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Biomedical subjects

Q Xu

Publications and source records attributed to Q Xu.

At least 109 records · Page 6Linked to original sources

[Effects of supplementing of calcium, iron and zinc on women's health during pregnancy].

OBJECTIVES: To determine the effects of supplementing biscuits fortified with calcium (Ca) and vitamin D (VD), iron (Fe), vitamin C (VC) and zinc (Zn) to pregnant women from the 5th month of gestation until delivery on their health, and to explore a way to improve their Ca, Fe and Zn nutritional status during pregnancy. METHODS: A total of 313 healthy and primary pregnant women were enrolled and divided into five study groups based on their order visiting the hospitals for prenatal care. Each woman of the study groups was given three pieces of biscuit fortified with VD, Ca and VD, Ca, Zn and VD (Ca + Zn + VD), Ca, Fe, VC and VD (Ca + Fe + VD), Ca, Fe, VC, Zn and VD (Ca + Fe + Zn + VD), respectively, from the 15th month of gestation until delivery (24 weeks in total) daily. The fortified levels were 10 micrograms VD, 400 mg Ca from carbonate calcium, 10 mg Zn from lactate zinc, 10 mg Fe from ferrous lactate, and 50 mg VC, respectively. A parturient women was selected from the same hospital as control after one trial subject for each study groups selected. RESULTS: The daily dietary intakes of Ca, Zn and Fe in pregnant women were only 47.7%, 54.7% and 86.7% of the Recommended Dietary Allowances for Chinese. Incidence of anemia for mid-term pregnant women was 35.2%, and Fe-supplementation could significantly improved their hemoglobin level (P < 0.05). Prevalence of anemia in the groups of Ca + Fe + Zn + VD and Ca + Fe + VD was 35.3% and 40.7%, respectively, before Fe supplementation and reduced to zero and 4.0%, respectively, after Fe supplementation. Whereas, prevalence of anemia in the other groups without Fe supplementation still kept in a relatively high level. In the groups supplemented with Ca, their plasma Ca level increased, especially with the best results in Ca + VD group. Plasma level of Zn declined with length of gestation, which could be improved by Zn supplementation. Serum level of alkaline phosphatase activity increased a little bit with length of gestation. There was no significant difference in radial and ulnar bone mineral density (BMD) between trial groups and controls two months after delivery. Maternal radial and ulnar BMD correlated significantly with their dietary Ca intakes in Ca + VD group. CONCLUSION: The best way to improve maternal nutritional status is supplementation of Ca + Fe + Zn + VitD, based on the Recommended Dietary Allowances for Chinese.

Adult↗

[Effects of supplementing calcium, iron and zinc on the fetus development and growth during pregnancy].

OBJECTIVES: The purpose of the present study is to determine the effects of supplementing the biscuits fortified with calcium (Ca), iron (Fe) and zinc (Zn) for pregnant women from the 5th month of gestation until delivery on the growth and development of fetus and to explore the best way to improve infant growth. METHODS: A total of 313 healthy and primary pregnant women were enrolled and divided into five study groups based on their order visiting the hospitals for prenatal care. Each woman of the study groups was given three pieces of biscuit fortified with VD, Ca and VD, Ca, Zn and VD (Ca + Zn + VD), Ca, Fe, VC and VD (Ca + Fe + VD), Ca, Fe, VC, Zn and VD (Ca + Fe + Zn + VD), respectively, from the 5th month of gestation until delivery (24 weeks in total) daily. The fortified levels were 10 micrograms Ca from carbonate calcium, 10 mg Zn from lactate zinc, 10 mg Fe from ferrous lactate, and 50 mg VC, respectively. A parturient women was selected from the same hospital as control after one trial subject for each study groups selected. Placenta was weighed and umbilical cord venous blood and placenta tissue samples were collected after delivery for measuring Ca and other trace elements. Body weight and height of the new-born babies were measured. RESULTS: The weight of placenta in control group (551.1 +/- 64.2) g was significantly (P < 0.05) heavier than other trial groups with Ca + Fe + Zn + VD (467.1 +/- 36.6) g, but contents of Ca and other trace elements in placenta of the control group were lower, which probably because of the lower nutrients intake of mothers in control group that would result in a compensation enlargement of placenta to get enough nutrients for fetus from mother. The Hb level in cord venous blood was significantly higher than that of maternal blood. There was no significant difference in activity of alkaline phosphatase between cord venous blood and material blood. The contents of Ca, Fe and Zn in cord venous plasma were all significantly higher than those in maternal plasma. Birth weight and height in Ca + Fe + Zn + VD group were the highest in all the groups, with birth weight of (3.53 +/- 0.33) kg, as compared with (3.28 +/- 0.54) kg in the control group. There was significant correlation between birth weight, weight for age and intake of Ca, Fe and Zn during pregnancy. CONCLUSION: Supplementation of Ca + Fe + Zn + VitD during pregnancy is the best way to improve infant development and growth, based on the current Recommended Dietary Allowances (RDA) for pregnant women.

