Absence of Proteinase-Activated Receptor-1 Signaling Affords Protection from Bleomycin-Induced Lung Inflammation and Fibrosis
- 1 May 2005
- journal article
- Published by Elsevier in The American Journal of Pathology
- Vol. 166 (5) , 1353-1365
- https://doi.org/10.1016/s0002-9440(10)62354-1
Abstract
No abstract availableKeywords
This publication has 83 references indexed in Scilit:
- Proteinase-activated receptors and the pathophysiology of pulmonary fibrosisDrug Development Research, 2003
- Protease‐activated receptor (PAR)‐1 and PAR‐2 participate in the cell growth of alveolar capillary endothelium in primary lung adenocarcinomasCancer, 2003
- Thrombin contributes to bronchoalveolar lavage fluid mitogenicity in lung disease of the premature infantPediatric Pulmonology, 2002
- Coagulation cascade proteases and tissue fibrosisBiochemical Society Transactions, 2002
- Thrombin Differentiates Normal Lung Fibroblasts to a Myofibroblast Phenotype via the Proteolytically Activated Receptor-1 and a Protein Kinase C-dependent PathwayPublished by Elsevier ,2001
- Direct Thrombin Inhibition Reduces Lung Collagen, Accumulation, and Connective Tissue Growth Factor mRNA Levels in Bleomycin-Induced Pulmonary FibrosisThe American Journal of Pathology, 2001
- A Total Fibrinogen Deficiency Is Compatible with the Development of Pulmonary Fibrosis in MiceThe American Journal of Pathology, 2000
- Thrombin stimulates production of transforming growth factor-beta by cultured human mesangial cellsNephrology Dialysis Transplantation, 1997
- Thrombin functions as an inflammatory mediator through activation of its receptor.The Journal of Experimental Medicine, 1996
- Mechanisms of bleomycin-induced lung damageArchives of Toxicology, 1991