Regulation of human airway smooth muscle cell migration and relevance to asthma

نویسندگان

  • Brittany Salter
  • Cara Pray
  • Katherine Radford
  • James G. Martin
  • Parameswaran Nair
چکیده

Airway remodelling is an important feature of asthma pathogenesis. A key structural change inherent in airway remodelling is increased airway smooth muscle mass. There is emerging evidence to suggest that the migration of airway smooth muscle cells may contribute to cellular hyperplasia, and thus increased airway smooth muscle mass. The precise source of these cells remains unknown. Increased airway smooth muscle mass may be collectively due to airway infiltration of myofibroblasts, neighbouring airway smooth muscle cells in the bundle, or circulating hemopoietic progenitor cells. However, the relative contribution of each cell type is not well understood. In addition, although many studies have identified pro and anti-migratory agents of airway smooth muscle cells, whether these agents can impact airway remodelling in the context of human asthma, remains to be elucidated. As such, further research is required to determine the exact mechanism behind airway smooth muscle cell migration within the airways, how much this contributes to airway smooth muscle mass in asthma, and whether attenuating this migration may provide a therapeutic avenue for asthma. In this review article, we will discuss the current evidence with respect to the regulation of airway smooth muscle cell migration in asthma.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Selective stimulation of IL-4 receptor on smooth muscle induces airway hyperresponsiveness in mice

Production of the cytokines IL-4 and IL-13 is increased in both human asthma and mouse asthma models, and Stat6 activation by the common IL-4/IL-13R drives most mouse model pathophysiology, including airway hyperresponsiveness (AHR). However, the precise cellular mechanisms through which IL-4Rα induces AHR remain unclear. Overzealous bronchial smooth muscle constriction is thought to underlie A...

متن کامل

Migration of the contractile phenotype of human airway smooth muscle cells in response to supernatants from rhinovirus infected human bronchial epithelial cells

Rationale Human rhinovirus (HRV) infections during early childhood are associated with a significantly increased risk of developing asthma in subsequent years [1]. There is published evidence that airway remodeling is present in pre-school children, often before the diagnosis of asthma is established [1]. It is thought that this increased risk relates to the fact that HRV infections facilitate ...

متن کامل

The role of autophagy in advanced glycation end product-induced proliferation and migration in rat vascular smooth muscle cells

Objective(s): To investigate the role of autophagy in advanced glycation end products (AGEs)-induced proliferation and migration in rat vascular smooth muscle cells (VSMCs).Materials and Methods: After culture, VSMCs were treated with 0, 1, 10, and 100 μg/ml concentrations of AGEs. Autophagy specific protein light chain 3 (LC3)-I/II was determined by western blotting, autophagosomes were observ...

متن کامل

Extracellular matrix regulates human airway smooth muscle cell migration.

Extracellular matrix proteins regulate the survival and proliferation of smooth muscle cells. Their effect on airway smooth muscle cell migration is not known. Their role in leukotriene-primed (0.1 microM leukotriene E4) chemotaxis of cultured human airway smooth muscle cells towards platelet-derived growth factor BB (1 ng.mL(-1)) was investigated. Migration of cells was greater on membranes co...

متن کامل

Inflammation signals airway smooth muscle cell proliferation in asthma pathogenesis

UNLABELLED BACKGROUND Airway inflammation stimulates proliferation of airway smooth muscle cell, which contributes to the development of hyperplasia and hypertrophy of smooth muscle cell. The increase in airway smooth muscle cell mass is believed to be due to an up-regulation of inflammatory mediators in the airway. It is now well recognized that chronic inflammation as well as airway hyper-...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره 18  شماره 

صفحات  -

تاریخ انتشار 2017