אסיף מאגר המחקר החקלאי

Growth Hormone Receptors in Avian Epiphyseal Growth-Plate Chondrocytes

Year:

1993

Source of publication :

Authors :

Volume :

92

Co-Authors:

Monsonego, E., Institute of Animal Science, Agricultural Research Organization, The Volcani Center, Bet Pagan 50250, Israel
and Department of Animal Science and Department of Biochemistry and Human Nutrition, The Hebrew University of Jerusalem, Faculty of Agriculture, Rehovot 76100, Israel
Halevy, O., The Faculty of Agriculture.
Gertler, A., The Faculty of Agriculture.
Volokita, M., Institute of Animal Science, Agricultural Research Organization, The Volcani Center, Bet Pagan 50250, Israel
Schickler, M., Institute of Animal Science, Agricultural Research Organization, The Volcani Center, Bet Pagan 50250, Israel
Hurwitz, S., Institute of Animal Science, Agricultural Research Organization, The Volcani Center, Bet Pagan 50250, Israel
Pines, M., Institute of Animal Science, Agricultural Research Organization, The Volcani Center, Bet Pagan 50250, Israel

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Abstract:

Growth hormone receptor (GH-R) gene expression was evaluated in avian growth-plate cartilage by Northern blot and hybridization using the avian GH-R probe. A single transcript of ∼5.2 kb was demonstrated in cultured growth-plate chondrocytes as well as in growth-plate extracts. GH receptor gene expression was inhibited by chicken GH (cGH) in a dose-and time-dependent manner. Chicken GH was more potent in down-regulating the GH-R gene expression than hGH, but on the other hand cGH exhibited a lower affinity to avian chondrocytes receptor than did the human hormone. Addition of ascorbic acid to the culture media caused cell differentiation: induction of alkaline phosphatase activity and attenuation of collagen type II gene expression. No differences in the GH-R gene expression were observed in the nondifferentiated cells compared with the differentiated cells. Chicken GH did not form any complex with the purified hGH binding protein (hGHBP), did not bind to human lymphocytes GH receptor, and did not affect Nb2 cell proliferation. These systems represent somatogenic and lactogenic types of GH receptors, respectively. In summary, avian growth-plate chondrocytes in situ and in culture exhibit GH-R and these receptors are capable of binding GH. Thus, the failure of GH to affect avian chondrocytes' proliferation was not due to either the absence of receptors on the cell membrane or to a lack in its binding activity, but rather may be due to events farther downstream. © 1993 Academic Press. All rights reserved.

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