Localization and activity of calmodulin is involved in cell–cell adhesion of tumor cells and endothelial cells in response to hypoxic stress

Shen, Weishou; Peng, Wan-Xin; Shao, Yue; Xu, Jinling; Dai, Gaole; Zhang, Y.; Pan, Fei; Li, Chao Jun

doi:10.1007/s10565-006-0157-2

Cited by 11 publications

(8 citation statements)

References 43 publications

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“…Media containing 100 U/mL penicillin and 100 lg/mL streptomycin and cells were maintained at 37 C in a humidified atmosphere of 5% CO 2 . Cells were cultured in hypoxic conditions, as previously described (Shen et al, 2007), in a tightly sealed hypoxic culture chamber (Changjin Science Technologies, Changsha, China). The cells were placed in the humidified chamber flushed with a gas mixture of 1% O 2 , 5% CO 2 that was balanced with nitrogen (N 2 ).…”

Section: Materials and Methods Cell Culture And Hypoxia Treatmentmentioning

confidence: 99%

Hypoxia Stabilizes Microtubule Networks and Decreases Tumor Cell Chemosensitivity to Anticancer Drugs Through Egr‐1

Peng¹,

Pan²,

Liu³

et al. 2010

The Anatomical Record

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The hypoxic environment of solid tumor causes the tumor cells survive and which could protect them from death by facilitating resistance to therapy. Here, we provide evidence that hypoxia can increase tumor cell viability and proliferation through an Egr-1-dependant pathway. Hypoxia protected the microtubules from disassembly, and Egr-1 was colocalized with microtubules in different cell cycle stages. Knockdown of Egr-1 with its siRNA overcame the protection effect of hypoxia and increased the sensitivity of tumor cells to vinblastine under hypoxic conditions. Our results suggest a novel approach for increasing the sensitivity of tumor cells to chemotherapeutics that target microtubule assembly. Anat Rec, 293:414-420, 2010. V V C 2010 Wiley-Liss, Inc.

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Section: Materials and Methods Cell Culture And Hypoxia Treatmentmentioning

confidence: 99%

Hypoxia Stabilizes Microtubule Networks and Decreases Tumor Cell Chemosensitivity to Anticancer Drugs Through Egr‐1

Peng¹,

Pan²,

Liu³

et al. 2010

The Anatomical Record

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“…Endothelial cells in the coronary arteries form the inner surface of the vessels and drive a response to hypoxic conditions in ischemic heart disease, including coronary atherosclerotic disease or acute coronary syndrome [16]. In response to hypoxic conditions, a number of genes are upregulated by signaling cascades, such as p38 mitogen-activated protein kinase (MAPK), Jun N-terminal kinase (JNK), hypoxia induce factor-1alpha (HIF-1alpha) and ERK, in vascular endothelial cells [17–20]. These responses include vascular-endothelial-cell proliferation, migration, and subsequently angiogenesis, but also growth arrest and apoptosis.…”

Section: Introductionmentioning

confidence: 99%

Tumor Necrosis Factor-Alpha and the ERK Pathway Drive Chemerin Expression in Response to Hypoxia in Cultured Human Coronary Artery Endothelial Cells

