Hyperthermia at 43°C for 2h Inhibits the Proliferation of Vascular Smooth Muscle Cells, but not Endothelial Cells

Orihara, Koji; Biro, Sadatoshi; Hamasaki, Shuichi; Eto, Hideyuki; Miyata, Masaaki; Ikeda, Yoshiyuki

doi:10.1006/jmcc.2002.2071

Cited by 29 publications

(11 citation statements)

References 40 publications

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“…Indeed, studies performed in various cellular systems, demonstrated the ability of heat shock to decrease cell survival rate [26][27][28][29]. In agreement with those data, our results demonstrated as well that exposure of MEFs to heat shock resulted in a timedependent decrease in cell survival.…”

Section: Discussionsupporting

confidence: 93%

“…Indeed, a heat-shock-induced decrease in proliferation rate was demonstrated in several experimental systems, such as human fibroblasts, vascular smooth muscle, melanoma or malignant glioma cells [28,29,31,32]. In agreement with those studies, our data showed as well that exposure of MEFs to heat shock resulted in a clear decrease in the percentage of cells that incorporated BrdU, which was again more prominent in p65 À/À cells.…”

Section: Discussionsupporting

confidence: 92%

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NF-κB regulates the response of embryonic cells to heat shock

Savion

Sofer

Brengauz-Breitmann

et al. 2007

International Journal of Hyperthermia

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NF-kappaB was shown previously to regulate apoptotic cell death processes in various experimental systems. However, its role in controlling teratogen-induced cell death has not been established yet. Therefore, the objective of the present study was to explore the involvement of the p65 subunit of NF-kappaB in the response of mouse embryonic fibroblasts (MEFs) to heat shock, using p65 knockout (p65-/-) cells. Indeed, we found p65-/- MEFs to be more susceptible to the exposure to heat shock, as compared with wild-type (WT) MEFs, as they demonstrated a more prominent decrease in cell survival and proliferation as well as the appearance of cells undergoing apoptotic cell death. These heat-shock-induced effects were preceded by a decrease in p65 expression in WT cells, which was accompanied by a decrease in IkappaBalpha expression in WT MEFs, while disappearing completely in p65-/- MEFs and accordingly, by an increase in p-IkappaBalpha expression in both cell lines, which was found to be more prominent in p65-/- MEFs. Interestingly, the heat shock-induced decrease in p65 expression was accompanied by an increase in HSP70 expression in both cell lines. However, it was again found to be more prominent in p65-/- MEFs. Taken together, our results suggest a protective role for the p65 subunit of NF-kappaB in mechanisms underlying the response of embryonic cells to heat shock.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 92%

NF-κB regulates the response of embryonic cells to heat shock

Savion

Sofer

Brengauz-Breitmann

et al. 2007

International Journal of Hyperthermia

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“…Orihara et al [19] reported that exposure of vascular smooth muscle cells to 43°C for 2 hours inhibited cell proliferation. Further work is required to assess whether HSP20 is involved in this response.…”

Section: Discussionmentioning

confidence: 99%

Heat induced HSP20 phosphorylation without increased cyclic nucleotide levels in swine carotid media

Rembold

Kaufman

2003

BMC Physiol

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“…The results from the cell cycle analysis demonstrated that there was significantly less progression to the G0/G1 phase in MSH-treated cells than in the control group 24 h following the heat treatment, suggesting S and G2/M phase arrest. Orihara et al (15) evaluated the effect of heating on VSMCs from the rat thoracic aorta and revealed that the results indicated G1 arrest (15). Two plausible explanations may account for the difference between the two observations: There was an interspecies difference between the two studies and the two heating approaches, i.e.…”

Section: Discussionmentioning

confidence: 99%

“…It has been revealed that repeated whole-body hyperthermia may improve vascular endothelial and cardiac functions in patients with chronic heart failure (14). Furthermore, Orihara et al showed that hyperthermia treatment (43°C, 2 h) was capable of inhibiting the proliferation of the dividing VSMCs without damaging the quiescent VSMCs (15). However, with regard to restenosis, which normally occurs at the site of the stent in the coronary artery, there is a requirement for localized or targeted heating.…”

Section: Introductionmentioning

confidence: 99%

In vitro study on the feasibility of magnetic stent hyperthermia for the treatment of cardiovascular restenosis

Wang

Shi

et al. 2013

Experimental and Therapeutic Medicine

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Thermal treatment or hyperthermia has received considerable attention in recent years due to its high efficiency, safety and relatively few side-effects. In this study, we investigated whether it was possible to utilize targeted thermal or instent thermal treatments for the treatment of restenosis following percutaneous transluminal coronary angioplasty (PTCA) through magnetic stent hyperthermia (MSH). A 316L stainless steel stent and rabbit vascular smooth muscle cells (VSMCs) were used in the present study, in which the inductive heating characteristics of the stent under alternative magnetic field (AMF) exposure, as well as the effect of MSH on the proliferation, apoptosis, cell cycle and proliferating cell nuclear antigen (PCNA) expression of the rabbit VSMCs, were evaluated. The results demonstrated that 316L stainless steel coronary stents possess ideal inductive heating characteristics under 300 kHz AMF exposure. The heating properties were shown to be affected by the field intensity of the AMF, as well as the orientation the stent axis. MSH had a significant effect on the proliferation and apoptosis of VSMCs, and the effect was temperature-dependent. While a mild temperature of 43°C demonstrated negligible effects on the growth of VSMCs, MSH treatment above 47°C effectively inhibited the VSMC proliferation and induced apoptosis. Furthermore, a 47°C treatment exhibited a significant and long-term inhibitory effect on VSMC migration. The results strongly suggested that MSH may be potentially applied in the clinic as an alternative approach for the prevention and treatment of restenosis.

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Hyperthermia at 43°C for 2h Inhibits the Proliferation of Vascular Smooth Muscle Cells, but not Endothelial Cells

Cited by 29 publications

References 40 publications

NF-κB regulates the response of embryonic cells to heat shock

NF-κB regulates the response of embryonic cells to heat shock

Heat induced HSP20 phosphorylation without increased cyclic nucleotide levels in swine carotid media

In vitro study on the feasibility of magnetic stent hyperthermia for the treatment of cardiovascular restenosis

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