scholarly journals Iloprost suppresses connective tissue growth factor production in fibroblasts and in the skin of scleroderma patients

2001 ◽  
Vol 108 (2) ◽  
pp. 241-250 ◽  
Author(s):  
Richard Stratton ◽  
Xu Shiwen ◽  
Giorgia Martini ◽  
Alan Holmes ◽  
Andrew Leask ◽  
...  
Oral Oncology ◽  
2009 ◽  
Vol 45 (9) ◽  
pp. e99-e105 ◽  
Author(s):  
Yi-Ting Deng ◽  
Hsin-Ming Chen ◽  
Shih-Jung Cheng ◽  
Chun-Pin Chiang ◽  
Mark Yen-Ping Kuo

2013 ◽  
Vol 456 (1) ◽  
pp. 109-118 ◽  
Author(s):  
Su Jin Lee ◽  
Jeong Han Kang ◽  
Soo Young Choi ◽  
Oh-Shin Kwon

In the present study, we demonstrated that PKCδ-stimulated RhoA/ROCK activation resulted in a reduction in PPM1A, thereby up-regulating Smad-dependent gene induction for extended periods. These findings indicated that PKCδ plays a critical role in TGF-β1-induced CTGF production in HepG2 cells.


2013 ◽  
Vol 305 (2) ◽  
pp. G139-G150 ◽  
Author(s):  
Song Han ◽  
Ella W. Englander ◽  
Guillermo A. Gomez ◽  
Judith F. Aronson ◽  
Cristiana Rastellini ◽  
...  

Pancreatitis is classified into acute pancreatitis (AP) and chronic pancreatitis (CP). Apelin, a small regulatory peptide, is the endogenous ligand for the APJ receptor. Apelin and APJ are expressed in the pancreas. The aims of this study were to examine whether apelin influences the inflammatory and fibrosis responses to pancreatitis in mice and to identify mechanisms behind apelin's activities. Supramaximal cerulein induction of AP or CP caused significant ( P < 0.05) elevations in pancreatic apelin and APJ expression. Levels declined during the recovery phases. In apelin gene-knockout mice with pancreatitis, pancreatic neutrophil invasion and myeloperoxidase activity were enhanced significantly, and apelin treatment suppressed both. Apelin exposure reduced CP-induced elevations of extracellular matrix-associated proteins. Apelin inhibited PDGF-simulated connective tissue growth factor production and proliferation of pancreatic stellate cells (PSCs). Serum granulocyte colony-stimulating factor and keratinocyte cytokine levels were higher in apelin gene-knockout than wild-type mice with pancreatitis. Apelin reduced AP- and CP-induced elevations in pancreatic NF-κB activation. Together, these findings imply that the pancreatic apelin-APJ system functions to curb the inflammatory and fibrosis responses during pancreatitis. Furthermore, findings suggest that apelin reduces inflammation and fibrosis by reducing neutrophil recruitment and PSC activity. Inhibition of neutrophil invasion may be mediated by reduced keratinocyte cytokine and granulocyte colony-stimulating factor secretion. Apelin-induced reductions in PSC proliferation and connective tissue growth factor production are putative mechanisms underlying apelin's inhibition of extracellular matrix production. The apelin-associated changes in NF-κB binding may be linked to apelin's regulation of pancreatic inflammatory and fibrosis responses during pancreatitis.


Hepatology ◽  
2009 ◽  
pp. NA-NA
Author(s):  
Ieva Peredniene ◽  
Eddy van de Leur ◽  
Birgit Lahme ◽  
Monika Siluschek ◽  
Axel M. Gressner ◽  
...  

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