Direct mitogenic effects of human somatomedin on human embryonic lung fibroblasts

Weidman, E. Russell; Bala, R. M.

doi:10.1016/0006-291x(80)90372-1

Cited by 24 publications

(11 citation statements)

References 22 publications

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“…They are thought to be critical in postnatal growth (15,16). Studies to date have shown that IGF receptors are widespread in many fetal tissues (17,18), and a variety of fetal tissues respond to (19,20) and produce IGF (21)(22)(23). In addition, the concentrations of IGF in fetal and cord blood are correlated with fetal birth size (24).…”

mentioning

confidence: 99%

Expression of insulin-like growth factor II in human placentas from normal and diabetic pregnancies.

Shen¹,

Wang²,

Nelson³

et al. 1986

Proc. Natl. Acad. Sci. U.S.A.

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The growth and development of the placenta is critical to fetal growth and development; however, little is known regarding the mechanisms controlling placental growth and development. Human placental membranes are known to possess receptors for insulin-like growth factors I and II (IGF-I and IGF-II) from early gestation, and increasing evidence supports a major role for IGF-I and/or IGF-II in fetal growth and development. Therefore, the IGFs may also play a significant role in regulating placental growth and development. We report here that an adult human liver IGF-II cDNA hybridizes to poly(A)+ RNAs of human placentas from different gestational ages. There are four placental poly(A)I RNA species that hybridize to IGF-II cDNA, the major one ofwhich is about 6000 bases. The sizes of the hybridized transcripts are the same for placentas of different gestational ages. Furthermore, the IGF-II sequences expressed in the human placenta were quantitated by dot blot hybridization. The second trimester placenta expresses more IGF-ll mRNA sequences than placenta of first trimester and term. Interestingly, the term placentas from diabetic pregnancies also express more of these sequences than those from normal pregnancies. These results suggest that there are developmental changes in the expression ofthe IGF-II gene in the placenta and that IGF-ll may promote placental growth by way of an autocrine and/or paracrine mechanism. Moreover, fetuses developing in diabetic pregnancies receive a large influx of glucose, which in turn may stimulate the expression of IGF-ll sequences in placenta, resulting in higher utilization of glucose and overgrowth of placenta. This may explain the macrosomia and high incidence of malformations and stillbirths known to result from pregnancies in diabetics.

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mentioning

confidence: 99%

Expression of insulin-like growth factor II in human placentas from normal and diabetic pregnancies.

Shen¹,

Wang²,

Nelson³

et al. 1986

Proc. Natl. Acad. Sci. U.S.A.

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“…In normal fetuses between 16 and 22 weeks gestational age, the value corrected for the effect of heparin was found to be 4.10 ± 1.63 U/ml. This was a 4-fold increase over the adult range.…”

Section: Resultsmentioning

confidence: 99%

“…Fetal blood was sampled, without contamination by amniotic fluid or maternal blood, by fetoscopy between 16 and 23 weeks gestational age as detailed by Rodeck and Campbell (26). Gestational age was determined by dates and by ultrasound.…”

Section: Methodsmentioning

confidence: 99%

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Human embryonic somatomedin.

Sara¹,

Hall²,

Rodeck³

et al. 1981

Proc. Natl. Acad. Sci. U.S.A.

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A radioreceptor assay utilizing human fetal brain plasma membrane as matrix and somatomedin A as ligand (fetal brain RRA-SMA) was developed. Increased levels of fetal brain RRA-SMA were found in the fetal circulation. The concentration was approximately 4-fold higher in the fetal as compared to the adult human. At birth, values fell within the adult range. In contrast, adult somatomedins determined by somatomedin radioimmunoassay were undetectable in the fetus and below the adult range at birth. Levels of fetal brain RRA-SMA were decreased in fetuses with different clinical disorders. In healthy newborns at cesarean section a significant correlation between serum fetal brain RRA-SMA values and birth weight and length was found. These results indicate the presence of an embryonic somatomedin in humans. The fetal brain RRA-SMA may provide a reliable index of fetal growth.

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“…Thigh muscle was removed, weighed and frozen in liquid nitrogen and stored at -20 °C for later measurement of DNA, RNA and protein content (Wannemacher et al, 1965;Munro and Fleck, 1966;Abraham et al, 1972 Ashton and Francis, 1978;Weidman and Bala, 1980) and the ability of tissues such as chick liver cells (Haselbacher et al, 1980) and chick cartilage (Burch et al, 1986), to synthesize IGF-I (d'Ercole et al, 1976), it is widely believed that IGF-11 may be the somatomedin involved in growth promotion in the fetus (Moses et al, 1980). IGF-I blood levels are low in fetal life compared to postnatal values (Gluckman et al, 1983;Spencer GSG et al, 1983); in contrast, IGF-11 levels were found to be high in the fetus of some species (Moses et al, 1980).…”

Section: Methodsmentioning

confidence: 99%

Lack of effect of exogenous insulin-like growth factor-I (IGF-I) on chick embryo growth rate

Spencer¹,

Garssen²,

Gerrits³

et al. 1990

Reprod. Nutr. Dévelop.

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Direct mitogenic effects of human somatomedin on human embryonic lung fibroblasts

Cited by 24 publications

References 22 publications

Expression of insulin-like growth factor II in human placentas from normal and diabetic pregnancies.

Expression of insulin-like growth factor II in human placentas from normal and diabetic pregnancies.

Human embryonic somatomedin.

Lack of effect of exogenous insulin-like growth factor-I (IGF-I) on chick embryo growth rate

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