Transforming growth factor-β inhibits cellular adenylate cyclase activity in cultured human arterial endothelial cells

1989 ◽  
Vol 25 (1) ◽  
pp. 101-104 ◽  
Author(s):  
Hiroyuki Mioh ◽  
Jan-Kan Chen
Keyword(s):  
Endothelial Cells ◽  
Growth Factor ◽  
Adenylate Cyclase ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Arterial Endothelial Cells

Transforming growth factor-beta 1 regulation of signal transduction in two renal epithelial cell lines

1993 ◽  
Vol 265 (4) ◽  
pp. F584-F591
Author(s):  
R. J. Anderson ◽  
H. T. Sponsel ◽  
R. Breckon ◽  
T. Marcell ◽  
J. P. Hoeffler
Keyword(s):  
Growth Factor ◽  
Adenylate Cyclase ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Tgf Beta ◽  
Renal Epithelial Cell ◽  
Epithelial Cell Lines ◽  
Growth Factor Beta

The present studies examine the effect of transforming growth factor-beta 1 (TGF-beta 1) on signal transduction pathways in two cultured renal epithelial cell lines. TGF-beta 1 promotes basal and agonist-stimulated adenylate cyclase activity in LLC-PK1 but not MDCK cell membranes. TGF-beta 1 stimulation of LLC-PK1 membrane adenylate cyclase activity occurs quickly and can be attenuated by pertussis toxin pretreatment. Both TGF-beta 1 and adenosine 3',5'-cyclic monophosphate (cAMP) exert comparable effects on [3H]thymidine uptake in LLC-PK1 cells, suggesting that TGF-beta 1 regulation of adenylate cyclase activity potentially plays a role in mediating biological responses to TGF-beta 1. The activities of protein kinase C and phospholipase A are not affected by TGF-beta 1 in either LLC-PK1 or MDCK cells. Both TGF-beta 1 and epidermal growth factor (EGF) increase expression and induce the appearance of new forms of the cAMP response element binding protein (CREB) in LLC-PK1 cells. These effects of TGF-beta 1 and EGF on CREB appear to be specific since neither TGF-beta 1 nor EGF alters expression of an activating transcription factor in LLC-PK1 cells. The effect of TGF-beta 1 and EGF to alter expression of CREB does not affect CREB binding to its regulatory element in LLC-PK1 cell lysates. These results suggest that some of the biological effects of TGF-beta 1 may be attributed to stimulation of adenylate cyclase activity and cAMP formation as well as to enhanced expression and/or modification of the CREB transcription factor in LLC-PK1 cells.

Modulation of adenylate cyclase activity in cultured bovine pulmonary arterial endothelial cells

1989 ◽  
Vol 38 (3) ◽  
pp. 423-430 ◽  
Author(s):  
Alain B. Legrand ◽  
Tanjore K. Narayanan ◽  
Una S. Ryan ◽  
Robert S. Aronstam ◽  
John D. Catravas
Keyword(s):  
Endothelial Cells ◽  
Adenylate Cyclase ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Pulmonary Arterial ◽  
Arterial Endothelial Cells

Intracisternal administration of transforming growth factor-β evokes fever through the induction of cyclooxygenase-2 in brain endothelial cells

2008 ◽  
Vol 294 (1) ◽  
pp. R266-R275 ◽  
Author(s):  
Shigenobu Matsumura ◽  
Tetsuro Shibakusa ◽  
Teppei Fujikawa ◽  
Hiroyuki Yamada ◽  
Kiyoshi Matsumura ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Growth Factor ◽  
Proinflammatory Cytokines ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Cyclooxygenase 2 ◽  
Dependent Manner ◽  
Cox 2 ◽  
Β Receptor

Transforming growth factor-β (TGF-β), a pleiotropic cytokine, regulates cell proliferation, differentiation, and apoptosis, and plays a key role in development and tissue homeostasis. TGF-β functions as an anti-inflammatory cytokine because it suppresses microglia and B-lymphocyte functions, as well as the production of proinflammatory cytokines. However, we previously demonstrated that the intracisternal administration of TGF-β induces fever like that produced by proinflammatory cytokines. In this study, we investigated the mechanism of TGF-β-induced fever. The intracisternal administration of TGF-β increased body temperature in a dose-dependent manner. Pretreatment with cyclooxygenase-2 (COX-2)-selective inhibitor significantly suppressed TGF-β-induced fever. COX-2 is known as one of the rate-limiting enzymes of the PGE2 synthesis pathway, suggesting that fever induced by TGF-β is COX-2 and PGE2 dependent. TGF-β increased PGE2 levels in cerebrospinal fluid and increased the expression of COX-2 in the brain. Double immunostaining of COX-2 and von Willebrand factor (vWF, an endothelial cell marker) revealed that COX-2-expressing cells were mainly endothelial cells. Although not all COX-2-immunoreactive cells express TGF-β receptor, some COX-2-immunoreactive cells express activin receptor-like kinase-1 (ALK-1, an endothelial cell-specific TGF-β receptor), suggesting that TGF-β directly or indirectly acts on endothelial cells to induce COX-2 expression. These findings suggest a novel function of TGF-β as a proinflammatory cytokine in the central nervous system.

Epidermal growth factor receptors and adenylate cyclase activity in human thyroid tissues

1990 ◽  
Vol 14 (3) ◽  
pp. 410-417 ◽  
Author(s):  
Quan-Yang Duh ◽  
Allan E. Siperstein ◽  
Rebecca A. Miller ◽  
Joan J. Sancho ◽  
Michael J. Demeure ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Adenylate Cyclase ◽  
Growth Factor Receptors ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Human Thyroid ◽  
Epidermal Growth Factor Receptors ◽  
Epidermal Growth

Transforming Growth Factor-β: Role in Mediating Serum-Induced Endothelin Production by Vascular Endothelial Cells*

Endocrinology ◽  
1991 ◽  
Vol 129 (5) ◽  
pp. 2355-2360 ◽  
Author(s):  
MARVIN R. BROWN ◽  
JOAN VAUGHAN ◽  
LETICIA L. JIMENEZ ◽  
WYLIE VALE ◽  
ANDREW BAIRD
Keyword(s):  
Endothelial Cells ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Vascular Endothelial Cells ◽  
Transforming Growth Factor Β ◽  
Vascular Endothelial
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