Adult↗

[Biomass, sporulation and aphid-infecting virulence of Pandora neoaphidis mycelia produced in repeated liquid culture].

Repeated culture of entomophthoraceous isolates is a suspectable factor leading to their virulence decline of biological variation. In the present study, an isolate of Pandora neoaphidis, F98028, was repeatedly cultured six times at the regime of 20 degrees C and 80 r/min in Sabouraud dextrose broth(SDB) at three inoculation ratio of 1/20, 2/20, and 4/20 (seed culture over fresh SDB). Mycelial biomass(MB), sporulation capacity(SC), and virulence to the green peach aphid, Myzus persicae, were assessed for each of the subcultures. The repeated liquid cultures, initiating from seed culture with MB 8.84 mg/mL ad SC 7.22 x 10(5) conidia/mg, yielded MB and SC in a range of 6.4-10.0 mg/mL and 7.3 x 10(5)-10.8 x 10(5) conidia/mg at the ratio of 1/20(72 h culture), 5.7-8.5 mg/mL and 10.0 x 10(5)-12.1 x 10(5) condia/mg at 2/20(60 h culture), and 5.5-10.9 mg/mL and 6.4 x 10(5)-10.9 x 10(5) conidia/mg at 4/20(48 h culture), respectively. There was no significant difference in both MB and SC among the cultures(F = 0.299, P = 0.903) or the three inoculation ratios (F = 0.561, P = 0.587). Inocula from each of the cultures at the inoculation ratio of 1/20 were repeatedly bioassayed on the second and third instar colonies of M. periscae. Based on time-dose-mortality analysis, the estimates of LD50 s for all batches of the inocula were 22.8-162, 4.7-49.4, 2.8-16.7, 2.3-9.5, and 1.8-5.2 conidia/mm2 3-7 d after inoculation, respectively. All the estimates for the repeated cultures fell within a range previously reported. Thus, the method used for repeated liquid culture in this study did not cause a visible decline in the virulence of P. neoaphidis F98028.

Animals↗

[Evaluation on the growth and development of children from gangsan primary school in Kundulun district of Baotou City].

In order to evaluate the growth and development of primary school children and the effect of anemia on body height and weihgt, a routine examination on anthropometry and heomoglobin was carried out among the children from Gangsan Primary School in the Kundulun District of Baotou City, including 580 boys and 561 girls for anthropometry and 579 boys and 560 girls for hemoglobin in the Spring of 2001. The results showed that the growth and development of children were higher than the average results of children published in 1992 National Nutrition Survey, and also higher than the results from the Chinese school children physique development in 1995. The average prevalence of anemia was 26.2%, and the girls suffered from anemia were much higher than the boys (30.9% and 21.8% respectively). The highest prevalence of anemia in boys was in the second grades(29.3% and 28.9%), however, the highest prevalence of anemia in girls was in the second grade(43.2%). Compared with normal children, the children suffered from anemia were in lower height, lower body weight and lower body mass index significantly(P < 0.001); The present study indicated that anemia might have adverse effects on the growth and development of children.

Anemia, Iron-Deficiency↗

Progress in DNA chip technology.

DNA chip technology employs light-directed in situ oligonucleotide synthesis and/or DNA microarray printing device to produce arrays of large number of probes in the tiny surface of silicon substrates, which makes it possible that the gene detection be conducted efficiently with high speed and sensitivity. The DNA chip may take important part in genome research, gene diagnoses and so on.

Animals↗

[Simultaneous determination of hydride forming and non-hydride forming elements in human hair by hydride generation-inductively coupled plasma atomic emission spectrometry].

