TY - JOUR
T1 - Methodologic advancements in the study of airway smooth muscle
AU - Kotlikoff, Michael I.
AU - Kannan, Mathur S.
AU - Solway, Julian
AU - Deng, Ke Yu
AU - Deshpande, Deepak A.
AU - Dowell, Maria
AU - Feldman, Morris
AU - Green, Kai Su
AU - Ji, Guangju
AU - Johnston, Robyn
AU - Lakser, Oren
AU - Lee, Jane
AU - Lund, Frances E.
AU - Milla, Carlos
AU - Mitchell, Richard W.
AU - Nakai, Junichi
AU - Rishniw, Mark
AU - Walseth, Timothy F.
AU - White, Thomas A.
AU - Wilson, Jason
AU - Xin, Hong Bo
AU - Woodruff, Prescott G.
N1 - Funding Information:
Supported by grants HL45239, DK58795, and DK065992 from the National Institutes of Health (Dr Kotlikoff), grants from the Academic Health Center, University of Minnesota (Dr Walseth and Dr Kannan), grants HL56399, AI56352, and HL07605 from the National Institutes of Health (Dr Solway), and support by K23 RR17002 and the General Clinical Research Center, Moffitt Hospital, University of California, San Francisco, with funds provided by the National Center for Research Resources, 5 M01 RR-00079, US Public Health Service (Dr Woodruff).
PY - 2004/8
Y1 - 2004/8
N2 - The study of isolated airway myocytes has provided important information relative to specific processes that regulate contraction, proliferation, and synthetic properties of airway smooth muscle (ASM). To place this information in physiological context, however, improved methods to examine airway biology in vivo are needed. Advances in genetic, biochemical, and optical methods provide unprecedented opportunities to improve our understanding of in vivo physiology and pathophysiology. This article describes 4 important methodologic advances in the study of ASM: (1) the development of transgenic mice that could be used to investigate ASM proliferation and phenotype switching during the development of hypersensitivity, and to investigate excitation-contraction coupling; (2) the use of CD38-deficient mice to confirm the role of CD38-dependent, cyclic adenosine diphosphate-ribose-mediated calcium release in airway responsiveness; (3) investigation of the role of actin filament length and p38 mitogen-activated protein kinase activity in regulating the mechanical plasticity-elasticity balance in contracted ASM; and (d) the use of bronchial biopsies to study ASM structure and phenotype in respiratory science.
AB - The study of isolated airway myocytes has provided important information relative to specific processes that regulate contraction, proliferation, and synthetic properties of airway smooth muscle (ASM). To place this information in physiological context, however, improved methods to examine airway biology in vivo are needed. Advances in genetic, biochemical, and optical methods provide unprecedented opportunities to improve our understanding of in vivo physiology and pathophysiology. This article describes 4 important methodologic advances in the study of ASM: (1) the development of transgenic mice that could be used to investigate ASM proliferation and phenotype switching during the development of hypersensitivity, and to investigate excitation-contraction coupling; (2) the use of CD38-deficient mice to confirm the role of CD38-dependent, cyclic adenosine diphosphate-ribose-mediated calcium release in airway responsiveness; (3) investigation of the role of actin filament length and p38 mitogen-activated protein kinase activity in regulating the mechanical plasticity-elasticity balance in contracted ASM; and (d) the use of bronchial biopsies to study ASM structure and phenotype in respiratory science.
KW - ASM
KW - Airway smooth muscle
KW - Asthma
KW - CD38/cyclic ADP-ribose pathway
KW - airway smooth muscle
KW - bronchial biopsy
KW - cADPR
KW - calcium homeostasis
KW - excitation-contraction coupling
KW - morphometric changes
KW - phenotype
KW - plasticity- elasticity balance
KW - proliferation
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U2 - 10.1016/j.jaci.2004.04.040
DO - 10.1016/j.jaci.2004.04.040
M3 - Article
C2 - 15309016
AN - SCOPUS:4043174779
SN - 0091-6749
VL - 114
SP - S18-S31
JO - Journal of Allergy and Clinical Immunology
JF - Journal of Allergy and Clinical Immunology
IS - 2 SUPPL.
ER -