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Alveolar type II cells escape stress failure caused by tonic stretch through transient focal adhesion disassembly.

Liu XY, Chen XF, Ren YH, Zhan QY, Wang C, Yang C - Int. J. Biol. Sci. (2011)

Bottom Line: Avoiding cellular stress failure is crucial to ventilator-induced lung injury (VILI) treatment.In addition, immunofluorescence and immunoblots assay showed that the cells experienced an expansion-contraction-reexpansion process, accompanied by partial focal adhesion (FA) disassembly during contraction.Finally, a simplified numerical model was established to reveal that adequate disassembly of FAs reduced the forces transmitting throughout the cell.

View Article: PubMed Central - PubMed

Affiliation: Beijing Chao-Yang Hospital, Capital Medical University, China.

ABSTRACT
Mechanical ventilation-induced excessive stretch of alveoli is reported to induce cellular stress failure and subsequent lung injury, and is therefore an injurious factor to the lung. Avoiding cellular stress failure is crucial to ventilator-induced lung injury (VILI) treatment. In the present study, primary rat alveolar type II (ATII) cells were isolated to evaluate their viability and the mechanism of their survival under tonic stretch. By the annexin V/ PI staining and flow cytometry assay, we demonstrated that tonic stretch-induced cell death is an immediate injury of mechanical stress. In addition, immunofluorescence and immunoblots assay showed that the cells experienced an expansion-contraction-reexpansion process, accompanied by partial focal adhesion (FA) disassembly during contraction. Manipulation of integrin adherent affinity by altering bivalent cation levels in the culture medium and applying an integrin neutralizing antibody showed that facilitated adhesion affinity promoted cell death under tonic stretch, while lower level of adhesion protected the cells from stretch-induced stress failure. Finally, a simplified numerical model was established to reveal that adequate disassembly of FAs reduced the forces transmitting throughout the cell. Taken together, these results indicate that ATII cells escape stress failure caused by tonic stretch via active cell morphological remodeling, during which cells transiently disassemble FAs to unload mechanical forces.

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The homogeneous standard linear solid (SLS) model. The whole cell is modeled as a homogeneous viscoelastic SLS.
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FS1: The homogeneous standard linear solid (SLS) model. The whole cell is modeled as a homogeneous viscoelastic SLS.

Mentions: Living cells exhibit viscoelastic behavior. Specifically, adherent cells can be represented by a three element standard linear solid model (Fig. S1) that is analogous to a spring and fluid-like viscoelastic Maxwell model because of its solid-like character. The constitutive relation of the SLS model takes the form


Alveolar type II cells escape stress failure caused by tonic stretch through transient focal adhesion disassembly.

Liu XY, Chen XF, Ren YH, Zhan QY, Wang C, Yang C - Int. J. Biol. Sci. (2011)

The homogeneous standard linear solid (SLS) model. The whole cell is modeled as a homogeneous viscoelastic SLS.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3101527&req=5

FS1: The homogeneous standard linear solid (SLS) model. The whole cell is modeled as a homogeneous viscoelastic SLS.
Mentions: Living cells exhibit viscoelastic behavior. Specifically, adherent cells can be represented by a three element standard linear solid model (Fig. S1) that is analogous to a spring and fluid-like viscoelastic Maxwell model because of its solid-like character. The constitutive relation of the SLS model takes the form

Bottom Line: Avoiding cellular stress failure is crucial to ventilator-induced lung injury (VILI) treatment.In addition, immunofluorescence and immunoblots assay showed that the cells experienced an expansion-contraction-reexpansion process, accompanied by partial focal adhesion (FA) disassembly during contraction.Finally, a simplified numerical model was established to reveal that adequate disassembly of FAs reduced the forces transmitting throughout the cell.

View Article: PubMed Central - PubMed

Affiliation: Beijing Chao-Yang Hospital, Capital Medical University, China.

ABSTRACT
Mechanical ventilation-induced excessive stretch of alveoli is reported to induce cellular stress failure and subsequent lung injury, and is therefore an injurious factor to the lung. Avoiding cellular stress failure is crucial to ventilator-induced lung injury (VILI) treatment. In the present study, primary rat alveolar type II (ATII) cells were isolated to evaluate their viability and the mechanism of their survival under tonic stretch. By the annexin V/ PI staining and flow cytometry assay, we demonstrated that tonic stretch-induced cell death is an immediate injury of mechanical stress. In addition, immunofluorescence and immunoblots assay showed that the cells experienced an expansion-contraction-reexpansion process, accompanied by partial focal adhesion (FA) disassembly during contraction. Manipulation of integrin adherent affinity by altering bivalent cation levels in the culture medium and applying an integrin neutralizing antibody showed that facilitated adhesion affinity promoted cell death under tonic stretch, while lower level of adhesion protected the cells from stretch-induced stress failure. Finally, a simplified numerical model was established to reveal that adequate disassembly of FAs reduced the forces transmitting throughout the cell. Taken together, these results indicate that ATII cells escape stress failure caused by tonic stretch via active cell morphological remodeling, during which cells transiently disassemble FAs to unload mechanical forces.

Show MeSH
Related in: MedlinePlus