A method for simultaneous determination of both hydride forming and non-hydride forming elements in human hair has also been successful. The influence of HCl concentration, NaBH4 concentration, carrier gas flow rate and rinse time on hydride forming elements intensity, and the effect of between nebulization and hydride-nebulization system on non-hydride forming elements have been studied. The optimum experimental conditions are selected. This method has been applied to the analysis of standard human hair with satisfactory results.

Arsenic↗

The insulin-like growth factor-phosphatidylinositol 3-kinase-Akt signaling pathway regulates myogenin expression in normal myogenic cells but not in rhabdomyosarcoma-derived RD cells.

Insulin-like growth factors (IGFs) can stimulate skeletal muscle differentiation. One of the molecular mechanisms underlying IGF-stimulated myogenesis is transcriptional induction of myogenin. The current work is aimed to elucidate the signaling pathways mediating the IGF effect on myogenin promoter in mouse C2C12 myogenic cells. We show that phosphatidylinositol 3-kinase (PI3K)/Akt and p70(S6K) are crucial signaling molecules mediating the stimulatory effect of IGFs on myogenin expression. We have identified three cis-elements, namely the E box, MEF2, and MEF3 sites, within the 133-base pair mouse proximal myogenin promoter that are under the control of the IGF/PI3K/Akt pathway. Simultaneous mutation of all three elements completely abolishes activation of the myogenin promoter by PI3K/Akt. We demonstrate that PI3K/Akt can increase both the MyoD and the MEF2-dependent reporter activity by enhancing the transcriptional activity of MyoD and MEF2. Interestingly, IGF1 does not enhance myogenin expression in Rhabdomyosarcoma-derived RD cells. Consistently, the constitutively active PI3K/Akt fail to activate the myogenic reporters, suggesting the IGF/PI3K/Akt pathway is defective in RD cells and the defect(s) is downstream to PI3K/Akt. This is the first time that a defect in the IGF/PI3K/Akt pathway has been revealed in RD cells which provides another clue to future therapeutic treatment of Rhabdomyosarcoma.

Amino Acid Sequence↗

Isolation and characterization of apolipoproteins from murine microglia. Identification of a low density lipoprotein-like apolipoprotein J-rich but E-poor spherical particle.

Amyloid Abeta deposition is a neuropathologic hallmark of Alzheimer's disease. Activated microglia are intimately associated with plaques and appear to facilitate Abeta deposition, an event believed to contribute to pathogenesis. It is unclear if microglia can modulate pathogenesis of Alzheimer's disease by secreting lipoprotein particles. Here we show that cultured BV2 murine microglial cells, like astrocytes, secrete apolipoprotein E (apoE) and apolipoprotein J (apoJ) in a time-dependent manner. To isolate and identify BV2 microglial particles, gel filtration chromatography was employed to fractionate BV2-conditioned medium. Analyses by Western blot, lipid determination, electron microscopy, and native gel electrophoresis demonstrate that BV2 microglial cells release spherical low density lipoprotein (LDL)-like lipid-containing particles rich in apoJ but poor in apoE. These microglial particles are dissimilar in size, shape, and lipoprotein composition to astrocyte-derived particles. The microglial-derived particles were tested for functional activity. Under conditions of suppressed de novo cholesterol synthesis, the LDL-like particles effectively rescued primary rat cortical neurons from mevastatin-induced neurotoxicity. The particles were also shown to bind Abeta. We speculate that the LDL-like apoJ-rich apoE-poor microglial lipoproteins preferentially bind the lipoprotein receptor, recognizing apoJ, which is abundant in the choroid plexus, facilitating Abeta clearance from the brain. BV2 cells also secrete an apoE-rich lipid-poor species that binds Abeta. Consistent with the role of apoE in Abeta fibril formation and deposition, this microglial species may promote plaque formation.

Alzheimer Disease↗

Infections, immunity, and atherosclerosis: associations of antibodies to Chlamydia pneumoniae, Helicobacter pylori, and cytomegalovirus with immune reactions to heat-shock protein 60 and carotid or femoral atherosclerosis.

