Insulin-like growth factor I rescues SH-SY5Y human neuroblastoma cells from hyperosmotic induced programmed cell death

Matthews, Christopher C.; Feldman, Eva L.

doi:10.1002/(sici)1097-4652(199602)166:2<323::aid-jcp10>3.0.co;2-c

Cited by 159 publications

(44 citation statements)

References 51 publications

(46 reference statements)

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“…These results are supported by other studies illustrating that both IGF-I and IGF-II promote survival in many neuronal systems (Lindholm et al, 1996;D'Mello et al, 1993;Neff et al, 1993;Aizenman and de Vellis, 1987). The mechanism by which IGF-I mediates effects in other systems involves IGF-I receptor activation and PI3K pathways (Singleton et al, 1996a,b;Matthews and Feldman, 1996;D'Mello et al, 1997), and results presented here indicate a similar mechanism is used by immature telencephalic cells. IGF-I, IGF-II, and IGF-I receptors are expressed in the CNS by the early developmental period studied (Bondy et al, 1990;Rotwein et al, 1988), and activation of IGF-I receptors may therefore promote survival of immature telencephalic cells in vivo.…”

Section: Discussionsupporting

confidence: 90%

“…IGF-I promotes telencephalic survival through the IGF-I receptor and PI3K signaling IGF-I has been shown previously to promote survival in some neuronal systems by activating the IGF-I receptor and PI3K signaling pathway (Singleton et al, 1996a,b;Matthews and Feldman, 1996;D'Mello et al, 1997). To determine if these pathways are similarly involved in IGF-I mediated survival of E12 telencephalic cells, cultures grown in 100 ng ml 71 IGF-I were treated with either 2 mg ml 71 a-IR 3 or 100 mM wortmannin, concentrations which have been used previously to block IGF-I receptor activation and PI3K, respectively (Matthews and Feldman, 1996;D'Mello et al, 1997).…”

Section: Igf Receptor Ligands Promote Telencephalic Cell Survival Indmentioning

confidence: 99%

“…To determine if these pathways are similarly involved in IGF-I mediated survival of E12 telencephalic cells, cultures grown in 100 ng ml 71 IGF-I were treated with either 2 mg ml 71 a-IR 3 or 100 mM wortmannin, concentrations which have been used previously to block IGF-I receptor activation and PI3K, respectively (Matthews and Feldman, 1996;D'Mello et al, 1997). Differences in apoptosis were not found among wild-type or bcl-x 7/7 E12 telencephalic cultures grown in DMEM, DMEM and a-IR 3 or DMEM and wortmannin (data not shown).…”

Section: Igf Receptor Ligands Promote Telencephalic Cell Survival Indmentioning

confidence: 99%

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Trophic support promotes survival of bcl-x-deficient telencephalic cells in vitro

et al. 1998

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Survival of immature neurons is regulated by Bcl-x L , as targeted disruption of bcl-x significantly increases cell death in vivo and in vitro. Death of cultured bcl-x-deficient and wildtype telencephalic cells can be prevented by fetal calf serum or chemically-defined medium (ITS), suggesting trophic factors in these media potentiate survival through a pathway independent of Bcl-x L . Addition of trophic factors to basal medium revealed that insulin and insulin-like growth factors (IGFs), but not other trophic factors, reduced apoptosis of wild-type and bcl-x-deficient telencephalic cells. Antibodies raised against IGF-I receptors and wortmannin both attenuated the effects of IGF-I, indicating survival was mediated by IGF-I receptors and phosphatidylinositol 3'-kinase signaling, whereas effects of ITS were only partially reduced by these agents. The survival promoting effects of ITS were reduced in cells lacking both bcl-x and bcl-2, indicating Bcl-2 plays a supportive role to Bcl-x L in maintaining telencephalic cell survival. Furthermore, the ratio of expression of the pro-apoptotic bax gene to the anti-apoptotic bcl-2 gene was reduced in bcl-x-deficient cultures grown in ITS, suggesting that the interaction between these bcl-2 family members may, in part, regulate a Bcl-x L independent survival pathway. Finally, the pro-apoptotic bad gene does not appear to play a role in these interactions as targeted disruption of bad did not alter apoptosis in telencephalic cultures.

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Section: Discussionsupporting

confidence: 90%

Section: Igf Receptor Ligands Promote Telencephalic Cell Survival Indmentioning

confidence: 99%

Section: Igf Receptor Ligands Promote Telencephalic Cell Survival Indmentioning

confidence: 99%

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Trophic support promotes survival of bcl-x-deficient telencephalic cells in vitro

et al. 1998

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“…The results for the most sensitive cell line SW403 are presented in Figure 1b. While long exposure (24 h) to hypertonic media can affect cell viability 8,9 our results indicate that a short hypertonic challenge is harmless. As results were similar for the other two colon cancer cell lines, these data are not shown.…”

Section: Introductionmentioning

confidence: 71%

Water induces autocrine stimulation of tumor cell killing through ATP release and P2 receptor binding