Chua

Shyu²,

Lin

et al. 2016

PLoS ONE

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BackgroundChemerin, a novel adipokine, plays a role in the inflammation status of vascular endothelial cells. Hypoxia causes endothelial-cell proliferation, migration, and angiogenesis. This study was aimed at evaluating the protein and mRNA expression of chemerin after exposure of human coronary artery endothelial cells (HCAECs) to hypoxia.Methods and ResultsCultured HCAECs underwent hypoxia for different time points. Chemerin protein levels increased after 4 h of hypoxia at 2.5% O2, with a peak of expression of tumor necrosis factor-alpha (TNF-alpha) at 1 h. Both hypoxia and exogenously added TNF-alpha during normoxia stimulated chemerin expression, whereas an ERK inhibitor (PD98059), ERK small interfering RNA (siRNA), or an anti-TNF-alpha antibody attenuated the chemerin upregulation induced by hypoxia. A gel shift assay indicated that hypoxia induced an increase in DNA-protein binding between the chemerin promoter and transcription factor SP1. A luciferase assay confirmed an increase in transcriptional activity of SP1 on the chemerin promoter during hypoxia. Hypoxia significantly increased the tube formation and migration of HCAECs, whereas PD98059, the anti-TNF-alpha antibody, and chemerin siRNA each attenuated these effects.ConclusionHypoxia activates chemerin expression in cultured HCAECs. Hypoxia-induced chemerin expression is mediated by TNF-alpha and at least in part by the ERK pathway. Chemerin increases early processes of angiogenesis by HCAECs after hypoxic treatment.

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“…Hypoxic treatment. Hypoxic exposure was performed using a tightly sealed molecular incubator chamber (Billups-Rothenberg, Inc., Del Mar, CA, USA), which was tightly sealed and flushed with a gas mixture containing 1% O 2 , 94% N 2 and 5% CO 2 , as previously described (15,16), with the cell culture dishes containing 1x10 5 cells/well placed in the chamber and incubated at 37˚C for 24 h.…”

Section: Methodsmentioning

confidence: 99%

Cysteine-rich 61 RNA interference inhibits pathological angiogenesis via the phosphatidylinositol 3-kinase/Akt-vascular endothelial growth factor signaling pathway in endothelial cells

Zhang

Hui

et al. 2016

Molecular Medicine Reports

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Hypoxia is a key factor in the pathogenesis of angiogenesis, and cysteine‑rich 61 (CCN1), an angiogenic factor, is involved in the development of pathological angiogenesis. The aim of the present study was to investigate the mechanism of CCN1 RNA interference (RNAi)‑induced inhibition of hypoxia‑induced pathological angiogenesis in endothelial cells. Human umbilical vein endothelial cells (HUVECs) were cultured under hypoxic conditions in vitro. The effects of inhibiting phosphoinositide 3‑kinase (PI3K)/Akt signaling using LY294002 were investigated in hypoxic HUVECs. The proliferation and apoptosis of HUVECs under hypoxia were assessed using CCN1 RNAi. The CCN1‑PI3K/Akt‑vascular endothelial growth factor (VEGF) pathway was analyzed under hypoxic conditions using reverse transcription‑quantitative polymerase chain reaction and western blotting. CCN1 RNAi inhibited the proliferation and induced the apoptosis of the HUVECs under hypoxia, with hypoxia significantly increasing the mRNA and protein expression levels of CCN1, Akt and VEGF. By contrast, CCN1 RNAi reduced the mRNA and protein expression levels of CCN1, Akt and VEGF in the HUVECs (P<0.05). Furthermore, LY294002 reduced the mRNA and protein expression levels of CCN1 in the hypoxic cells (P<0.05). These data indicated that CCN1 inhibits apoptosis and promotes proliferation in HUVECs. Therefore, CCN1 RNAi may offer a novel therapeutic strategy, which may aid in the treatment of pathological angiogenesis via inhibition of the PI3K/Akt‑VEGF pathway.

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Localization and activity of calmodulin is involved in cell–cell adhesion of tumor cells and endothelial cells in response to hypoxic stress

Cited by 11 publications

References 43 publications

Hypoxia Stabilizes Microtubule Networks and Decreases Tumor Cell Chemosensitivity to Anticancer Drugs Through Egr‐1

Hypoxia Stabilizes Microtubule Networks and Decreases Tumor Cell Chemosensitivity to Anticancer Drugs Through Egr‐1

Tumor Necrosis Factor-Alpha and the ERK Pathway Drive Chemerin Expression in Response to Hypoxia in Cultured Human Coronary Artery Endothelial Cells

Cysteine-rich 61 RNA interference inhibits pathological angiogenesis via the phosphatidylinositol 3-kinase/Akt-vascular endothelial growth factor signaling pathway in endothelial cells

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