Heat-shock response is associated with enhanced contractility of vascular smooth muscle in isolated rat aorta

Kim, In Kyeom; Park, Tae-Gyu; Kim, Yeung‐Hyen; Cho, Jun Woo; Kang, Bong-Seok; Kim, Choong-Young

doi:10.1007/s00210-004-0880-2

Cited by 31 publications

(21 citation statements)

References 34 publications

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“…Anti-mouse IgM (goat), conjugated with horseradish peroxidase, was used as a secondary antibody (1:4000; Assay Designs, Inc., Ann Arbor, MI). The bands containing myosin light chains were visualized with enhanced chemiluminescence on films and then analyzed by NIH Image as described (Kim et al, 2004).…”

Section: Methodsmentioning

confidence: 99%

Isoflavone Attenuates Vascular Contraction through Inhibition of the RhoA/Rho-Kinase Signaling Pathway

Seok¹,

Baek²,

Kim³

et al. 2008

J Pharmacol Exp Ther

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Isoflavones decrease blood pressure, improve lipid profiles, and restore vascular function. We hypothesized that isoflavone attenuates vascular contraction by inhibiting RhoA/Rho-kinase signaling pathway. Rat aortic rings were denuded of endothelium, mounted in organ baths, and contracted with 11,9 epoxymethano-prostaglandin F 2␣ (U46619), a thromboxane A2 analog, or KCl 30 min after the pretreatment with genistein (4Ј,5,7-trihydroxyisoflavone), daidzein (4Ј,7-dihydroxyisoflavone), or vehicle. We determined the phosphorylation level of the myosin light chain (MLC 20 ), myosin phosphatase-targeting subunit 1 (MYPT1), and protein kinase C-potentiated inhibitory protein for heterotrimeric myosin light-chain phosphatase of 17 kDa (CPI17) by means of the Western blot. We also measured the amount of GTP RhoA as a marker regarding RhoA activation. The cumulative additions of U46619 or KCl increased vascular tension in a concentration-dependent manner, which were inhibited by pretreatment with genistein or daidzein. Both U46619 (30 nM) and KCl (50 mM) increased MLC 20 phosphorylation levels, which were inhibited by genistein and daidzein. Furthermore, both genistein and daidzein decreased the amount of GTP RhoA activated by either U46619 or KCl. U46619 (30 nM) increased phosphorylation of the MYPT1 Thr855 and CPI17 Thr38 , which were also inhibited by genistein or daidzein. However, neither genistein nor daidzein inhibited phorbol 12,13-dibutyrate-induced vascular contraction and CPI17 phosphorylation. In conclusion, isoflavone attenuates vascular contraction, at least in part, through inhibition of the RhoA/Rho-kinase signaling pathway.

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Section: Methodsmentioning

confidence: 99%

Isoflavone Attenuates Vascular Contraction through Inhibition of the RhoA/Rho-Kinase Signaling Pathway

Seok¹,

Baek²,

Kim³

et al. 2008

J Pharmacol Exp Ther

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“…Indeed, Hsp25/27 and Hsp20/ α B-crystallin may reciprocally assist in controlling venous tone [113]. Hsp70 may modulate vascular contractility through thick filament regulation [114], and Hsp90 is intricately involved in activation of endothelial nitric oxide synthase (eNOS) and the subsequent release of nitric oxide (NO) and vascular relaxation [115]. …”

Section: Vascular Function Of Hspmentioning

confidence: 99%

Impact of Exercise and Metabolic Disorders on Heat Shock Proteins and Vascular Inflammation

Noble

Shen

2012

Autoimmune Diseases

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Heat shock proteins (Hsp) play critical roles in the body's self-defense under a variety of stresses, including heat shock, oxidative stress, radiation, and wounds, through the regulation of folding and functions of relevant cellular proteins. Exercise increases the levels of Hsp through elevated temperature, hormones, calcium fluxes, reactive oxygen species (ROS), or mechanical deformation of tissues. Isotonic contractions and endurance- type activities tend to increase Hsp60 and Hsp70. Eccentric muscle contractions lead to phosphorylation and translocation of Hsp25/27. Exercise-induced transient increases of Hsp inhibit the generation of inflammatory mediators and vascular inflammation. Metabolic disorders (hyperglycemia and dyslipidemia) are associated with type 1 diabetes (an autoimmune disease), type 2 diabetes (the common type of diabetes usually associated with obesity), and atherosclerotic cardiovascular disease. Metabolic disorders activate HSF/Hsp pathway, which was associated with oxidative stress, increased generation of inflammatory mediators, vascular inflammation, and cell injury. Knock down of heat shock factor-1 (HSF1) reduced the activation of key inflammatory mediators in vascular cells. Accumulating lines of evidence suggest that the activation of HSF/Hsp induced by exercise or metabolic disorders may play a dual role in inflammation. The benefits of exercise on inflammation and metabolism depend on the type, intensity, and duration of physical activity.

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“…We expected potassium large KCNMB1, CALM1, ACTN1, TMSB4X, DNCL1, MRCL3, CFL2, TPM1, ARHGEF2, ARHGDIA and ARHGAP18 genes to be increased but it was found no significant change on them. Our laboratory reported that direct heat shock of rat isolated aorta at 42℃ for 45 minutes augmented its contractility several hours later 16). However, these regulated genes have not been characterized with respect to contractile functions so far.…”

Section: Discussionmentioning

confidence: 99%

Probing Regulatory Proteins for Vascular Contraction by Deoxyribonucleic Acid Microarray

Kim

2012

Korean Circ J

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Background and ObjectivesThe heat-shock response modulates contractility of vascular smooth muscles. With complementary deoxyribonucleic acid microarray, we tried to identify the novel genes that are involved in the regulation of vascular contraction after heat shock.Materials and MethodsHuman radial artery strips were mounted in organ baths, exposed at 42℃ for 45 minutes, and returned to equilibrate at 37℃. This study examined gene expression profile associated with heat-shock response in radial arteries of patients with hyperlipidemia by using a microarray that contained 5763 human cDNA. The results of microarray hybridization experiments from the radial arteries of 4 different subjects were analyzed and classified by the cluster program.ResultsAmong these differentially-expressed genes, Hsp70, Hsp10, αB-crystallin, and Hsp60 were significantly increased by the heat shock response. Of non-HSP genes, 15 genes increased, while 22 genes decreased. Among these 37 genes, αB-crystallin (CRYAB) (up 1.92-fold), myosin, light polypeptide kinase transcript variant 8, 6 (up 1.70-fold, up 1.68-fold), catenin (cadherin-associated protein, alpha-like 1) (down-0.57 fold) and tropomyosin 3 (down 0.68-fold) were thought to be related with the contraction. Real-time quantitative polymerase chain reaction showed that Hsp70, Hsp10 and αB-crystallin were significantly increased.ConclusionGene expression profile by heat shock provides information about genes implicated in augmentation of vascular contraction after heat shock.

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Heat-shock response is associated with enhanced contractility of vascular smooth muscle in isolated rat aorta

Cited by 31 publications

References 34 publications

Isoflavone Attenuates Vascular Contraction through Inhibition of the RhoA/Rho-Kinase Signaling Pathway

Isoflavone Attenuates Vascular Contraction through Inhibition of the RhoA/Rho-Kinase Signaling Pathway

Impact of Exercise and Metabolic Disorders on Heat Shock Proteins and Vascular Inflammation

Probing Regulatory Proteins for Vascular Contraction by Deoxyribonucleic Acid Microarray

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