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Effects of Inflammatory Cytokines on Ca2+ Homeostasis in Airway Smooth Muscle Cells

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Calcium Signaling In Airway Smooth Muscle Cells

Abstract

Crosstalk between airway inflammation and airway smooth muscle cells (ASMCs) contributes to airway hyperresponsiveness, a cardinal feature of asthma. The main putative mechanism underlying the agonist-induced intracellular Ca2+ ([Ca2+]i) transients in ASMCs is Ca2+ release from the sarcoplasmic reticulum (SR) via the inositol 1,4,5-trisphosphate (IP3) receptor and ryanodine receptor (RyR). Ca2+ depletion in SR then triggers store-operated Ca2+ entry (SOCE), Ca2+ influx from extracellular space. These mechanisms are modulated by inflammatory cytokines, such as tumor necrosis factor (TNF)-α and interleukin (IL)-13, which have pivotal roles in asthma and chronic obstructive pulmonary disease (COPD).

TNF-α upregulates Gq and Gi protein expression, and interleukin (IL)-13 enhances histamine H1 receptor and cysteinyl leukotriene receptor 1, which enhances agonist-induced IP3/IP3 receptor signaling. Expression of CD38, which affects Ca2+ release from the SR via RyR, is upregulated with TNF-α, IL-13, and, to a lesser extent, interferon-γ and IL-1β pretreatment. TNF-α and IL-13 also augment SOCE and expression of caveolin-1, a scaffolding protein in caveolae, flask-shaped plasma membrane invaginations, which play a key role in Ca2+ signaling. Furthermore, both TNF-α and IL-13 decrease the expression of sarcoendoplasmic reticulum Ca2+ ATPase SERCA2, which transfers Ca2+ from the cytosol of the cell to the lumen of the SR to replenish Ca2+ in the SR. The downregulation of SERCA2 mimics altered Ca2+ homeostasis observed in asthma. This chapter describes the mechanisms that underlie the inflammatory cytokine-mediated modulation of [Ca2+]i in ASMCs.

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Abbreviations

ACh:

Acetylcholine

AHR:

Airway hyperresponsiveness

ASMC:

Airway smooth muscle cell

β2AR:

β2 adrenergic receptor

BKCa :

High-conductance Ca2+-activated potassium

[Ca2+]i :

Intracellular Ca2+

cADPR:

Cyclic ADP-ribose

CICR:

Ca2+-induced Ca2+ release

COPD:

Chronic obstructive pulmonary disease

CysLT1R:

Cysteinyl leukotriene receptor

DAG:

1,2-diacylglycerol

ERK:

Extracellular signal-regulated kinase

HASMC:

Human ASMC

IFN:

Interferon

IL:

Interleukin

IP3 :

Inositol 1,4,5-trisphosphate

JAK:

Janus kinase

JNK:

c-Jun N-terminal kinase

LTD4:

Leukotriene D4

MLCK:

Myosin light chain kinase

MLCP:

Myosin light chain phosphatase

PKA:

Protein kinase A

PKC:

Protein kinase C

ROCC:

Receptor-operated Ca2+ channels

ROCE:

Receptor-operated Ca2+ entry

RyR:

Ryanodine receptor

SERCA:

Sarcoendoplasmic reticulum Ca2+ ATPase

STAT:

Signal transducer and activator of transcription

STIM:

Stromal-interacting molecule

SOCC:

Store-operated Ca2+ channel

SOCE:

Store-operated Ca2+ entry

SR:

Sarcoplasmic reticulum

TGF:

Transforming growth factor

TNF:

Tumor necrosis factor

TNFR:

Tumor necrosis factor receptor

TRPC:

Transient receptor potential channels

TSLP:

Thymic stromal lymphopoietin

VOCC:

Voltage-operated Ca2+ channel

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Authors and Affiliations

  1. Department of Respiratory Medicine, Kyoto University, 54, Kawahara-cho, Shogoin, Sakyo-ku, Kyoto, 606-8507, Japan

    Hisako Matsumoto M.D., Ph.D.

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  1. Hisako Matsumoto M.D., Ph.D.
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Correspondence to Hisako Matsumoto M.D., Ph.D. .

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  1. Albany Medical College Center for Cardiovascular Sciences, Albany, New York, USA

    Yong-Xiao Wang

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Matsumoto, H. (2014). Effects of Inflammatory Cytokines on Ca2+ Homeostasis in Airway Smooth Muscle Cells. In: Wang, YX. (eds) Calcium Signaling In Airway Smooth Muscle Cells. Springer, Cham. https://doi.org/10.1007/978-3-319-01312-1_20

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