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Biomedical subjects

Y S Chyun

Publications and source records attributed to Y S Chyun.

3 recordsLinked to original sources
PubMed1984

Stimulation of bone formation by prostaglandin E2.

We examined the effect of prostaglandin E2 (PGE2), in the presence or absence of cortisol, on bone formation in 21-day fetal rat calvaria maintained in organ culture for 24 to 96 h. [3H]Thymidine and [3H] proline incorporation were used to assess DNA and collagen synthesis, respectively. Changes in dry weight and DNA content were assessed after 96 h. PGE2 (10(-7) M) stimulated both DNA and collagen synthesis in calvaria. The effect on DNA synthesis was early (24 h), transient and limited to the periosteum. Collagen synthesis was stimulated at a later time (96 h), predominantly in the central bone. Cortisol (10(-7) M) inhibited DNA and collagen synthesis. The addition of PGE2 reversed the inhibitory effects of cortisol on DNA synthesis and content and increased collagen synthesis in central bone to levels above control untreated cultures. We conclude that PGE2 has stimulatory effects on bone formation and can reverse the inhibitory effects of cortisol. Hence the effects of cortisol may be mediated in part by their ability to reduce the endogenous production of prostaglandins.

Animals↗
PubMed1984

Cortisol decreases bone formation by inhibiting periosteal cell proliferation.

We tested the hypothesis that the inhibitory effect of cortisol on bone growth is primarily on the periosteum. Fetal rat calvaria were maintained in organ culture, labeled with radioactive proline or thymidine, and then dissected to separate periosteum from the osteoblast-rich central bone. There was a dose- and time-dependent inhibition of thymidine incorporation into DNA in the periosteum which was significant at 24 h. These observations were further supported by decreases in the dry weight and DNA content of the periosteum at 96 h. Incorporation of thymidine and proline into the central bone were decreased only at 96 h. Pulse-chase studies using a high concentration of cortisol (10(-6) M) indicated that increased cell attrition may also play a role in the inhibitory effect of cortisol. We propose that the primary effect of cortisol on bone growth is an inhibition of proliferation of the periosteal cells which give rise to osteoblasts. The subsequent decrease in the incorporation of proline into the central bone may be the consequence of this inhibition.

Animals↗