PMID- 9528978
OWN - NLM
STAT- MEDLINE
DCOM- 19980414
LR  - 20181201
IS  - 0013-7227 (Print)
IS  - 0013-7227 (Linking)
VI  - 139
IP  - 4
DP  - 1998 Apr
TI  - Regulation of endothelial production of C-type natriuretic peptide by interaction 
      between endothelial cells and macrophages.
PG  - 1920-6
AB  - We demonstrated endothelial production of C-type natriuretic peptide (CNP), the 
      third member of the natriuretic peptide family, and its regulation by cytokines, 
      including tumor necrosis factor-alpha (TNF alpha). We thus proposed that CNP can 
      control vascular tone and growth as an endothelium-derived relaxing peptide. We 
      also revealed the marked elevation of plasma CNP concentration in patients with 
      septic shock, in which TNF alpha plays a significant part. As the interaction 
      between endothelial cells (EC) and monocytes-macrophages plays a pivotal role in 
      the pathogenesis of atherosclerosis, we investigated the effect of coculture of 
      EC and macrophages on endothelial production of CNP. We used a human monocytic 
      leukemia cell line, THP-1, which differentiates into macrophages when treated 
      with phorbol 12-myristate 13-acetate. The coculture of EC and THP-1-derived 
      macrophages enhanced CNP secretion by more than 10-fold compared with the single 
      culture of EC or the coculture of EC and THP-1 without phorbol 12-myristate 
      13-acetate treatment. Prevention of direct contact between EC and THP-1-derived 
      macrophages did not attenuate the increase in CNP secretion. Northern blotting 
      revealed the augmentation of CNP messenger RNA expression in EC in the coculture. 
      We detected TNF alpha in the conditioned medium from the coculture of EC and 
      THP-1-derived macrophages. Furthermore, anti-TNF alpha antibody inhibited the 
      stimulation of CNP secretion in the coculture. CNP at a concentration of 1 nM did 
      not stimulate cGMP production in EC or THP-1-derived macrophages, but it elevated 
      cGMP production significantly in vascular smooth muscle cells. These results 
      indicate that endothelial production of CNP is stimulated mainly by TNF alpha 
      released from THP-1-derived macrophages in the coculture. Endothelial CNP at the 
      enhanced level may be one of the vascular mediators to regulate local vascular 
      tone and growth through cGMP production by vascular smooth muscle cells, 
      suggesting the potential significance of endothelial CNP in atherosclerosis.
FAU - Suga, S I
AU  - Suga SI
AD  - Department of Medicine and Clinical Science, Kyoto University Graduate School of 
      Medicine, Japan.
FAU - Itoh, H
AU  - Itoh H
FAU - Komatsu, Y
AU  - Komatsu Y
FAU - Ishida, H
AU  - Ishida H
FAU - Igaki, T
AU  - Igaki T
FAU - Yamashita, J
AU  - Yamashita J
FAU - Doi, K
AU  - Doi K
FAU - Chun, T H
AU  - Chun TH
FAU - Yoshimasa, T
AU  - Yoshimasa T
FAU - Tanaka, I
AU  - Tanaka I
FAU - Nakao, K
AU  - Nakao K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Endocrinology
JT  - Endocrinology
JID - 0375040
RN  - 0 (Culture Media, Conditioned)
RN  - 0 (Immune Sera)
RN  - 0 (Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 127869-51-6 (Natriuretic Peptide, C-Type)
RN  - 85637-73-6 (Atrial Natriuretic Factor)
RN  - H2D2X058MU (Cyclic GMP)
SB  - IM
MH  - Animals
MH  - Atrial Natriuretic Factor/pharmacology
MH  - Carotid Arteries
MH  - Cattle
MH  - Cell Communication
MH  - Cell Line
MH  - Cells, Cultured
MH  - *Coculture Techniques
MH  - Culture Media, Conditioned
MH  - Cyclic GMP/biosynthesis
MH  - Endothelium, Vascular/*cytology/*metabolism
MH  - Gene Expression
MH  - Humans
MH  - Immune Sera/pharmacology
MH  - Macrophages/*physiology
MH  - Natriuretic Peptide, C-Type
MH  - *Protein Biosynthesis
MH  - Proteins/genetics/metabolism
MH  - RNA, Messenger/metabolism
MH  - Tumor Necrosis Factor-alpha/antagonists & inhibitors/metabolism
EDAT- 1998/04/07 00:00
MHDA- 1998/04/07 00:01
CRDT- 1998/04/07 00:00
PHST- 1998/04/07 00:00 [pubmed]
PHST- 1998/04/07 00:01 [medline]
PHST- 1998/04/07 00:00 [entrez]
AID - 10.1210/endo.139.4.5918 [doi]
PST - ppublish
SO  - Endocrinology. 1998 Apr;139(4):1920-6. doi: 10.1210/endo.139.4.5918.