Distinct Effects of Ca2+ Sparks on Cerebral Artery and Airway Smooth Muscle Cell Tone in Mice and Humans

Chronic airway diseases, such as asthma or chronic obstructive pulmonary disease, are characterized by the presence in the airways of inflammation factors, growth factors and cytokines, which promote airway wall remodelling. The aim of this study was to investigate the effect of cytokines and growth factors on airway smooth muscle cell (ASMC) proliferation, phenotype and responsiveness. Incubation of serum starved human bronchial ASMCs with TNF-α, TGF, bFGF, and PDGF, but not IL-1β, increased methyl-[3H]thymidine incorporation and cell number, mediated by the PI3K and MAPK signalling pathways. Regarding rabbit tracheal ASMC proliferation, TNF-α, IL-1β, TGF, and PDGF increased methyl-[3H]thymidine incorporation in a PI3K- and MAPK-dependent manner. bFGF increased both methyl-[3H]thymidine incorporation and cell number. Moreover, incubation with TGF, bFGF and PDGF appears to drive human ASMCs towards a synthetic phenotype, as shown by the reduction of the percentage of cells expressing SM-α actin. In addition, the responsiveness of epithelium-denuded rabbit tracheal strips to carbachol was not significantly altered after 3-day treatment with bFGF. In conclusion, all the tested cytokines and growth factors increased ASMC proliferation to a different degree, depending on the specific cell type, with bronchial ASMCs being more prone to proliferation than tracheal ASMCs.

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Human airway smooth muscle cell proliferation from asthmatics is negatively regulated by semaphorin3A

Oncotarget ◽

10.18632/oncotarget.12884 ◽

2016 ◽

Vol 7 (49) ◽

pp. 80238-80251 ◽

Cited By ~ 17

Author(s):

Hesam Movassagh ◽

Nazanin Tatari ◽

Lianyu Shan ◽

Latifa Koussih ◽

Duaa Alsubait ◽

...

Keyword(s):

Cell Proliferation ◽

Smooth Muscle ◽

Smooth Muscle Cell ◽

Airway Smooth Muscle ◽

Muscle Cell ◽

Airway Smooth Muscle Cell ◽

Smooth Muscle Cell Proliferation ◽

Human Airway Smooth Muscle ◽

Human Airway

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Effects of hypoxia on rat airway smooth muscle cell proliferation

Journal of Applied Physiology ◽

10.1152/japplphysiol.00363.2002 ◽

2003 ◽

Vol 94 (4) ◽

pp. 1403-1409 ◽

Cited By ~ 21

Author(s):

A. Cogo ◽

G. Napolitano ◽

M. C. Michoud ◽

D. Ramos Barbon ◽

M. Ward ◽

...

Keyword(s):

Cell Proliferation ◽

Smooth Muscle ◽

Cell Growth ◽

Smooth Muscle Cells ◽

Smooth Muscle Cell ◽

Airway Smooth Muscle ◽

Muscle Cell ◽

Muscle Cells ◽

Airway Smooth Muscle Cell ◽

Gf 109203X

Although it is well known that hypoxemia induces pulmonary vasoconstriction and vascular remodeling, due to the proliferation of both vascular smooth muscle cells and fibroblasts, the effects of hypoxemia on airway smooth muscle cells are not well characterized. The present study was designed to assess the in vitro effects of hypoxia (1 or 3% O2) on rat airway smooth muscle cell growth and response to mitogens (PDGF and 5-HT). Cell growth was assessed by cell counting and cell cycle analysis. Compared with normoxia (21% O2), there was a 42.2% increase in the rate of proliferation of cells exposed to 3% O2 (72 h, P = 0.006), as well as an enhanced response to PDGF (13.9% increase; P = 0.023) and to 5-HT (17.2% increase; P = 0.039). Exposure to 1% O2 (72 h) decreased cell proliferation by 21.0% ( P = 0.017) and reduced the increase in cell proliferation induced by PGDF and 5-HT by 16.2 and 15.7%, respectively ( P = 0.019 and P = 0.011). A significant inhibition in hypoxia-induced cell proliferation was observed after the administration of bisindolylmaleimide GF-109203X (a specific PKC inhibitor) or downregulation of PKC with PMA. Pretreatment with GF-109203X decreased proliferation by 21.5% ( P = 0.004) and PMA by 31.5% ( P = 0.005). These results show that hypoxia induces airway smooth muscle cell proliferation, which is at least partially dependent on PKC activation. They suggest that hypoxia could contribute to airway remodeling in patients suffering from chronic, severe respiratory diseases.

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