Insulin-like growth factors act synergistically withbasic fibroblast growth factor and nerve growth factor to promote chromaffincell proliferation.

Frödin, Morten; Gammeltoft, Steen

doi:10.1073/pnas.91.5.1771

Cited by 62 publications

(28 citation statements)

References 48 publications

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“…In this regulatory loop FGF-2 and IGF-1 might act synergistically as survival factors for oligodendrocytes or induce remyelination. A synergism between FGF-2 and IGF-1 was indeed shown for chromaffin cell proliferation (Frodin and Gammeltoft, 1994). In conclusion, FGF-2 signaling from activated microglia may have autocrine effects on the activation and recruitment of microglia and direct paracrine effects on oligodendrocytes.…”

Section: Discussionmentioning

confidence: 95%

Basic FGF and FGF receptor 1 are expressed in microglia during experimental autoimmune encephalomyelitis: Temporally distinct expression of midkine and pleiotrophen

Liu

Mashour

Webster

et al. 1998

Glia

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Section: Discussionmentioning

confidence: 95%

Basic FGF and FGF receptor 1 are expressed in microglia during experimental autoimmune encephalomyelitis: Temporally distinct expression of midkine and pleiotrophen

Liu

Mashour

Webster

et al. 1998

Glia

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“…FGF-2, IGF-II, and NGF are potent promoters of chromaffin cell proliferation in vitro (Lillien and Claude, 1985;Tischler et al, 1989;Frödin and Gammeltoft, 1994;Wolf et al, 1999). PACAP has been identified as a negative regulator of chromaffin cell proliferation in vitro (Frödin et al, 1995).…”

Section: Discussionmentioning

confidence: 99%

Reduction of endogenous TGF-? increases proliferation of developing adrenal chromaffin cells in vivo

2000

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Chromaffin cells and sympathetic neurons are derivatives of the sympathoadrenal cell lineage of the neural crest. Although they are similar with respect to many cell biological aspects, chromaffin cells, in contrast to sympathetic neurons, continue to synthesize DNA and proliferate through their whole life span. Large numbers of neural and hormonal signals have been implicated in the regulation of chromaffin cell proliferation based on in vitro studies. We have previously shown that chromaffin cells synthesize and release transforming growth factor-beta (TGF-beta) and that exogenously applied TGF-beta suppresses chromaffin cell proliferation in vitro. We show now that TGF-beta is also a physiologically relevant factor in the control of cell division in developing chromaffin cells. We have neutralized endogenous TGF-beta in quail embryos using a monoclonal antibody recognizing all three TGF-beta isoforms, TGF-beta1, -beta2, and -beta3. Embryos deprived of TGF-beta show a prominent increase in numbers of tyrosine hydroxylase (TH)-immunoreactive adrenal chromaffin cells and TH-positive cells incorporating 5'-bromo-2'deoxyuridine. This is the first documentation of the physiological significance of a factor that has been suggested to play a role in the regulation of chromaffin cell mitosis based on in vitro experiments.

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“…In adult adrenal medulla and sympathetic ganglia, gene expression of IGF-I and IGF-II and their receptors was proven at the mRNA level (Haselbacher et al 1987, Gelato & Vassalotti 1990, Ilvesmäki et al 1993. IGFs have been shown to promote chromaffin cell survival and proliferation in vivo (Frödin & Gammeltoft 1994); moreover IGF-I enhances catecholamine synthesis (Hwang & Choi 1996) and secretion (Dahmer et al 1990) in these cells.…”

Section: Introductionmentioning

confidence: 99%

Overexpression of the insulin-like growth factor I receptor in human pheochromocytomas

Fottner

Minnemann²,

Kalmbach³

et al. 2006

Journal of Molecular Endocrinology

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In order to determine the role of the IGF-I receptor (IGF-IR) in human pheochromocytomas we have compared the expression of the IGF-IR in normal tissues and in pheochromocytomas with regard to the IGF-IR mRNA levels and ligand binding. By semiquantitative reverse transcription polymerase chain reaction (RT-PCR), the mRNA of the IGF-IR could be detected in all samples of normal adrenomedullary cells (n=13) and pheochromocytomas (n=16). However, pheochromocytomas exhibited 2·8-fold higher mean IGF-IR mRNA levels than normal adrenomedullary cells (2·8±0·5×10 5 molecules/µg RNA vs 7·8±1·2×10 5 molecules/µg RNA; P,0·001). This overexpression of the IGF-IR in pheochromocytomas could be confirmed at the protein level by binding studies. Radioligand assays and Scatchard analysis revealed a single class of high affinity IGF-IR binding sites with a similar dissociation constant (K d : 0·32±0·1 nmol/l vs 0·22±0·08 nmol/l) for both normal adrenomedullary cells and pheochromocytomas. However, specific 125 I-labeled IGF-I binding and the calculated receptor concentration were significantly elevated in pheochromocytomas as compared with normal adrenomedullary cells (58·3±5 vs 24·3±12 nmol/kg protein; P,0·05). In summary, our results demonstrate significant overexpression of the IGF-IR in human pheochromocytomas. This suggests a possible role of the IGF system in the pathogenesis of adrenal neoplasia and thus IGF-IR may be a target for future therapeutic approaches.

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Insulin-like growth factors act synergistically withbasic fibroblast growth factor and nerve growth factor to promote chromaffincell proliferation.

Cited by 62 publications

References 48 publications

Basic FGF and FGF receptor 1 are expressed in microglia during experimental autoimmune encephalomyelitis: Temporally distinct expression of midkine and pleiotrophen

Basic FGF and FGF receptor 1 are expressed in microglia during experimental autoimmune encephalomyelitis: Temporally distinct expression of midkine and pleiotrophen

Reduction of endogenous TGF-? increases proliferation of developing adrenal chromaffin cells in vivo

Overexpression of the insulin-like growth factor I receptor in human pheochromocytomas

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