Biaxial Mechanical Strain Research Articles

Electroluminescence from metal/oxide/strained-Si tunneling diodes

The metal-oxide-silicon light-emitting diode under biaxial tensile mechanical strain is studied. The emission line shape of the device can be fitted by the electron-hole-plasma recombination model. The energy gap of strained Si extracted by the light emission spectra at the temperature of 120 K is reduced by 15 meV under 0.13% biaxial tensile strain. The light intensity of the device under 0.13% biaxial tensile strain increases 9% as compared to the relaxed-Si device. The upshift of valence band edge under mechanical strain to increase the majority hole concentration at the oxide∕Si interface may be responsible for this light emission enhancement. The mechanical strain is measured by Raman spectroscopy, strain gauge, and analyzed by the finite element method.

Mechanically Strained Si–SiGe HBTs

The current gain (/spl beta/=I/sub C//I/sub B/) variations of the mechanically strained Si-SiGe heterojunction bipolar transistor (HBT) and Si bipolar junction transistor (BJT) devices are investigated experimentally and theoretically. The /spl beta/ change of HBT is found to be 4.2% and -7.8 under the biaxial compressive and tensile mechanical strain of 0.028%, respectively. For comparison, there are 4.9% and -5.0 /spl beta/ variations for BJT under the biaxial compressive and tensile mechanical strain of 0.028%, respectively. In HBT, the mechanical stress is competing with the compressive strain of SiGe base, inherited from the lattice misfit between SiGe and Si. The current change due to externally mechanical stress is the combinational effects of the dependence of the mobility and the intrinsic carrier concentration on strain.

Direct biomechanical induction of endogenous calcineurin inhibitor Down Syndrome Critical Region-1 in cardiac myocytes.

Signaling through the protein phosphatase calcineurin may play a critical role in cardiac hypertrophy. The gene for Down Syndrome Critical Region-1 (DSCR1) encodes a protein that is an endogenous calcineurin inhibitor. This study was designed to test the hypothesis that DSCR1 is directly induced by biomechanical stimuli. Neonatal rat cardiac myocytes were exposed to biaxial cyclic mechanical strain; mechanical strain upregulated DSCR1 mRNA expression in a time- and amplitude-dependent manner (3.4 +/- 0.2-fold at 8% strain for 6 h, n = 11, P < 0.01), and this induction was angiotensin II and endothelin I independent. Biomechanical induction of DSCR1 mRNA was partially blocked by calcineurin inhibition with cyclosporine A (30 +/- 5%, n = 3, P < 0.01). DSCR1 promoter-reporter experiments showed that mechanical strain induced DSCR1 promoter activity by 2.3-fold and that this induction was completely inhibited by cyclosporin A. Furthermore, DSCR1 gene expression was increased in the left ventricles of mice with pressure-overload hypertrophy induced by transverse aortic banding. These data demonstrate that biomechanical strain directly induces gene expression for the calcineurin inhibitor DSCR1 in cardiac myocytes, indicating that mechanically induced DSCR1 may regulate the hypertrophic response to mechanical overload.

Regulation of syndecan-4 expression with mechanical stress during the development of angioplasty-induced intimal thickening

In this study, we postulated that acute mechanical strain of the arterial wall induces changes in syndecan-4 expression that in turn may modulate cellular events, which promote neointima formation. Correlative in vivo and in vitro studies were performed to determine whether: (1) balloon injury of the rat carotid artery induces spatially and temporally regulated changes in syndecan-4 messenger RNA (mRNA) and protein expression; (2) the application of biaxial mechanical strain to cultured vascular wall cells regulates the expression of syndecan-4 mRNA and protein and its cell surface distribution and surface shedding; and (3) shed syndecan-4 directly effects cell motility behavior. We observed that syndecan-4 mRNA and protein expression were regulated in a temporally and spatially specific manner, such that initial expression of syndecan-4 was localized to adventitial cells followed by later expression in the neointima. Notably, in vitro stimulation of isolated adventitial fibroblasts with a mechanical stretch protocol that was designed to mimic in vivo balloon injury produced a rapid increase in syndecan-4 (4.3-fold increase; P < .001) that was accompanied both by enhanced protein shedding and by the disassembly of focal adhesions. Also significant was that shed syndecan-4, induced with mechanically conditioned media, appeared to be responsible for a chemotactic response of adventitial fibroblasts ( P = .005). These results indicate that mechanical strain tightly regulates syndecan-4 expression, which may, in part, provide a mechanism for the activation of myofibroblast migration from the tunica adventitia into the neointima. (J Vasc Surg 2002;36:361-70.)

Identification of mechanically induced genes in human monocytic cells by DNA microarrays.

