title: Severe acute pancreatitis is associated with upregulation of the ACE2-angiotensin-(1-7)-Mas axis and promotes increased circulating angiotensin-(1-7).
abstract: OBJECTIVE
  Angiotensin-converting enzyme 2 (ACE2), its product angiotensin-(1-7) and its receptor Mas may counteract the adverse effects of the ACE-angiotensin receptor II-AT(1) axis in many diseases. We examined the expression of these novel components of the rennin-angiotensin system in an experimental mouse model of severe acute pancreatitis (SAP).
  
  
  METHODS
  SAP was induced by six intraperitoneal injections of caerulein, and mice were sacrificed at 2, 12, 24, 48 and 72 h post disease-induction (normal control group mice were sacrificed at 2 h post disease-induction). Tissue and blood were collected for biochemical detection, gene and protein expression by qRT-PCR and western blot analysis, enzyme-linked immunosorbent assay and immunohistology detection.
  
  
  RESULTS
  Pancreatic ACE2 gene and protein expression, plasma and pancreatic angiotensin-(1-7) levels and Mas receptor gene and protein expression were significantly increased (p < 0.05) following SAP induction compared with the normal control group.
  
  
  CONCLUSIONS
  Severe acute pancreatitis is associated with upregulation of the ACE2-angiotensin-(1-7)-Mas axis and promotes increased circulating angiotensin-(1-7). These results support the presence of an ACE2-angiotensin-(1-7)-Mas axis in pancreatitis.
authors.affiliation: Emergency Department, Capital Medical University, Beijing Friendship Hospital, Beijing, China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Wang
authors.forename: Jing
authors.initials: J
authors.lastname: Wang
authors.forename: Ruixia
authors.initials: R
authors.lastname: Liu
authors.forename: Haiyu
authors.initials: H
authors.lastname: Qi
authors.forename: Yan
authors.initials: Y
authors.lastname: Wen
authors.forename: Fangfang
authors.initials: F
authors.lastname: Sun
authors.forename: Chenghong
authors.initials: C
authors.lastname: Yin
mesh_terms: D000208:Acute Disease; D000803:Angiotensin I / Q000097:blood*; D000085962:Angiotensin-Converting Enzyme 2; D000818:Animals; D002108:Ceruletide; D004195:Disease Models, Animal; D008297:Male; D051379:Mice; D010179:Pancreas / Q000378:metabolism; D010195:Pancreatitis / Q000139:chemically induced / Q000503:physiopathology*; D010446:Peptide Fragments / Q000097:blood*; D007703:Peptidyl-Dipeptidase A / Q000502:physiology*; D000090063:Proto-Oncogene Mas; D011518:Proto-Oncogene Proteins / Q000502:physiology*; D043562:Receptors, G-Protein-Coupled / Q000502:physiology*; D012084:Renin-Angiotensin System / Q000502:physiology*; D015854:Up-Regulation
chemical_list: D010446:Peptide Fragments; D000090063:Proto-Oncogene Mas; D011518:Proto-Oncogene Proteins; D043562:Receptors, G-Protein-Coupled; D002108:Ceruletide; D000803:Angiotensin I; D007703:Peptidyl-Dipeptidase A; C000705328:Ace2 protein, mouse; D000085962:Angiotensin-Converting Enzyme 2; C118790:angiotensin I (1-7)