Cathepsin G

02/01/2010 - "Dual inhibition of cathepsin G and chymase is effective in animal models of pulmonary inflammation."
05/01/2014 - "Cathepsin G degradation of phospholipid transfer protein (PLTP) augments pulmonary inflammation."
07/16/2004 - "Finally, the PAI-1 mutants were more effective in reducing the neutrophil elastase and cathepsin G activities in an in vivo model of lung inflammation than were their physiological inhibitors."
03/01/2003 - "During lung inflammation, airspaces are burdened by neutrophils that release elastase and cathepsin G, two serine proteinases. "
06/29/1999 - "Our data suggest that oxidation of MPI during chronic bronchitis may lead to cathepsin G-mediated lung tissue degradation and that heparin may be a useful adjuvant of MPI-based therapy of acute lung inflammation in cystic fibrosis."

02/01/2007 - "This study indicates that the monocyte chemotactic activity of cathepsin G may have a role in the pathogenesis of RA synovial inflammation."
06/27/2003 - "Collectively, these studies describe novel cardiac actions of cathepsin G that do not require PARs and are predicted to assume functional importance at sites of interstitial inflammation in the heart."
09/15/2002 - "The low activity of cathepsin G on synthetic substrates seriously impairs studies designed to clarify its role in tissue inflammation. "
05/07/2010 - "As cathepsin G is a serpin involved both in inflammation and coagulation activation, this confirms and expands the concept of a marked dysregulation of both inflammatory and hemostatic balances occurring after CABG. "
10/01/2007 - "It is a potent cathepsin G inhibitor thought to protect monocytes, neutrophils and bystander cells from ectopic cathepsin G during inflammation. "

02/15/1999 - "The frequency of severe lymphatic involvement in S-ADV was as high as in NS-ADV, and significantly greater than in SM-CA. The Ki-67, mitotic, and apoptotic indices for S-ADV were significantly increased compared with those for NS-ADV and/or SM-CA. Expression of cathepsin G in S-ADV tumor and stromal cells was significantly decreased compared with NS-ADV and/or SM-CA cases. "
08/01/2009 - "We showed that cathepsin G, which we have previously shown to be up-regulated at the tumor-bone interface, is capable of activating pro-MMP9. "
04/01/2009 - "We also show that in vivo inhibition of cathepsin G reduces the number of CD11b(+) osteoclast precursors and mature osteoclasts at the tumor-bone interface. "
07/15/2008 - "The major source of cathepsin G at the tumor-bone interface seems to be osteoclasts that up-regulate production of cathepsin G via interaction with tumor cells. "
01/01/1997 - "Result of our examinations indicate a relationship between cathepsin G activity, grade of tumor differentiation and particular clinical stages of disease."

01/01/2013 - "In a vaso-occlusive model of ischemic stroke, inhibition of cathepsin G and its congenital absence improved cerebral blood flow, reduced histologic brain injury, and improved neurobehavioral outcome. "

01/01/2013 - "In a vaso-occlusive model of ischemic stroke, inhibition of cathepsin G and its congenital absence improved cerebral blood flow, reduced histologic brain injury, and improved neurobehavioral outcome. "