Hypertension is a risk factor for coronary heart disease. Macrophages are critically involved in both atherogenesis and plaque instability. Although macrophages may be subjected to excess mechanical stress in these diseases, the way in which biomechanical forces affect macrophage function remains incompletely defined. To investigate the molecular response to mechanical force in macrophages. We used a DNA microarray with 1056 genes to describe the transcriptional profile of mechanically induced genes in human monocytic THP-1 cells. Mechanical deformation was applied to a thin and transparent membrane on which cells were cultured. After THP-1 cells were pre-incubated in the presence of phorbol 12-myristate 13-acetate (0.2 micromol/l) for 24 h, THP-1 cells attached to the membrane were subjected to biaxial mechanical strain. Interleukin-8 concentrations were determined using an enzyme-linked immunosorbent assay. In DNA microarray analysis, cyclic mechanical strain at 1 Hz induced only three genes more than 2.5-fold at 3 and 6 h in THP-1 cells: prostate apoptosis response-4 (3.0-fold at 3 h, 6.7-fold at 6 h), interleukin-8 (4.3-fold at 6 h) and the immediate-early response gene, IEX-1 (2.6-fold at 6 h). Real-time reverse transcriptase polymerase chain reaction analysis confirmed the amplitude-dependent induction of these three genes. In addition, mechanical strain increased interleukin-8 protein expression. The present study demonstrates that human monocytic cells respond to mechanical deformation with induction of immediate-early and inflammatory genes. These findings suggest that mechanical stress in vivo, such as that associated with hypertension, may play an important part in atherogenesis and instability of coronary artery plaques, through biomechanical effects on vascular macrophages.

Peroxisome proliferator-activated receptor gamma activators inhibit cardiac hypertrophy in cardiac myocytes.

Peroxisome proliferator-activated receptors (PPARs) are transcription factors belonging to the nuclear receptor superfamily. PPARgamma mRNA is present in cardiac myocytes; however, whether PPARgamma affects cardiac hypertrophy remains unknown. We investigated the effects of PPARgamma activators on cardiac hypertrophy in neonatal rat cardiac myocytes. Cyclic 4% biaxial mechanical strain caused enlargement of cardiac myocytes (1.3-fold versus control, P<0.0001), but the PPARgamma activators troglitazone and 15-deoxy-Delta(12-14)-prostaglandin J(2) (15d-PGJ(2)) (10 micromol/L) inhibited this effect (troglitazone, -72%, P<0.0005; 15d-PGJ(2), -88%, P<0.0002). Total cell protein was increased by mechanical strain (control, 164.3 microgram/dish; strain, 265.5, P<0.0002), and this effect was inhibited by troglitazone and 15d-PGJ(2) (troglitazone, -61%, P<0.005; 15d-PGJ(2), -72%, P<0.001). [(3)H]Leucine uptake was also increased by mechanical strain (1.9-fold versus control, P<0.002), and this increase was inhibited by troglitazone and 15d-PGJ(2) (troglitazone, -52% at 10 micromol/L, P<0.01; 15d-PGJ(2), -70% at 10 micromol/L, P<0.005). An increase in [(3)H]leucine uptake induced by angiotensin II or phenylephrine was significantly inhibited by troglitazone and 15d-PGJ(2). Mechanical strain induced mRNA expression for brain natriuretic peptide, but PPARgamma activators inhibited this induction. Furthermore, PPARgamma activators inhibited mechanically induced activation of nuclear factor (NF)-kappaB. Pyrrolidine dithiocarbamate, an inhibitor of NF-kappaB activation, inhibited strain-induced [(3)H]leucine uptake (-50% at 100 micromol/L, P<0.05). These results demonstrate that PPARgamma activators inhibit cardiac hypertrophy in cardiac myocytes and suggest that PPARgamma activators may regulate cardiomyocyte hypertrophy at least partially through the NF-kappaB pathway.

The proliferative response of isolated human tendon fibroblasts to cyclic biaxial mechanical strain.

At the cellular level, dynamic strain plays a key role in cell stimulation and organization of the extracellular matrix. Although positive effects of physical strain on tendon tissue are well known, little knowledge exists on how mechanical strain affects tendon cells. In this study, human tendon fibroblasts from patellar tendon were cultured on silicone dishes. Subsequently, cyclic biaxial mechanical strain was applied to the dishes for 15, 30, and 60 minutes using a specially developed cell stretching system. After the fibroblasts were strained, cells were tested for proliferation at 6, 12, and 24 hours. As a control, cells were grown on silicone dishes but did not receive any strain. A biphasic response in proliferation was observed for the 15- and 60-minute strain periods: at 6 hours and 24 hours there was more proliferation than at 12 hours. After a strain duration time of 30 minutes, a lower proliferation rate was measured compared with control levels. This study shows that application of mechanical stress to tendon fibroblasts resulted in an alteration of cellular proliferation depending on the stress time. Our results may implicate future modifications in the treatment of ligament and tendon injuries.

