Factors controlling smooth muscle proliferation and airway remodelling

2002 ◽  
Vol 2 (1) ◽  
pp. 47-51 ◽  
Author(s):  
Judith L. Black ◽  
Peter R.A. Johnson
Author(s):  
J.M. Minda ◽  
E. Dessy ◽  
G. G. Pietra

Pulmonary lymphangiomyomatosis (PLAM) is a rare disease occurring exclusively in women of reproductive age. It involves the lungs, lymph nodes and lymphatic ducts. In the lungs, it is characterized by the proliferation of smooth muscle cells around lymphatics in the bronchovascular bundles, lobular septa and pleura The nature of smooth muscle proliferation in PLAM is still unclear. Recently, reactivity of the smooth muscle cells for HMB-45, a melanoma-related antigen has been reported by immunohistochemistry. The purpose of this study was the ultrastructural localization of HMB-45 immunoreactivity in these cells using gold-labeled antibodies.Lung tissue from three cases of PLAM, referred to our Institution for lung transplantation, was embedded in either Poly/Bed 812 post-fixed in 1% osmium tetroxide, or in LR White, without osmication. For the immunogold technique, thin sections were placed on Nickel grids and incubated with affinity purified, monoclonal anti-melanoma antibody HMB-45 (1:1) (Enzo Diag. Co) overnight at 4°C. After extensive washing with PBS, grids were treated with Goat-anti-mouse-IgG-Gold (5nm) (1:10) (Amersham Life Sci) for 1 hour, at room temperature.


1985 ◽  
Vol 53 (03) ◽  
pp. 351-355 ◽  
Author(s):  
Robert G Schaub ◽  
James C Keith ◽  
Carol A Simmons ◽  
Clarence A Rawlings

Summary Dirofilaria immitis (DI) infection chronically injures canine pulmonary arteries. This injury produces endothelial cell loss, platelet/leukocyte adhesion, and smooth muscle proliferation. In the present study we assessed the effect of the cyclooxygenase inhibitor, U-53,059, on platelet function, platelet kinetics, coagulation, and smooth muscle proliferation in DI infected dogs.Platelet aggregation to the combination of arachidonic acid/ ADP was significantly inhibited by U-53,059. Coagulation and hematologic parameters were not effected by either DI infection or U-53,059 treatment. Platelet survival and the number of platelet dense granules were reduced in DI infection. Quantification of the lesions demonstrated that U-53,059 reduced both severity and density compared to non-treated dogs. U-53,059 is a potent and effective inhibitor of platelet aggregation which modifies smooth muscle proliferation produced by chronic vascular injury.


2008 ◽  
Vol 6 (32) ◽  
pp. 293-306 ◽  
Author(s):  
A Valentín ◽  
L Cardamone ◽  
S Baek ◽  
J.D Humphrey

Arteries exhibit a remarkable ability to adapt to sustained alterations in biomechanical loading, probably via mechanisms that are similarly involved in many arterial pathologies and responses to treatment. Of particular note, diverse data suggest that cell and matrix turnover within vasoaltered states enables arteries to adapt to sustained changes in blood flow and pressure. The goal herein is to show explicitly how altered smooth muscle contractility and matrix growth and remodelling work together to adapt the geometry, structure, stiffness and function of a representative basilar artery. Towards this end, we employ a continuum theory of constrained mixtures to model evolving changes in the wall, which depend on both wall shear stress-induced changes in vasoactive molecules (which alter smooth muscle proliferation and synthesis of matrix) and intramural stress-induced changes in growth factors (which alter cell and matrix turnover). Simulations show, for example, that such considerations help explain the different rates of experimentally observed adaptations to increased versus decreased flows as well as differences in rates of change in response to increased flows or pressures.


2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Hui Min Yap ◽  
Yu Zhao Lee ◽  
Hanis Hazeera Harith ◽  
Chau Ling Tham ◽  
Manraj Singh Cheema ◽  
...  

Metabolism ◽  
2005 ◽  
Vol 54 (5) ◽  
pp. 645-652 ◽  
Author(s):  
Subramanyam N. Murthy ◽  
Demian F. Obregon ◽  
Natasha N. Chattergoon ◽  
Neil A. Fonseca ◽  
Debasis Mondal ◽  
...  

2018 ◽  
Vol 99 (3) ◽  
pp. 387-398 ◽  
Author(s):  
Srinivasa Raju Datla ◽  
Lula L. Hilenski ◽  
Bonnie Seidel-Rogol ◽  
Anna E. Dikalova ◽  
Mark Harousseau ◽  
...  

1999 ◽  
Vol 277 (6) ◽  
pp. L1109-L1117 ◽  
Author(s):  
Simon Johnson ◽  
Alan Knox

Airway smooth muscle proliferation is important in asthma and is dependent on pro- and antimitogenic factors and cell-matrix interactions. Here we show an antiproliferative effect of protease inhibitors on human airway smooth muscle due to inhibition of autocrine-derived matrix metalloproteinase (MMP)-2. Proliferation in response to fetal bovine serum, thrombin, and platelet-derived growth factor was inhibited by the broad-spectrum protease inhibitor Complete and the MMP inhibitors EDTA and Ro-31-9790 but not by cysteine or serine protease inhibitors. Conditioned medium from airway smooth muscle cells contained 72-kDa gelatinase that was secreted by growth-arrested cells and increased by fetal bovine serum but not by thrombin or platelet-derived growth factor. Immunostaining of cultured human airway smooth muscle cells and normal lung biopsies confirmed this gelatinase to be MMP-2. Our results suggest a novel role for MMP-2 as an important autocrine factor required for airway smooth muscle proliferation. Inhibition of MMPs could provide a target for the prevention of smooth muscle hyperplasia and airway remodeling in asthma.


2017 ◽  
Vol 119 (4) ◽  
pp. 3267-3279 ◽  
Author(s):  
Xuehui Yang ◽  
Yan Gong ◽  
Qing He ◽  
Jonathan D. Licht ◽  
Lucy Liaw ◽  
...  

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