PMID- 24637240
OWN - NLM
STAT- MEDLINE
DCOM- 20140623
LR  - 20171116
IS  - 1873-2968 (Electronic)
IS  - 0006-2952 (Linking)
VI  - 89
IP  - 3
DP  - 2014 Jun 1
TI  - Catestatin decreases macrophage function in two mouse models of experimental 
      colitis.
PG  - 386-98
LID - S0006-2952(14)00161-0 [pii]
LID - 10.1016/j.bcp.2014.03.003 [doi]
AB  - Mucosal inflammation in patients with inflammatory bowel disease (IBD) is 
      characterized by an alteration of prohormone chromogranin A (CgA) production. The 
      recent demonstration of an implication of CgA in collagenous colitis and immune 
      regulation provides a potential link between CgA-derived peptides (catestatin, 
      CTS) and gut inflammation. Colitis was induced by administration of dextran 
      sulfate sodium or 2, 4 dinitrobenzenesulfonic acid to C57BL/6 mice. Treatment 
      with human (h)CTS or its proximal or distal part was started one day before 
      colitis induction and colonic inflammatory markers were determined. 
      Pro-inflammatory cytokines were evaluated in peritoneal isolated and bone marrow 
      derived macrophages (BMDMs); p-STAT3 level was studied. Serum levels of CgA and 
      CTS were assessed in experimental colitis and in a separate study in IBD patients 
      and healthy controls. We show that sera from IBD patients and that in 
      experimental colitis conditions the colonic level of mouse (m)CgA and mCTS are 
      significantly increased. Moreover, in vivo treatment with human (h)CTS reduces 
      the disease onset and suppresses exacerbated inflammatory responses in 
      preclinical settings of colitis associated with an increase of p-STAT3. In vitro, 
      hCTS treatment decreases proinflammatory cytokine release by peritoneal 
      macrophages and BMDMs and increases p-STAT3 levels. These results support the 
      hypothesis that CTS is increased during colitis and that hCTS modulates 
      intestinal inflammation via the macrophage population and through a STAT-3 
      dependent pathway in a murine model of colitis. Identification of the molecular 
      mechanism underlying the protective role of this peptide may lead to a novel 
      therapeutic option in IBD.
CI  - Copyright (c) 2014 Elsevier Inc. All rights reserved.
FAU - Rabbi, Mohammad F
AU  - Rabbi MF
AD  - University of Manitoba, Department of Immunology, Winnipeg, MB, Canada.
FAU - Labis, Benoit
AU  - Labis B
AD  - University of Manitoba, Department of Immunology, Winnipeg, MB, Canada.
FAU - Metz-Boutigue, Marie-Helene
AU  - Metz-Boutigue MH
AD  - Universite de Strasbourg, Biomateriaux et Ingenierie tissulaire, INSERM U1121, 1 
      Place de l'Hopital, 67091 Strasbourg, France.
FAU - Bernstein, Charles N
AU  - Bernstein CN
AD  - University of Manitoba, IBD Clinical and Research Centre and Section of 
      Gastroenterology, Winnipeg, MB, Canada.
FAU - Ghia, Jean-Eric
AU  - Ghia JE
AD  - University of Manitoba, Department of Immunology, Winnipeg, MB, Canada; 
      University of Manitoba, IBD Clinical and Research Centre and Section of 
      Gastroenterology, Winnipeg, MB, Canada. Electronic address: jeghia@yahoo.fr.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140314
PL  - England
TA  - Biochem Pharmacol
JT  - Biochemical pharmacology
JID - 0101032
RN  - 0 (Benzenesulfonates)
RN  - 0 (Chromogranin A)
RN  - 0 (Peptide Fragments)
RN  - 0 (STAT3 Transcription Factor)
RN  - 0 (chromogranin A (344-364))
RN  - 3WF0U675G6 (2,4-dinitrobenzenesulfonic acid)
RN  - 9042-14-2 (Dextran Sulfate)
SB  - IM
MH  - Animals
MH  - Benzenesulfonates/toxicity
MH  - Chromogranin A/*metabolism
MH  - Colitis/*chemically induced/*drug therapy
MH  - Dextran Sulfate/toxicity
MH  - Humans
MH  - Inflammation/metabolism
MH  - Macrophages/*drug effects
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Peptide Fragments/*metabolism
MH  - STAT3 Transcription Factor/genetics/metabolism
MH  - Serum
OTO - NOTNLM
OT  - Catestatin
OT  - Chromogranin A
OT  - Experimental colitis
OT  - Macrophages
OT  - STAT3
EDAT- 2014/03/19 06:00
MHDA- 2014/06/24 06:00
CRDT- 2014/03/19 06:00
PHST- 2013/12/27 00:00 [received]
PHST- 2014/03/04 00:00 [revised]
PHST- 2014/03/06 00:00 [accepted]
PHST- 2014/03/19 06:00 [entrez]
PHST- 2014/03/19 06:00 [pubmed]
PHST- 2014/06/24 06:00 [medline]
AID - S0006-2952(14)00161-0 [pii]
AID - 10.1016/j.bcp.2014.03.003 [doi]
PST - ppublish
SO  - Biochem Pharmacol. 2014 Jun 1;89(3):386-98. doi: 10.1016/j.bcp.2014.03.003. Epub 
      2014 Mar 14.