BACKGROUND: Atherogenesis involves inflammatory processes in which infections are incriminated as possible contributors. METHODS AND RESULTS: We evaluated cardiovascular risk factors as well as seropositivity to Chlamydia pneumoniae, Helicobacter pylori, and cytomegalovirus in a population-based study. A significant association between prevalence and severity of atherosclerosis in carotid and femoral arteries and IgA antibodies to C pneumoniae was demonstrated that was not substantially altered after adjustment for established risk factors. For anti-H pylori IgG antibodies, significant correlations to vascular disease were restricted to low social status and lesions in carotid arteries. In addition, the study design allowed us to monitor lesion progression over time. In this prospective analysis, C pneumoniae seropositivity emerged as a significant risk predictor. Antibody titers against cytomegalovirus were not a marker for prevalence or incidence of atherosclerosis in this population. Further infection parameters added to the predictive value of chlamydial serology in risk assessment: Mean odds ratios for the prevalence of carotid atherosclerosis were 4.2 and 6.3 for seropositive subjects with elevated C-reactive protein levels and clinical evidence for chronic respiratory infection, respectively. For subjects with all 3 infection parameters, the odds ratio of carotid atherosclerosis reached 10.3 (P<0.0001). Concomitantly, serum antibodies to mycobacterial heat-shock protein 65 (mHSP65) correlated with seropositivity to C pneumoniae and H pylori but not to cytomegalovirus. CONCLUSIONS: This prospective population-based study provides strong evidence for a potential atherogenic role of persistent bacterial infection, especially C pneumoniae, as indicated by serological and clinical data and demonstrates a correlation between immune reactions to mHSP65 and bacterial infections in atherogenesis.

Aged↗

Induction and modulation of cerebellar granule neuron death by E2F-1.

Growing evidence suggests that certain cell cycle regulators also mediate neuronal death. Of relevance, cyclin D1-associated kinase activity is increased and the retinoblastoma protein (Rb), a substrate of the cyclin D1-Cdk4/6 complex, is phosphorylated during K(+) deprivation-evoked death of cerebellar granule neurons (CGNs). Cyclin-dependent kinase (CDK) inhibitors block this death, suggesting a requirement for the cyclin D1/Cdk4/6-Rb pathway. However, the downstream target(s) of this pathway are not well defined. The transcription factor E2F-1 is regulated by Rb and is reported to evoke death in proliferating cells when overexpressed. Accordingly, we examined whether E2F-1 was sufficient to evoke death of CGNs and whether it was required for death evoked by low K(+). We show that adenovirus-mediated expression of E2F-1 in CGNs results in apoptotic death, which is independent of p53, dependent upon Bax, and associated with caspase 3-like activity. In addition, we demonstrate that levels of E2F-1 mRNA and protein increase during K(+) deprivation-evoked death. The increase in E2F-1 protein is blocked by the CDK inhibitor flavopiridol. Finally, E2F-1-deficient neurons are modestly resistant to death induced by low K(+). These results indicate that E2F-1 expression is sufficient to promote neuronal apoptosis and that endogenous E2F-1 modulates the death of CGNs evoked by low K(+).

Adenoviridae↗

Identification of type II restriction and modification systems in Helicobacter pylori reveals their substantial diversity among strains.

A total of 22 type II restriction endonucleases with 18 distinct specificities have been identified in six Helicobacter pylori strains. Among these 18 specificities are three completely new endonucleases, Hpy178III, Hpy99I, and Hpy188I, that specifically cleave DNA at TCNNGA, CGWCG, and TCNGA sites, respectively. The set of endonucleases identified in each strain varies, but all have four- or five-base recognition sequences. Among 16 H. pylori strains, examination of the DNA modification status at the recognition sites of 15 restriction endonucleases reveals that each strain has a substantially different complement of type II modification systems. We conclude that the type II restriction-modification systems in H. pylori are highly diverse between strains, a unique characteristic of H. pylori. The diverse methylation status of H. pylori chromosomal DNA may serve as a new typing system to discriminate H. pylori isolates for epidemiological and clinical purposes. This study also demonstrates that H. pylori is a rich source of type II restriction endonucleases.

Adult↗

Sp1 increases expression of cyclooxygenase-2 in hypoxic vascular endothelium. Implications for the mechanisms of aortic aneurysm and heart failure.

