PMID- 10642280
OWN - NLM
STAT- MEDLINE
DCOM- 20000209
LR  - 20190722
IS  - 0194-911X (Print)
IS  - 0194-911X (Linking)
VI  - 35
IP  - 1 Pt 1
DP  - 2000 Jan
TI  - Role of transforming growth factor-beta1 in cardiovascular inflammatory changes 
      induced by chronic inhibition of nitric oxide synthesis.
PG  - 86-90
AB  - We previously reported that chronic inhibition of nitric oxide (NO) synthesis 
      with N(omega)-nitro-L-arginine methyl ester (L-NAME) induces inflammatory changes 
      (monocyte infiltration, myofibroblast formation, and monocyte chemoattractant 
      protein-1 [MCP-1] and transforming growth factor-beta1 [TGF-beta1] expression) in 
      the rat heart and vessel. There is debate regarding whether TGF-beta1 exhibits 
      proinflammatory or anti-inflammatory activities. We used the rat model to 
      investigate the role of TGF-beta in the pathogenesis of such inflammatory 
      changes. We show here that infiltrating monocytes and myofibroblasts in the 
      inflammatory lesions produced TGF-beta1 on the third day of L-NAME 
      administration. Cotreatment with a monoclonal antibody against TGF-beta1, but not 
      with control IgG, prevented the L-NAME-induced cardiac inflammation. The antibody 
      also significantly inhibited the gene expression of MCP-1, P-selectin, and 
      intercellular adhesion molecule-1. In summary, the antibody against TGF-beta1 
      prevented inflammatory changes in rat heart and vessel induced by chronic 
      inhibition of NO synthesis, suggesting that increased production of TGF-beta1 is 
      involved in the inflammatory changes in this model.
FAU - Koyanagi, M
AU  - Koyanagi M
AD  - Department of Cardiovascular Medicine, Cardiovascular Science, Graduate School of 
      Medical Sciences, Kyushu University, Fukuoka, Japan.
FAU - Egashira, K
AU  - Egashira K
FAU - Kubo-Inoue, M
AU  - Kubo-Inoue M
FAU - Usui, M
AU  - Usui M
FAU - Kitamoto, S
AU  - Kitamoto S
FAU - Tomita, H
AU  - Tomita H
FAU - Shimokawa, H
AU  - Shimokawa H
FAU - Takeshita, A
AU  - Takeshita A
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Hypertension
JT  - Hypertension (Dallas, Tex. : 1979)
JID - 7906255
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Chemokine CCL2)
RN  - 0 (P-Selectin)
RN  - 0 (RNA, Messenger)
RN  - 0 (Transforming Growth Factor beta)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - V55S2QJN2X (NG-Nitroarginine Methyl Ester)
SB  - IM
MH  - Animals
MH  - Antibodies, Monoclonal/pharmacology
MH  - Cardiovascular Diseases/*etiology/pathology/physiopathology
MH  - Chemokine CCL2/genetics
MH  - Coronary Vessels/pathology/physiopathology
MH  - Gene Expression
MH  - Heart/physiopathology
MH  - Inflammation/*etiology/pathology/physiopathology
MH  - Intercellular Adhesion Molecule-1/genetics
MH  - Male
MH  - Monocytes/pathology/physiology
MH  - Myocardium/pathology
MH  - NG-Nitroarginine Methyl Ester/pharmacology
MH  - Nitric Oxide/biosynthesis
MH  - P-Selectin/genetics
MH  - RNA, Messenger/genetics/metabolism
MH  - Rats
MH  - Rats, Inbred WKY
MH  - Transforming Growth Factor beta/antagonists & inhibitors/*physiology
EDAT- 2000/01/21 00:00
MHDA- 2000/01/21 00:01
CRDT- 2000/01/21 00:00
PHST- 2000/01/21 00:00 [pubmed]
PHST- 2000/01/21 00:01 [medline]
PHST- 2000/01/21 00:00 [entrez]
AID - 10.1161/01.hyp.35.1.86 [doi]
PST - ppublish
SO  - Hypertension. 2000 Jan;35(1 Pt 1):86-90. doi: 10.1161/01.hyp.35.1.86.