© 1996 American Heart Association, Inc.
Articles |
Proliferating Arterial Smooth Muscle Cells After Balloon Injury Express TNF-
but Not Interleukin-1 or Basic Fibroblast Growth Factor
From the Department of Thoracic and Cardiovascular Surgery (H.T.), Tokyo Medical and Dental University, Japan, and the Vascular Medicine and Atherosclerosis Unit (G.S., D.S., P.L.), and the Cardiovascular Division (D.S., P.L.), Department of Medicine, Brigham and Women's Hospital, Boston, Mass.
Correspondence to Dr Peter Libby, Vascular Medicine and Atherosclerosis Unit, Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Longwood Medical Research Center, Room 307, 221 Longwood Ave, Boston, MA 02115.
Abstract We have recently reported that balloon withdrawal
injury to rabbit abdominal aortas induces sustained activation
indicated by the expression of certain adhesion molecules such as
vascular cell adhesion molecule-1 and intercellular adhesion molecule-1
in regenerating endothelial cells and/or proliferating
smooth muscle cells (SMCs). Local cytokine signaling may
contribute to ongoing modulation of cellular functions and
proliferation of intimal SMCs after acute vascular injury. We therefore
studied the expression of tumor necrosis factor-
(TNF-) and
interleukin-1ß (IL-1ß), proinflammatory and SMC
growth–promoting cytokines, and basic fibroblast growth
factor (bFGF) in SMCs of rabbit aorta at 2 (n=4), 5 (n=4), and
10 days
(n=6) after balloon injury. All animals were given bromodeoxyuridine
(BrdU, 10 mg/kg per day) continuously to label proliferating SMCs.
Frozen cross sections of injured vessels at each time point after
balloon injury were examined by immunoperoxidase staining with
monoclonal antibodies. As early as 2 days after injury, before intimal
thickening begins, foci of medial SMCs expressed TNF-, but not all
TNF-–positive medial SMCs had incorporated BrdU, suggesting
that TNF- expression by medial SMCs may precede their proliferation.
At 5 days, TNF-–bearing and BrdU-labeled medial SMCs increased
in number. At 10 days after injury, when uniform intimal thickening
occurred, almost all neointimal SMCs and foci of medial
SMCs labeled with BrdU. Most of the BrdU-positive (proliferating) SMCs
expressed immunoreactive TNF-. Reverse transcription polymerase
chain reaction showed increased TNF- mRNA at 10 days after
ballooning in the injured portion of the aorta. In contrast, regions of
SMC proliferation showed inconsistent IL-1ß expression,
and bFGF, abundant in normal rabbit arteries, was not detected in areas
of SMC replication. These data indicate that replication of
arterial SMCs after balloon injury occurs in regions of
TNF- but not IL-1ß expression and correlates inversely with the
presence of bFGF. These results indicate that SMC-derived TNF-
serves as a marker of modulated SMC phenotype after acute
vascular injury and may contribute to local cellular activation and
proliferation of SMCs at sites of arterial injury.
Key Words: smooth muscle cells • tumor necrosis factor– • balloon injury • proliferation
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