Cyclooxygenase-2 (COX-2) catalyzes prostaglandin synthesis from arachidonic acid and is expressed locally in aortic aneurysm and heart failure. Cellular hypoxia is also found in these conditions. We have previously shown that cox-2 is transcriptionally regulated by hypoxia in human umbilical vein endothelial cells (HUVEC) in culture via the transactivation factor NF-kappaB p65, leading to increased production of prostaglandin E(2), an inhibitor of vascular smooth muscle cell proliferation. Sp1 is a transactivation factor known to be important in the regulation of cytokine expression in association with NF-kappaB. We hypothesized that Sp1 is involved in the induction of cox-2 in hypoxic HUVEC. Electrophoretic mobility shift assays with hypoxic HUVEC nuclear protein showed that both Sp1 and the related protein Sp3 specifically bound to the cox-2 promoter. Immunoblotting demonstrated that hypoxia increased the nuclear localization of Sp1 but did not change the Sp3 content in HUVEC. Overexpression of Sp1 through transfection of HUVEC enhanced cox-2 promoter activity as measured by reporter gene expression and by the production of COX-2. The specificity of the results was confirmed by mutation of the Sp1-binding site in the cox-2 promoter construct and by reproducibility in an Sp-deficient Drosophila SL2 cell line. The regulatory role of Sp1 discovered in this work supports the concept that a mechanistic link exists between vascular cellular hypoxia and mediators of inflammation associated with aortic aneurysm and heart failure.

Base Sequence↗

Roles of Eph receptors and ephrins in segmental patterning.

Eph receptor tyrosine kinases and their membrane-bound ligands, ephrins, have key roles in patterning and morphogenesis. Interactions between these molecules are promiscuous, but largely fall into two groups: EphA receptors bind to glycosylphosphatidyl inositol-anchored ephrin-A ligands, and EphB receptors bind to transmembrane ephrin-B proteins. Ephrin-B proteins transduce signals, such that bidirectional signalling can occur upon interaction with the Eph receptor. In many tissues, there are complementary and overlapping expression domains of interacting Eph receptors and ephrins. An important role of Eph receptors and ephrins is to mediate cell contact-dependent repulsion, and this has been implicated in the pathfinding of axons and neural crest cells, and the restriction of cell intermingling between hindbrain segments. Studies in an in vitro system show that bidirectional activation is required to prevent intermingling between cell populations, whereas unidirectional activation can restrict cell communication via gap junctions. Recent work indicates that Eph receptors can also upregulate cell adhesion, but the biochemical basis of repulsion versus adhesion responses is unclear. Eph receptors and ephrins have thus emerged as key regulators that, in parallel with cell adhesion molecules, underlie the establishment and maintenance of patterns of cellular organization.

Animals↗

Determination of tripolyphosphate in frozen cod and scallop adductor by ion chromatography.

We introduce a method for the determination of tripolyphosphate in frozen cod and scallop adductor by using ion chromatography. The tripolyphosphate was extracted from minced cod and scallop adductor with deionized water by ultrasonic leaching, and then the proteins soluble in water were precipitated with trichloroacetic acid and removed by filtering. An ion chromatograph with an ionpac AS11-HC anion-exchange column, an ASRS (Anion Self Regenerating Suppression), a conductivity detector and a gradient pump (sodium hydroxide gradient) was used. The detection limit was below 5 mg tripolyphosphate/kg cod or scallop adductor. This method is applicable to the determination of polyphosphates in aquatic products and the procedures are easy to implement.

Chromatography, Ion Exchange↗

Serum soluble heat shock protein 60 is elevated in subjects with atherosclerosis in a general population.

BACKGROUND: Work from our laboratory has proven that increased titers of anti-heat shock protein 60 (HSP60) antibodies are associated with atherosclerosis and that HSP60-reactive T-cells are present in atherosclerotic lesions. Recent studies from others demonstrated that HSP60 directly activates endothelial cells and macrophages. METHODS AND RESULTS: To explore the possibility that HSP60 exists in the circulation, where it could exert its functions, we performed a population-based study with 826 subjects aged 40 to 79 years. The following items were measured in all participants: serum soluble HSP60 (sHSP60); anti-Escherichia coli lipopolysaccharide; anti-HSP65, anti-Chlamydia and anti-Helicobacter pylori antibodies; and a variety of acute phase reactants (C-reactive protein, alpha(1)-antitrypsin, and ceruloplasmin) and markers of systemic inflammation. Carotid atherosclerosis was assessed twice (1990 and 1995), and 15 other risk factors were evaluated. Our data show that levels of sHSP60 were significantly elevated in subjects with prevalent/incident carotid atherosclerosis and that these levels were correlated with common carotid artery intima/media thickness. Multiple logistic regression analysis documented these associations as independent of age, sex, and other risk factors. Interestingly, sHSP60 was also correlated with anti-lipopolysaccharide, anti-Chlamydia and anti-HSP60 antibodies, various markers of inflammation, and the presence of chronic infections. The risk of atherosclerosis associated with high sHSP60 levels was amplified when subjects had clinical and/or laboratory evidence of chronic infections. CONCLUSIONS: Our data provide the first evidence of a strong correlation between sHSP60 and atherosclerosis, suggesting that sHSP60 may play important roles in activating vascular cells and the immune system during the development of atherosclerosis.

