The proteome of mouse mucosal mast cell homologues: The role of transforming growth factor β1

PROTEOMICS ◽  
2006 ◽  
Vol 6 (2) ◽  
pp. 623-631 ◽  
Author(s):  
Alan D. Pemberton ◽  
Jeremy K. Brown ◽  
Steven H. Wright ◽  
Pamela A. Knight ◽  
Hugh R. P. Miller
Keyword(s):  
Mast Cell ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Mucosal Mast Cell

Role of tissue transforming growth factor-β1 in pancreatic fibrosis

1998 ◽  
Vol 114 ◽  
pp. A498 ◽  
Author(s):  
M. Shiozaki ◽  
Y. Takeda ◽  
H. Morikawa ◽  
Y. Nakagawa ◽  
K. Katsu
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Pancreatic Fibrosis

scholarly journals The Role of Transforming Growth Factor-β1 in Airway Inflammation of Childhood Asthma

2013 ◽  
Vol 26 (3) ◽  
pp. 725-738 ◽  
Author(s):  
R. Gagliardo ◽  
P. Chanez ◽  
M. Gjomarkaj ◽  
S. La Grutta ◽  
A. Bonanno ◽  
...  
Keyword(s):  
Growth Factor ◽  
Airway Inflammation ◽  
Childhood Asthma ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1

scholarly journals The fate of the primary cilium during myofibroblast transition

2014 ◽  
Vol 25 (5) ◽  
pp. 643-657 ◽  
Author(s):  
Matthew Rozycki ◽  
Monika Lodyga ◽  
Jessica Lam ◽  
Maria Zena Miranda ◽  
Károly Fátyol ◽  
...  
Keyword(s):  
Growth Factor ◽  
Sonic Hedgehog ◽  
Primary Cilium ◽  
Potential Role ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Related Transcription Factor ◽  
Necessary And Sufficient ◽  
Organ Fibrosis

Myofibroblasts, the culprit of organ fibrosis, can originate from mesenchymal and epithelial precursors through fibroblast–myofibroblast and epithelial–myofibroblast transition (EMyT). Because certain ciliopathies are associated with fibrogenesis, we sought to explore the fate and potential role of the primary cilium during myofibroblast formation. Here we show that myofibroblast transition from either precursor results in the loss of the primary cilium. During EMyT, initial cilium growth is followed by complete deciliation. Both EMyT and cilium loss require two-hit conditions: disassembly/absence of intercellular contacts and transforming growth factor-β1 (TGFβ) exposure. Loss of E-cadherin–dependent junctions induces cilium elongation, whereas both stimuli are needed for deciliation. Accordingly, in a scratch-wounded epithelium, TGFβ provokes cilium loss exclusively along the wound edge. Increased contractility, a key myofibroblast feature, is necessary and sufficient for deciliation, since constitutively active RhoA, Rac1, or myosin triggers, and down-regulation of myosin or myocardin-related transcription factor prevents, this process. Sustained myosin phosphorylation and consequent deciliation are mediated by a Smad3-, Rac1-, and reactive oxygen species–dependent process. Transitioned myofibroblasts exhibit impaired responsiveness to platelet-derived growth factor-AA and sonic hedgehog, two cilium-associated stimuli. Although the cilium is lost during EMyT, its initial presence contributes to the transition. Thus myofibroblasts represent a unique cilium-less entity with profoundly reprogrammed cilium-related signaling.

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