Faculty Opinions recommendation of Role of YKL-40 in bronchial smooth muscle remodeling in asthma.

Author(s):  
Judith Black ◽  
Brian Oliver ◽  
Janette Burgess
Author(s):  
Pauline Esteves ◽  
Landry Blanc ◽  
Alexis Celle ◽  
Isabelle Dupin ◽  
Elise Maurat ◽  
...  

Author(s):  
Pierre-Olivier Girodet ◽  
Benoit Allard ◽  
Matthieu Thumerel ◽  
Hugues Begueret ◽  
Isabelle Dupin ◽  
...  

2012 ◽  
Vol 185 (7) ◽  
pp. 715-722 ◽  
Author(s):  
Imane Bara ◽  
Annaig Ozier ◽  
Pierre-Olivier Girodet ◽  
Gabrielle Carvalho ◽  
Jennifer Cattiaux ◽  
...  

1992 ◽  
Vol 263 (3) ◽  
pp. L402-L408 ◽  
Author(s):  
Y. Gao ◽  
P. M. Vanhoutte

The present study was design to determine the role of prostaglandin E2 and I2 in the responses of isolated canine airways to H2O2. Rings of canine third-order bronchi, some of which had undergone mechanical denudation of the epithelium, were suspended in organ chambers; isometric tension was recorded. During contractions to acetylcholine, H2O2 induced concentration-dependent relaxations. The relaxations were attenuated significantly by indomethacin, acetylsalicylic acid, and methylene blue. H2O2 increased the release of prostaglandin E2 and 6-keto-prostaglandin F1 alpha and the content of adenosine 3',5'-cyclic monophosphate (cAMP). These effects were abolished by indomethacin or methylene blue. H2O2 did not affect the content of guanosine 3',5'-cyclic monophosphate significantly. These observations suggest that 1) H2O2 relaxes canine bronchial smooth muscle and 2) elevation of tissue content of cAMP induced by prostaglandin E2 and I2 may be involved. These phenomena did not appear to be modulated by the respiratory epithelium, since H2O2-induced relaxations and increases in the release of PGE2 and 6-ketoprostaglandin F1 alpha were similar in preparations with and without epithelium. However, after treatment with methylene blue, H2O2 induced contractions only in preparations with epithelium. These epithelium-dependent contractions were not affected by inhibitors of cyclooxygenase and lipoxygenase.


1997 ◽  
Vol 121 (4) ◽  
pp. 794-798 ◽  
Author(s):  
J. Tamaoki ◽  
E. Tagaya ◽  
K. Isono ◽  
M. Kondo ◽  
K. Konno

Author(s):  
Fabien Beaufils ◽  
Pauline Esteves ◽  
Raphaël Enaud ◽  
Ophélie Germande ◽  
Alexis Celle ◽  
...  

2020 ◽  
Vol 21 (21) ◽  
pp. 7982
Author(s):  
Yoshihiko Chiba ◽  
Mayumi Matsumoto ◽  
Motohiko Hanazaki ◽  
Hiroyasu Sakai

In allergic bronchial asthma, an increased smooth muscle contractility of the airways is one of the causes of the airway hyperresponsiveness (AHR). Increasing evidence also suggests a possible involvement of microRNAs (miRNAs) in airway diseases, including asthma, although their roles in function and pathology largely unknown. The current study aimed to determine the role of a miRNA, miR-140-3p, in the control of protein expression of CD38, which is believed to regulate the contraction of smooth muscles, including the airways. In bronchial smooth muscles (BSMs) of the mice that were actively sensitized and repeatedly challenged with ovalbumin antigen, an upregulation of CD38 protein concurrently with a significant reduction of miR-140-3p was observed. In cultured human BSM cells (hBSMCs), transfection with a synthetic miR-140-3p inhibitor caused an increase in CD38 protein, indicating that its basal protein expression is regulated by endogenous miR-140-3p. Treatment of the hBSMCs with interleukin-13 (IL-13), an asthma-related cytokine, caused both an upregulation of CD38 protein and a downregulation of miR-140-3p. Transfection of the hBSMCs with miR-140-3p mimic inhibited the CD38 protein upregulation induced by IL-13. On the other hand, neither a CD38 product cyclic ADP-ribose (cADPR) nor its antagonist 8-bromo-cADPR had an effect on the BSM contraction even in the antigen-challenged mice. Taken together, the current findings suggest that the downregulation of miR-140-3p induced by IL-13 might cause an upregulation of CD38 protein in BSM cells of the disease, although functional and pathological roles of the upregulated CD38 are still unclear.


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