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Mechanical Stretch and Cytokine Synthesis in Pulmonary Endothelial Cells

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Mechanical Stretch and Cytokines

Part of the book series: Mechanosensitivity in Cells and Tissues ((MECT,volume 5))

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Abstract

The respiratory system is dynamically exposed to physical forces derived from tidal breathing and blood flow. These physical forces are important for maintaining homeostasis of the respiratory system and normal lung development in vivo. In contrast, excessive mechanical forces lead to the pathogenesis of pulmonary diseases. Pulmonary endothelial cells serve as a barrier that regulates fluid balance and inflammatory cell accumulation in the lung. The functions of pulmonary endothelial cells are significantly affected by mechanical stimuli such as shear stress and mechanical stretch. For example, pulmonary endothelial cells produce cytokines/chemokines and nitric oxide in response to mechanical stimuli. The mechanotransduction pathways for mechanical force transmission into the intracellular signals are through mechanosensitive ion channels, integrins, actin cytoskeleton, and activation of mitogen-activated protein-kinases. Alterations in pulmonary endothelial cell properties due to excessive mechanical stress are suggested to play an important role in the disease progression of lung injury and inflammation. This chapter focuses on recent evidence regarding regulation of mechanical stress-induced cytokine/chemokine production by pulmonary endothelial cells and the role of pulmonary endothelial cells in the pathogenesis of pulmonary diseases related to mechanical stress.

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Abbreviations

ALI:

acute lung injury

ARDS:

acute respiratory distress syndrome

[Ca2+]I :

intracellular Ca2+ concentration

COPD:

chronic obstructive pulmonary disease

DAD:

diffuse alveolar damage

EC:

endothelial cell

ECM:

extracellular matrix

ELISA:

enzyme-linked immunosorbent assay

eNOS:

endothelial cell nitric oxide synthase

EPC:

endothelial progenitor cell

ERK:

extracellular signal-regulated kinase

GM-CSF:

granulocyte/macrophage colony stimulating factor

HUVEC:

human umbilical vein endothelial cell

IL:

interleukin

JNK:

c-Jun NH2-terminal kinase

LPS:

lipopolysaccharide

LVRS:

lung volume reduction surgery

MAP-kinase:

mitogen-activated protein-kinase

MCP-1:

monocyte chemoattractant protein-1

NO:

nitric oxide

PECAM-1:

platelet/endothelial cell adhesion molecule-1

TNF-α:

tumor necrosis factor-α

TRP:

transient receptor potential

VEGF:

vascular endothelial growth factor

VILI:

ventilator-induced lung injury

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Acknowledgements

This work was supported by Grants-in-Aid from the Ministry of Education, Culture, Sports, Science, and Technology of Japan (#19689017 and #22890837 to S.I.). We thank Dr. Béla Suki, Department of Biomedical Engineering, Boston University, for the helpful comments. We also thank Ms. Katherine Ono for providing language help.

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  1. Department of Respiratory Medicine, Nagoya University Graduate School of Medicine, Showa-ku, Nagoya, 466-8550, Japan

    Satoru Ito & Yoshinori Hasegawa

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  1. Satoru Ito
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  2. Yoshinori Hasegawa
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Correspondence to Satoru Ito .

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  1. Dept. Fundamental &, Applied Physiology, Russian State Medical University, Ostrovitjanova Str. 1, Moskva, 117997, Russian Federation

    Andre Kamkin

  2. , Department of Fundamental and Applied Ph, Russian State Medical University, Ostrovitjanova Str. 1, Moscow, 117997, Russian Federation

    Irina Kiseleva

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Ito, S., Hasegawa, Y. (2012). Mechanical Stretch and Cytokine Synthesis in Pulmonary Endothelial Cells. In: Kamkin, A., Kiseleva, I. (eds) Mechanical Stretch and Cytokines. Mechanosensitivity in Cells and Tissues, vol 5. Springer, Dordrecht. https://doi.org/10.1007/978-94-007-2004-6_7

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