Airway smooth muscle growth from the perspective of animal models.
Airway smooth muscle maintains airway tone and may assist in adjusting ventilation distribution within the normal lung. Alterations in the properties or the quantity of ASM are likely responsible for some instances of airways hyperresponsiveness to bronchoconstrictive stimuli that is a characteristic of diseases such as asthma. Morphometric studies have shown an increase in the mass of ASM in human asthmatic airways. Animal models have been developed that confirm that ASM can be induced to grow by allergic sensitization and challenge. Growth is in large part by hyperplasia as measured by incorporation of bromodeoxyuridine as a marker of the S-phase of the cell cycle. T cells, in particular CD4+ cells, may participate in the stimulation of growth of ASM by allergen challenge. The growth factors responsible for the increase in ASM are as yet unidentified but two mediators associated with allergic airway responses, cysteinyl leukotrienes and endothelin, have been implicated using specific receptor antagonists. The links between T cells and the biochemical mediators of growth have not been established.
D000222:Adaptation, Physiological; D000818:Animals; D001249:Asthma / Q000503:physiopathology*; D001980:Bronchi / Q000166:cytology; D016535:Bronchial Hyperreactivity / Q000503:physiopathology*; D004195:Disease Models, Animal; D004285:Dogs; D006801:Humans; D007091:Image Processing, Computer-Assisted; D051379:Mice; D009130:Muscle, Smooth / Q000166:cytology / Q000254:growth & development*; D032389:Myocytes, Smooth Muscle / Q000502:physiology*; D051381:Rats; D014132:Trachea / Q000166:cytology