Stress-induced fractal rearrangement of the endothelial cell cytoskeleton causes apoptosis

DeMeester, Susan L.; Cobb, J. Perren; Hotchkiss, Richard S.; Osborne, Dale F.; Karl, Irene E.; Tinsley, Kevin W.; Buchman, Timothy G.

doi:10.1067/msy.1998.90579

Cited by 4 publications

(3 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…4). Such heat-induced disruption of actin organization is consistent with previous observations obtained from endothelial cells cultured in flasks [19,20]. Romanov et al [20] found that short-lasting hyperthermia (1-4 h) triggered the disappearance of cytoplasmic actin filaments and their redistribution to areas of cell-to-cell contact.…”

Section: Discussionsupporting

confidence: 90%

“…Romanov et al [20] found that short-lasting hyperthermia (1-4 h) triggered the disappearance of cytoplasmic actin filaments and their redistribution to areas of cell-to-cell contact. DeMeester et al [19] found that inflammatory and/or heat shock treatments induced a dramatic cytoskeletal collapse in endothelial cells, suggesting that cytoskeletal rearrangement is likely a critical event in the pathway to apoptosis. In order to reveal the relationship between cytoskeletal collapse and apoptosis, we additionally examined including the nuclear factor-kappaB and mitogen-activated protein kinase pathways (for review, see [22]).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

A microfluidic cell culture system for monitoring of sequential changes in endothelial cells after heat stress

Tazawa¹,

Sato²,

Tsutiya³

et al. 2015

Thrombosis Research

View full text Add to dashboard Cite

Endothelial damage induced by a highly elevated body temperature is crucial in some diseases including viral hemorrhagic fevers. Here, we report the heat-induced sequential changes of endothelial cells under shear stress, which were determined with a microfluidic culture system. Although live cell imaging showed only minor changes in the appearance of heat-treated cells, Hsp70 mRNA expression analysis demonstrated that the endothelial cells in channels of the system responded well to heat treatment. F-actin staining also revealed clear changes in the bundles of actin filaments after heat treatment. Well-organized bundles of actin filaments in control cells disappeared in heat-treated cells cultured in the channel. Furthermore, the system enabled detection of sequential changes in plasminogen activator inhibitor-1 (PAI-1) secretion from endothelial cells. PAI-1 concentration in the effluent solution was significantly elevated for the first 15min after initiation of heat treatment, and then decreased subsequently. This study provides fundamental information on heat-induced endothelial changes under shear stress and introduces a potent tool for analyzing endothelial secretions.

show abstract

Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

A microfluidic cell culture system for monitoring of sequential changes in endothelial cells after heat stress

Tazawa¹,

Sato²,

Tsutiya³

et al. 2015

Thrombosis Research

View full text Add to dashboard Cite

show abstract

“…Thus, the adaptive response to hypovolemia is integrated simultaneously at the level of the cell and the organism. The hypothesis that organ dysfunction after injury results in part by alterations in intercellular interactions (communication) has only recently gained broad appeal [9][10][11][12].…”

Section: Figmentioning

confidence: 99%

Molecular Biology of Multiple Organ Dysfunction Syndrome: Injury, Adaptation, and Apoptosis

Cobb¹,

Buchman²,

Karl³

et al. 2000

Surgical Infections

Self Cite

View full text Add to dashboard Cite

Injury will equal or surpass communicable disease in the year 2020 as the number one cause of lost disability-adjusted life-years worldwide. The major cause of "late death" after trauma is organ dysfunction, commonly as a complication of shock or sepsis. The pathophysiology of injury-induced organ dysfunction is poorly characterized but has been linked to systemic inflammation as a result of infection (either obvious or occult) or massive tissue injury (systemic inflammatory response syndrome, SIRS). Subsequent complications of organ dysfunction, including death, may also stem from immunosuppression characteristic of what has been called the counter-regulatory anti-inflammatory response syndrome (CARS). At the cellular level, injurious stimuli trigger adaptive stress responses that include changes in gene expression. Multiple organ dysfunction syndrome (MODS) is the summation of these stress responses to severe systemic injury, integrated at the cellular, organ, and host levels. We hypothesize that a complete understanding at the molecular level of the stress responses induced by injury will aid in the development of therapeutic strategies for treating MODS in the critically ill surgical patient. This paper reviews recent data from our Cellular Injury and Adaptation Laboratory relevant to our understanding of MODS pathophysiology, particularly as it relates to stress-induced cell death by apoptosis. Our data suggest that inhibition of stress-induced apoptosis may improve survival after severe injury.

show abstract

Characterization of Melanophore Morphology by Fractal Dimension Analysis

Kimler¹,

Tracy-Bee²,

Ollie

et al. 2004

Pigment Cell Research

View full text Add to dashboard Cite

Fractal or focal dimension (FD) analysis is a valuable tool to identify physiologic stimuli at the cellular and tissue levels that allows for quantification of cell perimeter complexity. The FD analysis was determined on fluorescence images of caffeine- or epinephrine-treated (or untreated control) killifish Fundulus heteroclitus (Linneaus) melanophores in culture. Cell perimeters were indicated by rhodamine-phalloidin labeling of cortical microfilaments using box-counting FD analysis. Caffeine-treated melanophores displayed dispersed melanosomes in cells with less serrated edges and reduced FD and complexity. Complexity in epinephrine-treated cells was significantly higher than the caffeine-treated cells or in the control. Cytoarchitectural variability of the cell perimeter is expected because cells change shape when cued with agents. Epinephrine-treated melanophores demonstrated aggregated melanosomes in cells with more serrated edges, significantly higher FD and thus complexity. Melanophores not treated with caffeine or epinephrine produced variable distributions of melanosomes and resulted in cells with variably serrated edges and intermediate FD with a larger SE of the regression and greater range of complexity. Dispersion of melanosomes occurs with rearrangements of the cytoskeleton to accommodate centrifugal distribution of melanosomes throughout the cell and to the periphery. The loading of melanosomes onto cortical microfilaments may provide a less complex cell contour, with the even distribution of the cytoskeleton and melanosomes. Aggregation of melanosomes occurs with rearrangements of the cytoskeleton to accommodate centripetal distribution of melanosomes. The aggregation of melanosomes may contribute to centripetal retraction of the cytoskeleton and plasma membrane. The FD analysis is, therefore, a convenient method to measure contrasting morphologic changes within stimulated cells.

show abstract

Stress-induced fractal rearrangement of the endothelial cell cytoskeleton causes apoptosis

Cited by 4 publications

References 0 publications

A microfluidic cell culture system for monitoring of sequential changes in endothelial cells after heat stress

A microfluidic cell culture system for monitoring of sequential changes in endothelial cells after heat stress

Molecular Biology of Multiple Organ Dysfunction Syndrome: Injury, Adaptation, and Apoptosis

Characterization of Melanophore Morphology by Fractal Dimension Analysis

Contact Info

Product

Resources

About