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The Regulation of Growth Plate Chondrocytes by Transforming Growth Factor-Beta and Its Mechanism of Action | Spiral-bound

by Rosado E. Enrique (Author)

1 New starting at:

$23.95

Binding:

Spiral-bound

Publisher:

Storming Media

Page Count:

66 Pages

Publication Date:

2003

EDITORIAL REVIEWS

Product Description
This is a AIR FORCE INST OF TECH WRIGHT-PATTERSONAFB OH report procured by the Pentagon and made available for public release. It has been reproduced in the best form available to the Pentagon. It is not spiral-bound, but rather assembled with Velobinding in a soft, white linen cover. The Storming Media report number is A492514. The abstract provided by the Pentagon follows: Transforming growth factor-Beta 1(TGF-Beta 1) regulates chondrocytes through Smad protein-mediated mechanisms, and has been shown to increase PKC. To test whether other signaling pathways plan a role, this study examined if the physiologic response of rat costochondral growth zone (GC) chondrocytes to TGF- Beta 1 is through TGF-Beta 1 type II or III receptors and also the contribution of protein kinase C (PKC), protein kinase A (PKA), and G-proteins to this process. Growth zone chondrocytes were isolated from rat costochondral cartilage and cultured. Treatment of confluent growth plate chondrocytes with TGF-Beta 1 stimulated 3H-thymidine and 35S-sulfate incorporation as well as alkaline phosphatase and PKC specific activities. The receptor responsible for TGF-Beta 1-dependent PKC and the physiological response of GC cells to TGF-Beta 1 was tested using anti-type II TGF-Beta receptor antibody and soluble type II TGF- Beta 1 receptor. The results showed that TGF-Beta l mediates these effects through the type II receptor. Inhibition of PKC with chelerythrine, staurosporine, or H-7 caused a dose-dependent decrease in these parameters, indicating that PKC signaling was involved in the physiological response of the cells to TGF-Beta 1. The increase in 3H-thymidine incorporation and alkaline phosphatase specific activity were also regulated by protein kinase A (PKA) signaling, since the effects of TGF-Beta 1 were partially blocked by the PKA inhibitor H-8.