Selzner

Graf

et al. 2004

Cell Death Differ

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Although exposure of cells to extreme hypotonic stress appears to be a purely experimental set up, it has found an application in clinical routine. For years, surgeons have washed the abdominal cavity with distilled water to lyse isolated cancer cells left after surgery. No data are available supporting this practice or evaluating the potential mechanisms of cell injury under these circumstances. Recent evidence indicates that increases in cell volume stimulate release of adenosine triphosphate and autocrine stimulation of purinergic (P2) receptors in the plasma membrane of certain epithelial cell types. Under physiological conditions, purigenic stimulation can contribute to cell volume recovery through activation of solute efflux. In addition, adenosine triphosphate-P2 receptor binding might trigger other mechanisms affecting cell viability after profound hypotonic stress. This study demonstrates a novel pathway of cell death by apoptosis in human colon cancer cells following a short hypotonic stress. This pathway is induced by transitory cell swelling which leads to extracellular release of adenosine triphosphate (ATP) and specific binding of ATP to P2 receptors (probably P2X7). Extracellular ATP induced activation of caspases 3 and 8, annexin V, release of cytochrome c, and eventually cell death. The effect of ATP can be blocked by addition of (i) apyrase to hydrolyse extracellular ATP and (ii) suramin, a P2 receptor antagonist. Finally, (iii) gadolinium pretreatment, a blocker of ATP release, reduces sensitivity of the cells to hypotonic stress. The adenosine triphosphate-P2 receptor cell death pathway suggests that autocrine/paracrine signaling may contribute to regulation of viability in certain cancer cells disclosed with this pathway.

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“…This is also related to apoptosis and antiapoptosis, and is activated by cytokines or stress stimuli such as osmotic shock, UV light, and heat [9,18] . IGF-Ⅰ system has been reported to protect against a variety of chemical cellular injuries that induce apoptosis [19] . We previously showed that ethanol decreased the synthesis and secretion of IGF-Ⅰ and the activity of IGF-IR, an effect that is related to cell proliferation and differentiation [11] .…”

Section: Discussionmentioning

confidence: 99%

Effects of ethanol on insulin-like growth factor-I system in primary cultured rat hepatocytes: Implications of JNK1/2 and alcoholdehydrogenase

Kim²,

Kang³

2008

WJG

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AIM:To evaluate the effects of ethanol on the insulinlike growth factor-Ⅰ (IGF-Ⅰ) system involved in c-Jun N-terminal kinase (JNK1/2) and alcoholdehydrogenase (ADH) activity in primary cultured rat hepatocytes. M E T H O D S : H e p a t o c y t e s i s o l a t e d f r o m m a l eSprague-Dawley rats were incubated with various concentrations of ethanol for different durations of time. The cells were pretreated with SP600125 (10 μmol/L) and 4-MP (200 μmol/L), and then treated with ethanol (200 mmol/L). We then measured IGF-Ⅰ secretion, IGF-Ⅰ mRNA expression, cell viability and JNK1/2 activity by radioimmunoassay, RT-PCR, MTT assay and Western blot, respectively (n = 6). RESULTS: Ethanol induced the activity of phospho (p)-JNK1/2, reaching a maximum at 60 min and then decreasing at 180 min. The effects of ethanol on the IGF-Ⅰ system were increased at 60 min (secretion:7.11 ± 0.59 ng/mg protein vs 4.91 ± 0.51 ng/mg, mRNA expression: 150.2% ± 10.2% vs 101.5% ± 11.3%, P = 0.045) and then decreased at 180 min (secretion: 3.89 ± 0.25 ng/mg vs 5.4 ± 0.54 ng/mg protein; mRNA expression: 41.5% ± 10.4% vs 84.7% ± 12.1%, P = 0.04), however cell viability was decreased in a dose-and time-dependent manner. SP600125 blocked the ethanol-induced changes (at 60 min). Additionally, 4-methylpyrazole prevented the ethanol-induced decreases in the IGF-Ⅰ system, cell viability and p-JNK1/2 activity (at 180 min). CONCLUSION: This study suggests that ethanolinduced p-JNK1/2 activation is associated with the IGF-Ⅰ system and cell viability in hepatocytes. Furthermore, alcohol dehydrogenase is involved in the relationship between ethanol-induced inactivation of p-JNK1/2 and the changes of the IGF-Ⅰ system and cell viability. Oh YI, Kim JH, Kang CW. Effects of ethanol on insulin-like growth factor-Ⅰ system in primary cultured rat hepatocytes: Implications of JNK1/2 and alcoholdehydrogenase.

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Insulin-like growth factor I rescues SH-SY5Y human neuroblastoma cells from hyperosmotic induced programmed cell death

Cited by 159 publications

References 51 publications

Trophic support promotes survival of bcl-x-deficient telencephalic cells in vitro

Trophic support promotes survival of bcl-x-deficient telencephalic cells in vitro

Water induces autocrine stimulation of tumor cell killing through ATP release and P2 receptor binding

Effects of ethanol on insulin-like growth factor-I system in primary cultured rat hepatocytes: Implications of JNK1/2 and alcoholdehydrogenase

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