title: Phenotype modulation of airway smooth muscle in asthma.
abstract: The biological responses of airway smooth muscle (ASM) are diverse, in part due to ASM phenotype plasticity. ASM phenotype plasticity refers to the ability of ASM cells to change the degree of a variety of functions, including contractility, proliferation, migration and secretion of inflammatory mediators. This plasticity occurs due to intrinsic or acquired abnormalities in ASM cells, and these abnormalities or predisposition of the ASM cell may alter the ASM response and in some cases recapitulate disease hallmarks of asthma. These phenotypic changes are ultimately determined by multiple stimuli and occur due to alterations in the intricate balance or reversible state that maintains ASM cells in either a contractile or synthetic state, through processes termed maturation or modulation, respectively. To elucidate the role of ASM phenotype in disease states, numerous in vitro studies have suggested a phenotypic switch in ASM primary cell cultures as an explanation for the plethora of responses mediated by ASM cells. Moreover, there is overwhelming evidence suggesting that the immunomodulatory response of ASM is due to the acquisition of a synthetic phenotype; however, whether this degree of plasticity is present in vivo as opposed to cell culture-based models remains speculative. Nonetheless, this review will give an overall scope of ASM phenotypic markers, triggers of ASM phenotype modulation and novel therapeutic approaches to control ASM phenotype plasticity.
authors.affiliation: Medical Research Council and Asthma UK Centre in Allergic Mechanisms of Asthma, King's College London, London, United Kingdom.
authors.forename: David B
authors.initials: DB
authors.lastname: Wright
authors.forename: Thomas
authors.initials: T
authors.lastname: Trian
authors.forename: Sana
authors.initials: S
authors.lastname: Siddiqui
authors.forename: Chris D
authors.initials: CD
authors.lastname: Pascoe
authors.forename: Jill R
authors.initials: JR
authors.lastname: Johnson
authors.forename: Bart G J
authors.initials: BG
authors.lastname: Dekkers
authors.forename: Shyamala
authors.initials: S
authors.lastname: Dakshinamurti
authors.forename: Rushita
authors.initials: R
authors.lastname: Bagchi
authors.forename: Janette K
authors.initials: JK
authors.lastname: Burgess
authors.forename: Varsha
authors.initials: V
authors.lastname: Kanabar
authors.forename: Oluwaseun O
authors.initials: OO
authors.lastname: Ojo
mesh_terms: D000818:Animals; D001249:Asthma / Q000503:physiopathology*; D002465:Cell Movement; D049109:Cell Proliferation; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D009119:Muscle Contraction / Q000502:physiology; D009130:Muscle, Smooth / Q000166:cytology / Q000378:metabolism / Q000473:pathology*; D032389:Myocytes, Smooth Muscle / Q000378:metabolism / Q000473:pathology*; D010641:Phenotype
chemical_list: D018836:Inflammation Mediators