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Hormonal control of the replication of human fetal fibroblasts: role of somatomedin C/insulin-like growth factor I.
J Cell Physiol. 1986 Jul; 128(1):47-54.JC

Abstract

Sparse cultures of fetal and postnatal human fibroblasts were equivalent in their responsiveness to the mitogenic action of somatomedin C/insulin-like growth factor I (SM-C/IGF-I). At both developmental stages, the addition of SM-C/IGF-I (100 ng/ml) increased cell number at day 3 1.4-fold in serum-free medium and 2-fold in the presence of 0.25% human hypopituitary serum. Furthermore, dose-response curves indicated that there was no difference in the sensitivity of fetal and postnatal fibroblasts to the growth-promoting effects of SM-C/IGF-I, with a half-maximal response occurring at 6 ng/ml SM-C/IGF-I. This biological action of SM-C/IGF-I correlated with SM-C/IGF-I binding to fetal and postnatal fibroblast monolayers. Epidermal growth factor (EGF) and platelet-derived growth factor (PDGF) also stimulated replication of fetal and postnatal fibroblasts. The mitogenic effects of SM-C/IGF-I, EGF, and PDGF were additive. Dexamethasone, which alone had no effect, was synergistic with SM-C/IGF-I in stimulating replication of postnatal fibroblasts. The combination of SM-C/IGF-I (100 ng/ml), dexamethasone (10(-7) M), EGF (10 ng/ml), and PDGF (5 ng/ml) had the same mitogenic effectiveness as 10% calf serum (CS) in postnatal cells. In marked contrast, there was no mitogenic interaction between SM-C/IGF-I and dexamethasone in fetal fibroblasts. In fetal cells, SM-C/IGF-I + EGF + PDGF +/- dexamethasone could only account for 50% of the activity of 10% CS. Moreover, fetal cells were 50-100% more responsive than postnatal cells to the proliferative effect of serum.

Authors

Conover CA
No affiliation info available
Rosenfeld RG
No affiliation info available
Hintz RL
No affiliation info available

MeSH

Blood Physiological PhenomenaCell DivisionCulture MediaDexamethasoneEpidermal Growth FactorFetusFibroblastsHumansInsulin-Like Growth Factor IPeptide FragmentsPlatelet-Derived Growth FactorReceptors, Cell SurfaceReceptors, SomatomedinSomatomedins

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

3013906

Citation

Conover, C A., et al. "Hormonal Control of the Replication of Human Fetal Fibroblasts: Role of Somatomedin C/insulin-like Growth Factor I." Journal of Cellular Physiology, vol. 128, no. 1, 1986, pp. 47-54.
Conover CA, Rosenfeld RG, Hintz RL. Hormonal control of the replication of human fetal fibroblasts: role of somatomedin C/insulin-like growth factor I. J Cell Physiol. 1986;128(1):47-54.
Conover, C. A., Rosenfeld, R. G., & Hintz, R. L. (1986). Hormonal control of the replication of human fetal fibroblasts: role of somatomedin C/insulin-like growth factor I. Journal of Cellular Physiology, 128(1), 47-54.
Conover CA, Rosenfeld RG, Hintz RL. Hormonal Control of the Replication of Human Fetal Fibroblasts: Role of Somatomedin C/insulin-like Growth Factor I. J Cell Physiol. 1986;128(1):47-54. PubMed PMID: 3013906.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Hormonal control of the replication of human fetal fibroblasts: role of somatomedin C/insulin-like growth factor I. AU - Conover,C A, AU - Rosenfeld,R G, AU - Hintz,R L, PY - 1986/7/1/pubmed PY - 1986/7/1/medline PY - 1986/7/1/entrez SP - 47 EP - 54 JF - Journal of cellular physiology JO - J Cell Physiol VL - 128 IS - 1 N2 - Sparse cultures of fetal and postnatal human fibroblasts were equivalent in their responsiveness to the mitogenic action of somatomedin C/insulin-like growth factor I (SM-C/IGF-I). At both developmental stages, the addition of SM-C/IGF-I (100 ng/ml) increased cell number at day 3 1.4-fold in serum-free medium and 2-fold in the presence of 0.25% human hypopituitary serum. Furthermore, dose-response curves indicated that there was no difference in the sensitivity of fetal and postnatal fibroblasts to the growth-promoting effects of SM-C/IGF-I, with a half-maximal response occurring at 6 ng/ml SM-C/IGF-I. This biological action of SM-C/IGF-I correlated with SM-C/IGF-I binding to fetal and postnatal fibroblast monolayers. Epidermal growth factor (EGF) and platelet-derived growth factor (PDGF) also stimulated replication of fetal and postnatal fibroblasts. The mitogenic effects of SM-C/IGF-I, EGF, and PDGF were additive. Dexamethasone, which alone had no effect, was synergistic with SM-C/IGF-I in stimulating replication of postnatal fibroblasts. The combination of SM-C/IGF-I (100 ng/ml), dexamethasone (10(-7) M), EGF (10 ng/ml), and PDGF (5 ng/ml) had the same mitogenic effectiveness as 10% calf serum (CS) in postnatal cells. In marked contrast, there was no mitogenic interaction between SM-C/IGF-I and dexamethasone in fetal fibroblasts. In fetal cells, SM-C/IGF-I + EGF + PDGF +/- dexamethasone could only account for 50% of the activity of 10% CS. Moreover, fetal cells were 50-100% more responsive than postnatal cells to the proliferative effect of serum. SN - 0021-9541 UR - https://www.unboundmedicine.com/medline/citation/3013906/Hormonal_control_of_the_replication_of_human_fetal_fibroblasts:_role_of_somatomedin_C/insulin_like_growth_factor_I_ DB - PRIME DP - Unbound Medicine ER -