Effects of tri-iodothyronine and insulin-like growth factor-I (IGF-I) on alkaline phosphatase activity, [3H]thymidine incorporation and IGF-I receptor mRNA in cultured rat epiphyseal chondrocytes.

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Ohlsson, Claes,1965Gothenburg University,Göteborgs universitet,Institutionen för invärtesmedicin,Institute of Internal Medicine (författare)

Effects of tri-iodothyronine and insulin-like growth factor-I (IGF-I) on alkaline phosphatase activity, [3H]thymidine incorporation and IGF-I receptor mRNA in cultured rat epiphyseal chondrocytes.

Artikel/kapitelEngelska1992

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1992

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LIBRIS-ID:oai:gup.ub.gu.se/91652
https://gup.ub.gu.se/publication/91652URI

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Språk:engelska

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The effects of tri-iodothyronine (T3) and insulin-like growth factor-I (IGF-I) on [3H]thymidine incorporation, alkaline phosphatase (ALP) activity and IGF-I receptor mRNA levels were studied in rat epiphyseal chondrocytes cultured in monolayer. Chondrocytes from enzymatically digested rat tibia epiphyseal growth plates were seeded in monolayer culture and precultured for 7-14 days in Ham's F-12 medium supplemented with 10% (v/v) newborn calf serum and 1% (v/v) of a serum substitute. After preculture the medium was changed to Ham's F-12 medium containing 1% (v/v) serum from hypophysectomized rats, and the effects of T3 and/or IGF-I on DNA synthesis ([3H]thymidine incorporation), ALP activity (a late marker of differentiated epiphyseal chondrocytes) and IGF-I receptor mRNA levels were studied. ALP activity was increased by T3 in a dose-dependent manner with a maximal response at 10 micrograms T3/l (678 +/- 86% compared with control culture). The increase in ALP activity was accompanied by a concomitant decrease in [3H]thymidine incorporation (52 +/- 14% compared with control culture). Human GH (hGH; 50 micrograms/l) and IGF-I (25 micrograms/l) had no stimulatory effect on ALP activity. However IGF-I (10 micrograms/l) exerted an inhibition on the T3 (10 micrograms/l)-induced increase in ALP activity (64 +/- 9% compared with T3-treated culture). T3 (3 micrograms/l) inhibited the increase in [3H]thymidine incorporation caused by 25 micrograms IGF-I/l (51 +/- 13% compared with IGF-I-treated culture). Furthermore, IGF-I receptor mRNA levels were increased by 10 micrograms T3/l (137 +/- 4.2% compared with control culture) while no effect of hGH (50 micrograms/l) or IGF-I (25 micrograms/l) was demonstrated. Both T3 and IGF-I were shown to interact with epiphyseal chondrocytes and both substances seemed to affect cell proliferation and maturation and therefore longitudinal bone growth. Furthermore, the results indicated that IGF-I is important for proliferation of the cells while T3 initiates the terminal differentiation of epiphyseal chondrocytes.

Ämnesord och genrebeteckningar

Alkaline Phosphatase
metabolism
Animals
Cell Differentiation
drug effects
Cell Division
drug effects
Cells
Cultured
Growth Plate
cytology
drug effects
metabolism
Insulin-Like Growth Factor I
pharmacology
Male
RNA
Messenger
analysis
Rats
Rats
Sprague-Dawley
Receptor
IGF Type 1
genetics
Thymidine
metabolism
Triiodothyronine
pharmacology

Biuppslag (personer, institutioner, konferenser, titlar ...)

Nilsson, Anders,1958Gothenburg University,Göteborgs universitet,Institutionen för de kirurgiska disciplinerna, Avdelningen för ortopedi,Institute of Surgical Sciences, Department of Orthopaedics(Swepub:gu)xniand (författare)
Isaksson, Olle,1943Gothenburg University,Göteborgs universitet,Institutionen för invärtesmedicin,Institute of Internal Medicine(Swepub:gu)xisaol (författare)
Bentham, J (författare)
Lindahl, Anders,1954Gothenburg University,Göteborgs universitet,Institutionen för laboratoriemedicin, Avdelningen för klinisk kemi/transfusionsmedicin,Institute of Laboratory Medicine, Dept of Clinical Chemistry/Transfusion Medicine(Swepub:gu)xlandy (författare)
Göteborgs universitetInstitutionen för invärtesmedicin (creator_code:org_t)

Sammanhörande titlar

Ingår i:The Journal of endocrinology135:1, s. 115-230022-0795

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Av författaren/redakt...: Ohlsson, Claes, ...; Nilsson, Anders, ...; Isaksson, Olle, ...; Bentham, J; Lindahl, Anders, ...

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Av lärosätet: Göteborgs universitet

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