Anisotropic effective mass and scattering of electrons in mismatched heteroepitaxial films

InP layers grown epitaxially on silicon substrates show a pronounced anisotropy of the transverse magnetoresistance. We use this effect to study the ensuing anisotropy of the effective mass and scattering mechanisms of electrons. We investigated samples with an electron concentration from 7×1016 to 9.6×1017 cm−3 at temperatures ranging from 4.2 to 30 K in magnetic fields of up to 15 T. The sample with the lowest electron concentration showed an anisotropic negative magnetoresistance which we attribute to weak localization. This allows the characteristic times for inelastic scattering (coherence time) and for spin–orbit interaction to be determined. For the InP layers on Si of higher electron concentration we measured for the first time Shubnikov-de Haas oscillations, showing again anisotropy of the effective mass and of the Dingle temperature. We quantitatively ascribe differences from the bulk values to biaxial mechanical strain, distorting the Fermi sphere of bulk material to an ellipsoid. We assume that the observed anisotropies are due to a preferential orientation of crystal defects as a result of differences in the thermal expansion coefficient of the InP film and the Si substrate.

Mechanical Strain-Induced Proliferation of Osteoblastic Cells Parallels Increased TGF-β1 mRNA

It is well known that mechanical stimulation can prompt healing of bone fractures. However, the mechanism involved is less clear. In this study, we found that a 0.17% cyclic, biaxial mechanical strain delivered at 1 Hz increased proliferation of MC3T3-E1 cells, a clonal osteoblastic cell line. Mechanical strain also increased the level of TGF-β1 mRNA determined by quantitative reverse transcription/polymerase chain reaction. Previous reports have shown that neomycin and W-7, which are inhibitors in the inositol phosphate/calmodulin pathway, blocked mechanical strain-induced proliferation of the osteoblast cells. Interestingly, we found that neomycin and W-7 can also block mechanical stimulation-induced elevation of TGF-β1 mRNA. Finally, using an antibody which blocked the action of TGF-β1, we found that the increased MC3T3-E1 cell proliferation induced by mechanical strain did not depend on the action of TGF-β1.

The inositol phosphate pathway as a mediator in the proliferative response of rat calvarial bone cells to cyclical biaxial mechanical strain.

Isolated newborn rat calvarial bone cells grown in monolayer on polyurethane membranes in specially constructed culture chambers and subjected to a cyclical biaxial mechanical strain of 0.17% at a frequency of 1 Hz for 30 min demonstrated a 16% increase in DNA synthesis during the subsequent 24 h. The metabolites of the inositol phosphate pathway, shown to be an important second messenger in many cell types, were shown to be elevated using high-performance liquid chromatography to separate and quantitate the various inositol polyphosphates. Inositol 1,4,5-trisphosphate, inositol 1,4-bisphosphate, and inositol 1,3,4,5-tetrakisphosphate reached peak accumulations after 20 s of mechanical strain. Inositol 1,3,4-trisphosphate reached a peak accumulation after 2 min, and inositol 1,2,3,4,5,6 phosphate reached a peak accumulation after 60 min of mechanical strain. Neomycin, an inhibitor of phospholipase C, a membrane-bound enzyme that hydrolyzes phosphatidyl inositol 4,5-bisphosphate to start the inositol phosphate cascade, completely inhibited accumulation of the above inositol phosphates during mechanical straining of the bone cells. Neomycin also completely abolished the increase in DNA synthesis that was seen after a mechanical strain of 0.17%. It is concluded from this study that the inositol phosphate pathway is activated by mechanical strain in bone cells and that this pathway is an important and primary mediator in the transduction of mechanical strain into cellular proliferation in these cells.

The proliferative and synthetic response of isolated calvarial bone cells of rats to cyclic biaxial mechanical strain.

Isolated bone cells from the calvaria of newborn rats were grown in monolayer on polyurethane membranes in specially constructed culture chambers. These were subjected to cyclic biaxial mechanical strains of 0.02 per cent (200 microstrain), 0.04 per cent (400 microstrain), and 0.1 per cent (1000 microstrain) at a frequency of one hertz for periods ranging from fifteen minutes to seventy-two hours. DNA content, an index of proliferation, was significantly increased at a strain of 0.04 per cent applied for fifteen minutes and for twenty-four and forty-eight hours. DNA content was not increased at the other amplitudes of strain that were evaluated, nor was it increased after prolonged mechanical stimulation for forty-eight hours or longer. Synthesis of collagen, non-collagenous protein, and proteoglycan, as well as activity of alkaline phosphatase, all indicators of macromolecular synthesis, were significantly decreased at a strain of 0.04 per cent applied for fifteen minutes and for twenty-four, forty-eight, and seventy-two hours. Macromolecular synthesis was not affected by the other amplitudes of strain that were evaluated in this study. At a strain of 0.04 per cent, prostaglandin E2 content was significantly increased after five, fifteen, and thirty minutes of mechanical stimulation, whereas net cAMP content did not change significantly. This suggests that the described cellular events (increased proliferation and decreased macromolecular synthesis) that occur secondary to mechanical strain are mediated, at least in part, by prostaglandin E2.