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Titolo:
MECHANICAL STRAIN TIGHTLY CONTROLS FIBROBLAST GROWTH FACTOR-II RELEASE FROM CULTURED HUMAN VASCULAR SMOOTH-MUSCLE CELLS
Autore:
CHENG GC; BRIGGS WH; GERSON DS; LIBBY P; GRODZINSKY AJ; GRAY ML; LEE RT;
Indirizzi:
HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,DIV CARDIOVASC,75FRANCIS ST BOSTON MA 02115 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,DIV CARDIOVASC BOSTON MA 02115 MIT,DIV HLTH SCI & TECHNOL CAMBRIDGE MA 02139 MIT,DEPT MECH ENGN CAMBRIDGE MA 02139
Titolo Testata:
Circulation research
fascicolo: 1, volume: 80, anno: 1997,
pagine: 28 - 36
SICI:
0009-7330(1997)80:1<28:MSTCFG>2.0.ZU;2-Q
Fonte:
ISI
Lingua:
ENG
Soggetto:
PLASMINOGEN-ACTIVATOR PRODUCTION; CAPILLARY ENDOTHELIAL-CELLS; PLASMA-MEMBRANE DISRUPTIONS; SECRETORY SIGNAL SEQUENCE; EXTRACELLULAR-MATRIX; ATHEROSCLEROTIC PLAQUES; RECEPTOR; STRETCH; STRESS; EXPRESSION;
Keywords:
ATHEROSCLEROSIS; BIOMECHANICS; VASCULAR SMOOTH MUSCLE; FIBROBLAST GROWTH FACTOR;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
76
Recensione:
Indirizzi per estratti:
Citazione:
G.C. Cheng et al., "MECHANICAL STRAIN TIGHTLY CONTROLS FIBROBLAST GROWTH FACTOR-II RELEASE FROM CULTURED HUMAN VASCULAR SMOOTH-MUSCLE CELLS", Circulation research, 80(1), 1997, pp. 28-36

Abstract

Although fibroblast growth factor-2 (FGF-2) participates in the response to vascular injury, the role of cellular deformation in FGF-2 release is incompletely understood. To test the hypothesis that mechanicalstrain tightly controls FGF-2 release, a novel device was used to impose homogeneous and uniform biaxial strain to human vascular smooth muscle cells. Release of FGF-2 increased with the number of cycles of strain (14%, 1 Hz); 1; 9, and 90 cycles of strain, respectively, released 0.55+/-0.06%, 2.9+/-0.3%, and 5.5+/-1.3% of the total cellular FGF-2(versus 0.00+/-0.40% for control, P<.05), but release was not furtherincreased for strain of 90 to 90 000 cycles. Mechanical release of FGF-2 depended on both the frequency and amplitude of deformation. For example, strain (90 cycles, 1 Hz) at 4% amplitude released only 0.1+/-0.1% of the total FGF-2, but strain at 14% and 33% amplitudes, respectively, released 5.7+/-0.5% and 19.0+/-3.0% of the FGF-2 cellular pool (P<.05), suggesting a strain amplitude threshold for FGF-2 release. Injury to a subpopulation of cells increased with the frequency and amplitude of strain, but cells were not injured by strains below 10% amplitude. Strain following pretreatment with heparin released 12.6+/-1.6% of the total FGF-2 (versus 15.8+/-0.9% for strain alone, P<.05), indicating that most FGF-2 was liberated from the nuclear or cytoplasmic pools and not from low-affinity extracellular receptors. Conversely, strain in the presence of heparin released 25.2+/-3.5% of the total FGF-2 (versus 15.6+/-2.6% for strain alone, P<.05). Thus, cellular strain closely modulates the release of intracellular FGF-2 from human vascularsmooth muscle cells. but FGF-2 release is negligible in response to the smaller strains that occur in the normal artery. In addition, larger mechanical strains lead to transfer of intracellular FGF-2 to the extracellular low-affinity receptors, where FGF-2 may be displaced by heparin. These observations provide insight into the mechanisms by whichdeforming vascular injury, such as that produced by arterial interventions, may elicit a proliferative response.

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Documento generato il 30/11/20 alle ore 16:15:45