Classification of Signals for Blocking Apoptosis in Vascular Endothelial Cells

Hase, Makoto; Araki, Satohiko; Kaji, Koichi; Hayashi, Hiroshi

doi:10.1093/oxfordjournals.jbchem.a124614

Cited by 27 publications

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“…In the present study we investigated the possible relationship between adherent and detached endothelial cells and the formation of EMP. In line with previous studies, we found that detached endothelial cells are apoptotic, similar to other cells losing their association with the matrix [22–26], i.e. most of the detached cells stained for annexin V and PI, and contained caspase 3.…”

Section: Discussionsupporting

confidence: 91%

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Cell‐derived microparticles contain caspase 3 in vitro and in vivo

Hussein

Nieuwland

Hau

et al. 2005

Journal of Thrombosis and Haemostasis

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; 24 h). Cell fractions were analyzed by flow cytometry for annexin V binding, propidium iodide (PI) and caspase 3 staining (n ¼ 3). Caspase 3 in EMP was studied using Western blot (n ¼ 6) and flow cytometry (n ¼ 6). Plasma from healthy subjects and systemic lupus erythematosus patients (both n ¼ 3) were analyzed for caspase 3-containing (E)MP. Results: Detached but not adherent cells double-stained for annexin V and PI, confirming the apoptotic conditions of the detached cells and the viable nature of the adherent cells. Caspase 3 was solely present in the detached cells and procaspase 3 in the adherent cells. Caspase 3 was present in EMP from both control and IL1a-treated cultures. Counts of EMP and detached cells, but not adherent cells, highly correlated (r ¼ 0.959, P < 0.0001). In vivo circulating MP from nucleated (endothelial cells, monocytes) and anucleated cells (platelets, erythrocytes) contained caspase 3. Conclusions: EMP contain caspase 3 and may be mainly derived from detached (apoptotic) endothelial cells in vitro. The presence of caspase 3 in MP from anucleated cell types, however, suggests that its presence may not necessarily be related to apoptosis in vivo but may be associated with caspase 3 activation unrelated to apoptosis.

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Section: Discussionsupporting

confidence: 91%

“…In vitro , small fractions of endothelial cells appear as ‘floaters’ that display typical biochemical and morphological features of apoptosis [22–25]. This is a well‐known phenomenon, called anoikis (Greek for ‘homelessness’), i.e.…”

Section: Introductionmentioning

confidence: 99%

Cell‐derived microparticles contain caspase 3 in vitro and in vivo

Hussein

Nieuwland

Hau

et al. 2005

Journal of Thrombosis and Haemostasis

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“…Indeed, detached HBMEC displayed significant signs of apoptosis. On the other hand, endothelial cell detachment has been demonstrated as a late feature of endothelial cells undergoing apoptosis [56] and pathogenic Neisseriae have been shown to induce the expression of apoptosis-related genes and to trigger apoptosis in different cell types [40]–[42], [57]. Caspase 3 has been shown to act as an effector for the cytoskeletal remodelling involved in cell “rounding” that occurs before the apoptotic cell detaches [39].…”

Section: Discussionmentioning

confidence: 99%

Neisseria meningitidis Induces Brain Microvascular Endothelial Cell Detachment from the Matrix and Cleavage of Occludin: A Role for MMP-8

et al. 2010

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Disruption of the blood-brain barrier (BBB) is a hallmark event in the pathophysiology of bacterial meningitis. Several inflammatory mediators, such as tumor necrosis factor alpha (TNF-α), nitric oxide and matrix metalloproteinases (MMPs), contribute to this disruption. Here we show that infection of human brain microvascular endothelial cells (HBMEC) with Neisseria meningitidis induced an increase of permeability at prolonged time of infection. This was paralleled by an increase in MMP-8 activity in supernatants collected from infected cells. A detailed analysis revealed that MMP-8 was involved in the proteolytic cleavage of the tight junction protein occludin, resulting in its disappearance from the cell periphery and cleavage to a lower-sized 50-kDa protein in infected HBMEC. Abrogation of MMP-8 activity by specific inhibitors as well as transfection with MMP-8 siRNA abolished production of the cleavage fragment and occludin remained attached to the cell periphery. In addition, MMP-8 affected cell adherence to the underlying matrix. A similar temporal relationship was observed for MMP activity and cell detachment. Injury of the HBMEC monolayer suggested the requirement of direct cell contact because no detachment was observed when bacteria were placed above a transwell membrane or when bacterial supernatant was directly added to cells. Inhibition of MMP-8 partially prevented detachment of infected HBMEC and restored BBB permeability. Together, we established that MMP-8 activity plays a crucial role in disassembly of cell junction components and cell adhesion during meningococcal infection.

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“…6 The regulation of apoptosis is complex. In vitro, withdrawal of a growth factor is a well recognized trigger for apoptosis in many cells, including endothelial cells, 7 and these growth factors are frequently referred to as survival factors. The potential consequence of the loss of normal levels of growth factors in vivo has not been extensively addressed.…”

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confidence: 99%

Exposure to Hyperoxia Decreases the Expression of Vascular Endothelial Growth Factor and Its Receptors in Adult Rat Lungs

Klekamp

Jarzecka

Perkett

1999

The American Journal of Pathology

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Exposure to high levels of inspired oxygen leads to respiratory failure and death in many animal models. Endothelial cell death is an early finding , before the onset of respiratory failure. Vascular endothelial growth factor (VEGF) is highly expressed in the lungs of adult animals. In the present study , adult SpragueDawley rats were exposed to >95% FiO 2 for 24 or 48 hours. Northern blot analysis revealed a marked reduction in VEGF mRNA abundance by 24 hours, which decreased to less than 50% of control by 48 hours. In situ hybridization revealed that VEGF was highly expressed in distal airway epithelial cells in controls but disappeared in the oxygen-exposed ani- Supplemental oxygen therapy has marked beneficial effects in the treatment of numerous cardiorespiratory diseases, but oxygen use is limited by direct toxicity. Severe pulmonary damage from exposure to high levels of inspired oxygen has been well documented in animal models. For example, rats exposed to Ͼ95% FiO 2 are asymptomatic for 48 hours, but the animals then develop pulmonary edema and respiratory failure that progresses to death within 72 to 96 hours.

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Classification of Signals for Blocking Apoptosis in Vascular Endothelial Cells

Cited by 27 publications

References 0 publications

Cell‐derived microparticles contain caspase 3 in vitro and in vivo

Cell‐derived microparticles contain caspase 3 in vitro and in vivo

Neisseria meningitidis Induces Brain Microvascular Endothelial Cell Detachment from the Matrix and Cleavage of Occludin: A Role for MMP-8

Exposure to Hyperoxia Decreases the Expression of Vascular Endothelial Growth Factor and Its Receptors in Adult Rat Lungs

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