PMID- 8609426
OWN - NLM
STAT- MEDLINE
DCOM- 19960529
LR  - 20131121
IS  - 0022-1767 (Print)
IS  - 0022-1767 (Linking)
VI  - 156
IP  - 8
DP  - 1996 Apr 15
TI  - Estrogen suppression of connective tissue deposition in a murine model of 
      peritoneal adhesion formation.
PG  - 3036-42
AB  - Estrogen's involvement in inflammation and wound healing is poorly understood. To 
      examine the role of estrogen in peritoneal adhesion formation, we gave 
      ovariectomized female C57BL/6 mice time-release pellets containing placebo, 0.05 
      mg 17 beta-estradiol (low E2), or 5 mg 17 beta-estradiol (high E2) before i.p. 
      injection of talc in saline or saline alone. Analyses of abdominal wall 
      connective tissue thickness and peritoneal cell populations were performed. 
      Talc-treated mice receiving low and high E2 replacement had a decreased amount of 
      abdominal connective tissue deposition (29% and 65% decrease, respectively) as 
      compared with talc-treated mice receiving placebo pellets. At high E2 
      replacement, the difference in connective tissue deposition was significant 
      statistically (p less than 0.01). Immunohistochemical analysis revealed that the 
      number of macrophages in adhesion tissue was proportionate to the amount of 
      connective tissue present, regardless of the circulating levels of E2. Northern 
      blot analysis of abdominal wall tissue showed that five of six talc-treated 
      animals given placebo expressed mRNA for the murine monocyte chemoattractant 
      protein-1 (MCP-1), JE. Conversely, only one of five talc-treated animals that 
      received E2 replacement expressed JE/MCP-1 mRNA, suggesting that the hormone may 
      inhibit connective tissue deposition by altering the production of chemotactic 
      factors. Furthermore, E2 suppressed talc-induced expression of JE/MCP-1 mRNA in 
      murine macrophages. Since macrophages play a central role in the wound healing 
      process, these studies suggest that E2 inhibition of adhesion formation could be 
      mediated by suppressing macrophage activation and/or recruitment to inflammatory 
      sites.
FAU - Frazier-Jessen, M R
AU  - Frazier-Jessen MR
AD  - Department of Cell Biology, Loyola University, Maywood, IL 60153, USA.
FAU - Mott, F J
AU  - Mott FJ
FAU - Witte, P L
AU  - Witte PL
FAU - Kovacs, E J
AU  - Kovacs EJ
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Chemokine CCL2)
RN  - 0 (Immunosuppressive Agents)
RN  - 0 (RNA, Messenger)
RN  - 14807-96-6 (Talc)
RN  - 4TI98Z838E (Estradiol)
SB  - IM
MH  - Abdomen
MH  - Animals
MH  - Chemokine CCL2/genetics
MH  - Connective Tissue/chemistry/pathology
MH  - Disease Models, Animal
MH  - Estradiol/*therapeutic use
MH  - Female
MH  - Immunosuppressive Agents/*therapeutic use
MH  - Macrophages/drug effects/pathology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Organ Size/drug effects
MH  - Ovariectomy
MH  - Peritoneal Diseases/immunology/*pathology/*prevention & control
MH  - RNA, Messenger/biosynthesis/drug effects
MH  - Talc/toxicity
MH  - Tissue Adhesions
EDAT- 1996/04/15 00:00
MHDA- 1996/04/15 00:01
CRDT- 1996/04/15 00:00
PHST- 1996/04/15 00:00 [pubmed]
PHST- 1996/04/15 00:01 [medline]
PHST- 1996/04/15 00:00 [entrez]
PST - ppublish
SO  - J Immunol. 1996 Apr 15;156(8):3036-42.