Dose-specific or dose-dependent effect of growth hormone treatment on the proliferation and differentiation of cultured neuronal cells

Lyuh, Esther; Kim, Hyun-Jung; Kim, Manho; Lee, Jungkwon; Park, Kyong-Soo; Yoo, Keun-Young; Lee, Kwang-Woo; Ahn, Yoon‐Ok

doi:10.1016/j.ghir.2007.03.002

Cited by 32 publications

(32 citation statements)

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“…36 In view of the different cell types or the same cell type at different status, GH may function as a regulator for cell proliferation and/or differentiation. 37,38 In this study, we found that rhGH is incapable of supporting the survival or proliferation of HSCs or megakaryoblastic cells but has the ability to promote megakaryocyte differentiation. These results are consistent with the report that GH is inefficient in maintaining the survival/proliferation machinery of CD34 1 cells and Sca-1 1 cells in BM cultures, although it does promote B-lymphocyte differentiation.…”

Section: Discussionmentioning

confidence: 68%

hGH promotes megakaryocyte differentiation and exerts a complementary effect with c-Mpl ligands on thrombopoiesis

Xu¹,

Wang²,

Shen³

et al. 2014

Blood

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Section: Discussionmentioning

confidence: 68%

hGH promotes megakaryocyte differentiation and exerts a complementary effect with c-Mpl ligands on thrombopoiesis

Xu¹,

Wang²,

Shen³

et al. 2014

Blood

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“…This view is supported by Lyuh et al (2007), who found that GH induced the production of neurite outgrowths from cultured neuronal hybrid cells. Neurotrophic actions of GH in the nervous system are therefore still controversial.…”

Section: Introductionmentioning

confidence: 72%

Growth Hormone Production and Action in N1E-115 Neuroblastoma Cells

et al. 2009

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Neuroblastoma cells are undifferentiated cells derived from the neural crest and are commonly used as models for studying neural function. Mouse N1E-115 neuroblastoma cells are derived from cancerous tissue and provide a model for studying the oncogenesis of neural cells. As growth hormone (GH) has been implicated as an autocrine or paracrine involved in neural regulation and in the induction or progression of cancer, the possibility that N1E-115 cells are sites of GH production and GH action was assessed. Using RT-PCR, cultured N1E-115 cells were found to express the mouse GH and GH receptor (GHR) genes. Immunocytochemistry demonstrated that both of the translated proteins (GH and its receptor) were abundantly present in the cytoplasm of these cells and their co-localization was established by confocal cytochemistry. GH action in these cells was determined in cells cultured for 72 h in the presence or absence of 10(-6) M or 10(-9) M mouse GH, which induced neurite sprouting and increased axon growth. In summary, the expression of GH and its receptor in GH responsive tumor-derived N1E-115 neuroblastoma cells suggests they provide a useful experimental model to assess GH actions in neural function or neural oncogenesis.

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“…A mechanism that could account for the modest effects of bGH-Tg is the so-called bell-shaped dose response. The net effect of GH then becomes negative at high concentrations of GH (Lyuh et al 2007, Aberg et al 2009). This phenomenon occurs when excessive concentrations of GH homo-dimerise, thereby preventing binding to the GHR.…”

Section: Discussionmentioning

confidence: 99%

Local overexpression of GH and GH/IGF1 effects in the adult mouse hippocampus

Walser¹,

Samà²,

Wickelgren³

et al. 2012

Journal of Endocrinology

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GH therapy improves hippocampal functions mainly via circulating IGF1. However, the roles of local GH and IGF1 expression are not well understood. We investigated whether transgenic (TG) overexpression in the adult brain of bovine GH (bGH) under the control of the glial fibrillary acidic protein (GFAP) promoter affected cellular proliferation and the expression of transcripts known to be induced by systemic GH in the hippocampus. Cellular proliferation was examined by 5-bromo-2 0 -deoxyuridine immunohistochemistry. Quantitative PCR and western blots were performed. Although robustly expressed, bGH-Tg did not increase either cell proliferation or survival. However, bGH-Tg modestly increased Igf1 and Gfap mRNAs, whereas other GH-associated transcripts were unaffected, i.e. the GH receptor (Ghr), IGF1 receptor (Igf1r), 2 0 ,3 0 -cyclic nucleotide 3 0 -phosphodiesterase (Cnp), ionotropic glutamate receptor 2a (Nr2a (Grin2a)), opioid receptor delta (Dor), synapse-associated protein 90/postsynaptic density-95-associated protein (Sapap2 (Dlgap2)), haemoglobin beta (Hbb) and glutamine synthetase (Gs (Glul )). However, IGF1R was correlated with the expression of Dor, Nr2a, Sapap2, Gs and Gfap. In summary, although local bGH expression was robust, it activated local IGF1 very modestly, which is probably the reason for the low response of previous GH-associated response parameters. This would, in turn, indicate that hippocampal GH is less important than endocrine GH. However, as most transcripts were correlated with the expression of IGF1R, there is still a possibility for endogenous circulating or local GH to act via IGF1R signalling. Possible reasons for the relative bio-inactivity of bGH include the bell-shaped dose-response curve and cell-specific expression of bGH.

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Dose-specific or dose-dependent effect of growth hormone treatment on the proliferation and differentiation of cultured neuronal cells

Cited by 32 publications

References 50 publications

hGH promotes megakaryocyte differentiation and exerts a complementary effect with c-Mpl ligands on thrombopoiesis

hGH promotes megakaryocyte differentiation and exerts a complementary effect with c-Mpl ligands on thrombopoiesis

Growth Hormone Production and Action in N1E-115 Neuroblastoma Cells

Local overexpression of GH and GH/IGF1 effects in the adult mouse hippocampus

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