Adult↗

Prolonged survival of heart allografts from p53-deficient mice.

BACKGROUND: Acute rejection of the heart allograft is the major cause of heart failure in the first month after transplantation. Most studies on the prevention of acute rejection have concentrated on immune suppression of the recipients, whereas little is known about the effects of genetically manipulated donor organs on heart allograft survival. Herein, we describe a mouse model of heart allografts donated by p53-/- mice that can prolong the survival time of the grafts. METHODS: Hearts of p53-/- or p53+/+ C57BL/6J mice were grafted to the neck carotid artery and jugular vein of BALB/c mice using a cuff technique. The graft survival was observed daily. The hearts were analyzed using several techniques, including histology, immunofluorescence, terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL), and Western blot analysis. RESULTS: p53+/+ allografts ceased beating at 7.6+/-0.5 days, whereas p53-/- hearts were beating at 10.5+/-1.1 days after transplantation (P<0.01). Mean histological rejection scores were significantly lower in allografts donated by p53-deficient mice. Furthermore, apoptotic cells, determined by TUNEL and a reagent kit for detection of cardiac apoptosis, were of high numbers in the allograft sections from wild-type hearts but rare in p53-/- allografts (4.2+/-1.3 vs. 0.7+/-0.5/250x field). Immunofluorescence staining and Western blot analysis revealed that high levels of p53 and proapoptotic protein Bax were expressed in wild-type grafts but not p53-/- allografts. Interestingly, Bcl-2, an antiapoptotic protein, was abundant in cardiac allografts from p53-/- mice and almost undetectable in grafts from wild-type mice. CONCLUSIONS: Thus, p53 is involved in cardiac apoptosis induced by alloimmune reaction, and prolonged survival of heart allografts can be achieved when p53 is lacking.

Animals↗

Mechanical stress-induced heat shock protein 70 expression in vascular smooth muscle cells is regulated by Rac and Ras small G proteins but not mitogen-activated protein kinases.

-Previous studies have documented that acute elevation in blood pressure results in heat shock protein (hsp) 70-mRNA expression followed by hsp70-protein production in rat aortas. In this article, we provide evidence that mechanical forces evoke rapid activation of heat shock transcription factor (HSF) and hsp70 accumulation. In our study, Western blot analysis demonstrated that hsp70-protein induction peaked between 6 and 12 hours after treatment with cyclic stain stress (60 cycles/minute, up to 30% elongation). Elevated protein levels were preceded by hsp70-mRNA transcription, which was associated with HSF1 phosphorylation and activation stimulated by mechanical forces, suggesting that the response was regulated at the transcriptional level. Conditioned medium from cyclic strain-stressed vascular smooth muscle cells (VSMCs) did not result in HSF-DNA-binding activation. Furthermore, mitogen-activated protein kinases (MAPKs), including extracellular signal-regulated kinases, c-Jun NH(2)-terminal protein kinases or stress-activated protein kinases, and p38 MAPKs, were also highly activated in response to cyclic strain stress. Inhibition of extracellular signal-regulated kinase and p38-MAPK activation by their specific inhibitors (PD 98059 and SB 202190) did not influence HSF1 activation. Interestingly, VSMC lines stably expressing dominant-negative rac (rac N17) abolished hsp-protein production and HSF1 activation induced by cyclic strain stress, whereas a significant reduction of hsp70 expression was seen in ras N17-transfected VSMC lines. Thus, our findings demonstrate that cyclic strain stress-induced hsp70 expression is mediated by HSF1 activation and regulated by rac and ras GTP-binding proteins. Induction of hsp70 could be important in maintaining VSMC homeostasis during vascular remodeling in response to hemodynamic stimulation.

Animals↗