Expression and induction of the stress protein alpha-B-crystallin in vascular endothelial cells

Golenhofen, Nikola; Ness, Winfried; Wawrousek, Eric F.; Drenckhahn, Detlev

doi:10.1007/s00418-001-0378-7

Cited by 63 publications

(50 citation statements)

References 47 publications

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“…Hsp27 has been found to be increased in the myocardium during the development of heart failure (Tanonaka et al 2001). However, HSP27 has recently been found to respond differently from ␣B-crystallin in vascular endothelial cells (Golenhofen et al 2002). These observations warrant investigations at the subcellular level by immunohistochemistry.…”

Section: Discussionmentioning

confidence: 96%

Effects of hypoxia on stress proteins in the piglet heart at birth

Louapre

Grongnet²,

Tanguay

et al. 2005

Cell Stress Chaper

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Hypoxia at birth represents a very stressful event that can result in severe lifelong consequences in different tissues, including those of the heart. Heat shock and other associated stress proteins are involved in cellular protection, but their roles are not clearly defined at the time of birth. Newborn piglets were subjected to 5% oxygen and 95% nitrogen for either 1 or 4 hours. They were allowed to recover over periods of 1 to 68 hours. The relative levels of ␣B-crystallin, HspB8, Hsp20, Hsp27, Hsp60, and Hsp70 as well as nitric oxide synthases (NOS) (endothelial NOS, inducible NOS, neuronal NOS) were examined by Western blot analysis. Surprisingly, ␣B-crystallin expression was drastically increased in animals submitted to hypoxia. The hypoxia-associated factor HIFI␣ was also strongly and rapidly overexpressed. Heme oxygenase 1 was also increased. To a lesser extent, neuronal NOS was also increased in the left ventricle of animals submitted to hypoxia. This work clearly shows that the Hsp chaperone ␣B-crystallin is strongly overexpressed in the left ventricle of animals submitted to hypoxia. This observation dissociates the response to low oxygenation of ␣B-crystallin and other stress-associated proteins including Hsp27, and it indicates that heme oxygenase is not alone among HSPs in its oxygen-related gene expression.

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Section: Discussionmentioning

confidence: 96%

Effects of hypoxia on stress proteins in the piglet heart at birth

Louapre

Grongnet²,

Tanguay

et al. 2005

Cell Stress Chaper

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show abstract

“…Cells were passaged using a kit (Detach kit-30; PromoCell) and used between passages 2 and 5. Immortalized microvascular mouse myocardial endothelial cells (MyEnd) 17,18 were cultured on collagen 1-coated culture flasks and maintained in Dulbecco's modified Eagle's medium (SigmaAldrich, Munich, Germany) containing 10% fetal calf serum and 50 U/mL penicillin/50 g streptomycin. Primary porcine pulmonary artery endothelial cells (PAECs) were isolated by collagenase A treatment, as described elsewhere.…”

Section: Cell Culturementioning

confidence: 99%

Ultrastructural Analysis Reveals cAMP-Dependent Enhancement of Microvascular Endothelial Barrier Functions via Rac1-Mediated Reorganization of Intercellular Junctions

Spindler

Peter

Harms

et al. 2011

The American Journal of Pathology

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The barrier between blood and the surrounding interstitium, limiting the exchange of fluid and solutes, is provided by a single layer of endothelial cells that are coupled by intercellular junctions. Various pathological conditions in humans, such as edema, hemorrhagic stroke, and vascular malformations, have been, at least in part, caused by impaired endothelial barrier function and disruption of cell junctions.

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“…The cells were cultured as described (23). The microvascular endothelial cell line MyEND was obtained from mouse myocardium and characterized by positive staining for VE-cadherin, a-, h-, and g-catenin, ZO-1, and Claudin-5 as well as von Willebrand factor (44). The cells were cultured as described (45).…”

Section: Cell Culturementioning

confidence: 99%

Up-Regulation of Connective Tissue Growth Factor in Endothelial Cells by the Microtubule-Destabilizing Agent Combretastatin A-4

Samarin

Rehm²,

Krueger³

et al. 2009

Molecular Cancer Research

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Incubation of microvascular endothelial cells with combretastatin A-4 phosphate (CA-4P), a microtubule-destabilizing compound that preferentially targets tumor vessels, altered cell morphology and induced scattering of Golgi stacks. Concomitantly, CA-4P up-regulated connective tissue growth factor (CTGF/CCN2), a pleiotropic factor with antiangiogenic properties. In contrast to the effects of other microtubule-targeting agents such as colchicine or nocodazole, up-regulation of CTGF was only detectable in sparse cells, which were not embedded in a cell monolayer. Furthermore, CA-4P induced CTGF expression in endothelial cells, forming tube-like structures on basement membrane gels. Up-regulation of CTGF by CA-4P was dependent on Rho kinase signaling and was increased when p42/44 mitogen-activated protein kinase was inhibited. Additionally, FoxO transcription factors were identified as potent regulators of CTGF expression in endothelial cells. Activation of FoxO transcription factors by inhibition of phosphatidylinositol 3-kinase/AKT signaling resulted in a synergistic increase in CA-4P-mediated CTGF induction. CA-4P-mediated expression of CTGF was thus potentiated by the inhibition of kinase pathways, which are targets of novel antineoplastic drugs. Up-regulation of CTGF by low concentrations of CA-4P may thus occur in newly formed tumor vessels and contribute to the microvessel destabilization and antiangiogenic effects of CA-4P observed in vivo. (Mol Cancer Res 2009;7(2):180–8)

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Expression and induction of the stress protein alpha-B-crystallin in vascular endothelial cells

Cited by 63 publications

References 47 publications

Effects of hypoxia on stress proteins in the piglet heart at birth

Effects of hypoxia on stress proteins in the piglet heart at birth

Ultrastructural Analysis Reveals cAMP-Dependent Enhancement of Microvascular Endothelial Barrier Functions via Rac1-Mediated Reorganization of Intercellular Junctions

Up-Regulation of Connective Tissue Growth Factor in Endothelial Cells by the Microtubule-Destabilizing Agent Combretastatin A-4

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