puts into context the recent articles which have advanced understanding of the functions of pancreatic acinar cells and the mechanisms by which these functions are regulated. Recent findings Receptors present on acinar cells, particularly those for cholecystokinin and secretin, have been better characterized as to the molecular nature of the ligand-receptor interaction. Other reports have described the potential regulation of acinar cells by GLP-1 and cannabinoids. Intracellular Ca2+ signaling remains at the center of stimulus secretion coupling and its regulation has been further defined. Recent studies have identified specific channels mediating Ca2+ release from intracellular stores and influx across the plasma membrane. Work downstream of intracellular mediators has focused on molecular mechanisms of exocytosis particularly involving small G proteins, SNARE proteins and chaperone molecules. In addition to secretion, recent studies have further defined the regulation of pancreatic growth both in adaptive regulation to diet and hormones in the regeneration that occurs after pancreatic damage. Lineage tracing has been used to show the contribution of different cell types. The importance of specific amino acids as signaling molecules to activate the mTOR pathway is being elucidated. Summary Understanding the mechanisms that regulate pancreatic acinar cell function is contributing to knowledge of normal pancreatic function and alterations in disease.
引用
收藏
页码:478 / 483
页数:6
相关论文
共 50 条
[1]  
Ahmad SR, 2008, NEW ENGL J MED, V358, P1970
[2]   ATP depletion inhibits Ca2+ release, influx and extrusion in pancreatic acinar cells but not pathological Ca2+ responses induced by bile [J].
Barrow, Stephanie L. ;
Voronina, Svetlana G. ;
Xavier, Gabriela da Silva ;
Chvanov, Misha A. ;
Longbottom, Rebecca E. ;
Gerasimenko, Oleg V. ;
Petersen, Ole H. ;
Rutter, Guy A. ;
Tepikin, Alexei V. .
PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY, 2008, 455 (06) :1025-1039
[3]   Gastrointestinal growth factors and hormones have divergent effects on Akt activation [J].
Berna, Marc J. ;
Tapia, Jose A. ;
Sancho, Veronica ;
Thill, Michelle ;
Pace, Andrea ;
Hoffmann, K. Martin ;
Gonzalez-Fernandez, Lauro ;
Jensen, Robert T. .
CELLULAR SIGNALLING, 2009, 21 (04) :622-638
[4]   Myosin 2 Maintains an Open Exocytic Fusion Pore in Secretory Epithelial Cells [J].
Bhat, Purnima ;
Thorn, Peter .
MOLECULAR BIOLOGY OF THE CELL, 2009, 20 (06) :1795-1803
[5]   Essential requirement for two-pore channel 1 in NAADP-mediated calcium signaling [J].
Brailoiu, Eugen ;
Churamani, Dev ;
Cai, Xinjiang ;
Schrlau, Michael G. ;
Brailoiu, G. Cristina ;
Gao, Xin ;
Hooper, Robert ;
Boulware, Michael J. ;
Dun, Nae J. ;
Marchant, Jonathan S. ;
Patel, Sandip .
JOURNAL OF CELL BIOLOGY, 2009, 186 (02) :201-209
[6]   STIMulating store-operated Ca2+ entry [J].
Cahalan, Michael D. .
NATURE CELL BIOLOGY, 2009, 11 (06) :669-677
[7]   NAADP mobilizes calcium from acidic organelles through two-pore channels [J].
Calcraft, Peter J. ;
Ruas, Margarida ;
Pan, Zui ;
Cheng, Xiaotong ;
Arredouani, Abdelilah ;
Hao, Xuemei ;
Tang, Jisen ;
Rietdorf, Katja ;
Teboul, Lydia ;
Chuang, Kai-Ting ;
Lin, Peihui ;
Xiao, Rui ;
Wang, Chunbo ;
Zhu, Yingmin ;
Lin, Yakang ;
Wyatt, Christopher N. ;
Parrington, John ;
Ma, Jianjie ;
Evans, A. Mark ;
Galione, Antony ;
Zhu, Michael X. .
NATURE, 2009, 459 (7246) :596-U130
[8]   Mechanism of induction of pancreatic acinar cell apoptosis by hydrogen sulfide [J].
Cao, Yang ;
Adhikari, Sharmila ;
Ang, Abel Damien ;
Moore, Philip K. ;
Bhatia, Madhav .
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY, 2006, 291 (03) :C503-C510
[9]   Therapeutic potential for novel drugs targeting the type 1 cholecystokinin receptor [J].
Cawston, Erin E. ;
Miller, Laurence J. .
BRITISH JOURNAL OF PHARMACOLOGY, 2010, 159 (05) :1009-1021
[10]   Cholecystokinin-58 and cholecystokinin-8 exhibit similar actions on calcium signaling, zymogen secretion, and cell fate in murine pancreatic acinar cells [J].
Criddle, David N. ;
Booth, David M. ;
Mukherjee, Rajarshi ;
McLaughlin, Euan ;
Green, Gary M. ;
Sutton, Robert ;
Petersen, Ole H. ;
Reeve, Joseph R., Jr. .
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY, 2009, 297 (06) :G1085-G1092