Hormonal regulation of insulin-like growth factor (IGF)-binding proteins secreted by isolated sheep thyroid epithelial cells: relationship with iodine organification

Wang, J. F.; Becks, G P; Hanada, Erika; Buckingham, K.D.; Phillips, Ian D.; Hill, D. J.

doi:10.1677/joe.0.1300129

Cited by 28 publications

(17 citation statements)

References 38 publications

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“…This observation, coupled with the finding that IGFBP-2 production by fetal lung epithelial cell cultures declines with increasing cell density (39), suggests that the decreased expression of IGFBP-2 on E21 may reflect the increase in epithelial cell density during this developmental period or changes in epithelial cell-cell interaction as differentiation proceeds. For example, in porcine follicular thyroid cells, the relative abundance of IGFBP-2 determines whether these cells respond to IGF-II by proliferating or by increasing differentiated cell function (40). Thus, these observations are consistent with IGFBP-2 facilitating the accumulation of IGF-I and IGF-II on the epithelial cell surface, possibly modulating the proliferative and/or differentiative effects of the IGFs on airway epithelium.…”

Section: Discussionsupporting

confidence: 58%

Regulation of the insulin-like growth factor system during normal rat lung development.

Moats‐Staats¹,

Price²,

Xu³

et al. 1995

Am J Respir Cell Mol Biol

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Insulin-like growth factor (IGF)-I and IGF-II are small peptide growth factors that interact with a specific membrane receptor, the type 1 IGF receptor, to stimulate cellular proliferation and/or differentiation. The actions of these growth factors and their availability to their receptors are modulated by specific binding proteins, IGF binding protein (IGFBP)-1 through -6, which together with the IGFs and IGF receptors form the IGF system. We have analyzed RNA extracted from fetal (gestation day 16 [E16] through 22 [E22]) and adult (60-day-old) rat lung for expression of each component of the IGF system. IGF-I and -II RNAs are expressed throughout fetal development. IGF-I mRNA remained relatively constant in fetal and adult lung, whereas IGF-II RNA decreased in later gestation to levels below detection by Northern analyses in adult lung. Type 1 IGF receptor expression varied little through all ages studied, whereas the type 2 IGF receptor RNA displayed developmental regulation with a decline in expression with advancing age. IGFBP-1 transcripts were not detected in fetal or adult lung. IGFBP-2 RNA was expressed from E16 to E22, although its abundance decreased in late gestation and in adult lung, with the lowest levels of expression on day E22. IGFBP-3, -4, and -5 had similar profiles of RNA abundance, with fetuses at ages E21 and E22 displaying higher levels of transcript abundance as compared with those aged E17 to E20; the lowest RNA abundance was seen at E20.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussionsupporting

confidence: 58%

Regulation of the insulin-like growth factor system during normal rat lung development.

Moats‐Staats¹,

Price²,

Xu³

et al. 1995

Am J Respir Cell Mol Biol

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“…However, in several other in vitro studies [37,38,39,40] IGFBP-2 expression was found to correlate positively with cell proliferation. It was thus concluded that IGFBP-2 represents an inducer of cell growth rather than an inhibitor.…”

Section: Investigation Of Igfbp-2 Functions In Cell Culture Studiesmentioning

confidence: 82%

Effects of IGFBP-2 overexpression in vitro and in vivo

Wolf¹,

Lahm²,

Wu³

et al. 2000

Pediatric Nephrology

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Insulin-like growth factor-binding proteins (IGFBPs) are important modulators of IGF actions and may have both stimulatory and inhibitory effects. Expression of IGFBP-2 is increased after fasting and in a variety of pathological conditions. However, the specific role of IGFBP-2 in growth physiology remains to be determined. In this review, we summarize data from in vitro and in vivo models suggesting that IGFBP-2 has mainly inhibitory effects on IGF actions. Since the growth hormone (GH)/IGF system is involved in a number of pathological alterations of the kidney and these changes may--at least in part--be due to increased IGF-I, local overexpression of inhibitory IGFBP-2 in the kidney might prevent IGF-I-induced lesions. This hypothesis will be tested by crossing GH transgenic mice, a common model of glomerulosclerosis, with transgenic mice characterized by systemic and renal overexpression of IGFBP-2.

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“…Secretion of several types of IGF binding proteins by thyrocytes has been demonstrated (16)(17)(18). Studies on mesenchymal as well as epithelial cells shows that the expression of general, as well as tissuespecific functions is influenced by the cellular organiza¬ tion, cell-cell contact and cell-substrate interaction (19)(20)(21)(22).…”

Section: G\l=o"\teborgswedenmentioning

confidence: 99%

Effects of insulin-like growth factor I on growth, epithelial barrier and iodide transport in polarized pig thyrocyte monolayers

Ericson

Nilsson²

1996

European Journal of Endocrinology

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The effects of insulin-like growth factor I (IGF-I) on mitogenesis, epithelial barrier function and transepithelial iodide transport were studied in confluent, polarized monolayers of pig thyrocytes cultured on filter in Transwell bicameral chambers. The growth rate in controls cultured in 1% fetal calf serum was low. Insulin-like growth factor I stimulated dose-dependently the incorporation of [3H]thymidine, maximally at 100 ng/ml, which corresponded to an increase of DNA content by 60% after 6 days. Thyrotropin (1 mU/ml) alone did not stimulate cell multiplication but inhibited partially the stimulatory effect of IGF-I. Insulin-like growth factor I (100 ng/ml) increased within 10 min the transepithelial potential difference, which remained elevated for several days, but did not significantly change the transepithelial resistance. When added together, IGF-I reinforced the effects of TSH on potential difference (increase) and resistance (decrease). A preserved epithelial barrier in IGF-I-treated cultures was confirmed by observing a normal immunolocalization of the tight junction protein ZO-1 and an unchanged ultrastructure of the junctional complex. Insulin-like growth factor I increased the transepithelial flux of 125I- in the basal-to-apical, but not in the opposite, direction. Stimulation of iodide transport by IGF-I was modest after 2 days and pronounced after 6 days. In comparison, TSH-stimulated iodide transport was higher after 2 days but lower after 6 days. Both TSH and IGF-I were strongly synergistic, after 6 days amounting to a 90-fold increase over the control basoapical 125I- transfer. The simultaneous accumulation of 125I- in the cell layer was increased two- to fourfold by IGF-I and/or TSH. In conclusion, IGF-I is able to induce growth in preformed monolayers of pig thyrocytes cultured on permeable filter. During these conditions, the mitogenic effect of IGF-I is partially inhibited by TSH, which has no growth-promoting action on its own. The transepithelial transport of iodide and bulk electrolytes is altered by IGF-I without affecting the epithelial barrier function. Specifically, IGF-I up-regulates the activity of the basolateral iodide pump and increases the iodide permeability of the apical plasma membrane. The action of IGF-I on iodide transport is independent of, although synergistic with, that of TSH. The findings support the notion that IGF-I may be an important regulator of thyroid growth and differentiated functions.

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Hormonal regulation of insulin-like growth factor (IGF)-binding proteins secreted by isolated sheep thyroid epithelial cells: relationship with iodine organification

Cited by 28 publications

References 38 publications

Regulation of the insulin-like growth factor system during normal rat lung development.

Regulation of the insulin-like growth factor system during normal rat lung development.

Effects of IGFBP-2 overexpression in vitro and in vivo

Effects of insulin-like growth factor I on growth, epithelial barrier and iodide transport in polarized pig thyrocyte monolayers

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