Study of heat shock response of human umbilical vein endothelial cells (HUVECs) using cDNA microarray

Zhou, Mingjie; Zhang, A.; Lin, Binyan; Liu, J.; Xu, Liang

doi:10.1080/02656730701295441

Cited by 15 publications

(11 citation statements)

References 27 publications

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“…First, both hyperthermia and hypoxia have a direct detrimental effect on endothelial cells. 35,36 As a result, sinusoids become leaky, which was observed in our experiments by the extravasation of FITC-dextran in the TZ. This is in accordance with reports describing a hyperaemic rim at the necrotic margin.…”

Section: Discussionmentioning

confidence: 66%

Accelerated Perinecrotic Outgrowth of Colorectal Liver Metastases Following Radiofrequency Ablation is a Hypoxia-Driven Phenomenon

et al. 2009

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Section: Discussionmentioning

confidence: 66%

Accelerated Perinecrotic Outgrowth of Colorectal Liver Metastases Following Radiofrequency Ablation is a Hypoxia-Driven Phenomenon

et al. 2009

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“…DNA microarray technique has been used to identify changes in gene expression induced by mild hyperthermia at 41 °C (Tabuchi et al., 2008) and hyperthermia at 43–44 °C (Borkamo et al., 2008; Hirano et al., 2005; Kato et al., 2003; Narita et al., 2002; Sonna et al., 2002; Wada et al., 2007; Zhou et al., 2007). Although this method is valuable in differential gene expression, there is an increasing need to move beyond this level of analysis.…”

Section: Introductionmentioning

confidence: 99%

Gene networks involved in apoptosis induced by hyperthermia in human lymphoma U937 cells

Furusawa¹,

Tabuchi²,

Takasaki³

et al. 2009

Cell Biology International

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To define the molecular mechanisms that mediate hyperthermia-induced apoptosis, we performed microarray and computational gene expression analyses. U937 cells, a human myelomonocytic lymphoma cell line, were treated with hyperthermia at 42 degrees C for 90 min and cultured at 37 degrees C. Apoptotic cells ( approximately 15%) were seen 6 h after hyperthermic treatment, and elevated expression of heat shock proteins (HSPs) including Hsp27, Hsp40, and Hsp70 was detected, following the activation of heat shock factor-1. Of the 54,675 probe sets analyzed, 1334 were upregulated and 4214 were downregulated by >2.0-fold in the cells treated with hyperthermia. A non-hierarchical gene clustering algorithm, K-means clustering, demonstrated 10 gene clusters. The gene network U1 or U2 that was obtained from up-regulated genes in cluster I or IX contained HSPA1B, DNAJB1, HSPH1, and TXN or PML, LYN, and DUSP1, and were mainly associated with cellular compromise, and cellular function and maintenance or death, and cancer, respectively. In the decreased gene cluster II, the gene network D1 including CCNE1 and CEBPE was associated with the cell cycle and cellular growth and proliferation. These findings will provide a basis for understanding the detailed molecular mechanisms of apoptosis induced by hyperthermia at 42 degrees C in cells.

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“…Zhou's study found that endothelial actin filament depolymerized and cytoskeleton denaturation occurred gradually after 20 minutes of heating [23]. The effect of heat on the endothelium especially the actin filament and cytoskeleton may be the major cause of the macromolecules extravasation in the peripheral region.…”

Section: Numerical Results and Discussionmentioning

confidence: 98%

Study of alternate cooling and heating treatment induced tumor microvasculature injury

Shen

Zhang

2010

Chin. Sci. Bull.

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Tumor microvasculature is important to tumor growth, metastasis and thus tumor treatment outcome. The alternate cooling and heating treatment has been confirmed to have advantages over single treatment of cooling or heating. The degree of tumor microvasculature damage induced by the alternate cooling and heating treatment and the mechanisms underlying are studied in this paper. The response of the tumor microvasculature to different treatments including alternate cooling and heating is observed in vivo through confocal microscopy using the nude mice dorsal skin fold tumor chamber model. Results show that alternate cooling and heating has induced much more severe damage to the microvessel structure throughout the entire tumor. Numerical simulations of the mechanical stresses on the tumor vessel wall has found that during the alternate treatment, the vessel wall suffer a rapid chang in thermal stresses in the opposite directions successively, which might caused damage to the peripheral microvasculature and micro-cracks in the central vessels. Reperfusion of blood flow after freezing also led to relatively large stresses on the vessel wall, especially when blood flow re-perfuses quickly during the subsequent heating. The quick increase of stresses on the blood vessel might be one of the key issues causing the blood vessel rupture referring to the experimental observation. The preliminary study has partly revealed the mechanism underlying serious tumor microvasculature damage caused by the alternate cooling and heating treatment.alternate cooling and heating treatment, tumor microvasculature injury, thermal stress, blood flow Citation:Shen Y Y, Zhang A L. Study of alternate cooling and heating treatment induced tumor microvasculature injury.

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Study of heat shock response of human umbilical vein endothelial cells (HUVECs) using cDNA microarray

Cited by 15 publications

References 27 publications

Accelerated Perinecrotic Outgrowth of Colorectal Liver Metastases Following Radiofrequency Ablation is a Hypoxia-Driven Phenomenon

Accelerated Perinecrotic Outgrowth of Colorectal Liver Metastases Following Radiofrequency Ablation is a Hypoxia-Driven Phenomenon

Gene networks involved in apoptosis induced by hyperthermia in human lymphoma U937 cells

Study of alternate cooling and heating treatment induced tumor microvasculature injury

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