Staurosporine induces neurite outgrowth in neuronal hybrids (PC12EN) lacking NGF receptors

Rasouly, D.; Shavit, D.; Zuniga, R.; Elejalde, Rafael B.; Unsworth, Brian R.; Yayon, Avner; Lelkes, Peter I.

doi:10.1016/s0304-3940(97)90166-x

Cited by 9 publications

(13 citation statements)

References 12 publications

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“…Our results indicated that the protein kinase A, but not protein kinase C, pathway is involved in the modulation of NPY gene expression in human pheochromocytoma cells, further demonstrating the difference between the rat PC12 cells and human pheochromocytoma cells. The general protein kinase inhibitor staurosporine can induce a mature neuronal phenotype in human neuroblastoma and rat PC12 cells through a protein kinase C-independent pathway in the absence of both the trk and p75 NGF receptors, suggesting staurosporine as a unique neurotropic compound (20,21). NPY mRNA was increased during staurosporineinduced differentiation of SH-SY5Y human neuroblastoma cells along the sympathetic neuronal lineage (20).…”

Section: Discussionmentioning

confidence: 99%

Regulation of neuropeptide Y mRNA expression in cultured human pheochromocytoma cells

Liu

Kahri

Heikkilä

et al. 1999

European Journal of Endocrinology

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The expression of the neuropeptide Y (NPY) gene varies considerably in human pheochromocytomas, but the mechanisms for this variation have not been clarified. To investigate the regulation pattern of the NPY gene in human pheochromocytomas, we screened 16 pheochromocytomas and 9 normal adrenal tissues with Northern blots. The expression level of NPY mRNA in normal adrenal medulla was low and relatively constant, while the pheochromocytomas showed a very wide variation in NPY mRNA levels in both malignant and benign tumors. This indicates that NPY gene expression is not correlated with malignancy in pheochromocytomas. In primary cultures of human pheochromocytoma cells, nerve growth factor treatment (causing neuronal differentiation) increased NPY mRNA accumulation 2-to 5-fold (P < 0:05). NPY mRNA levels were also induced by protein kinase modulators (Bu) 2 cAMP and staurosporine in the cultures (P < 0:05). In contrast, treatment with dexamethasone and IGF-II (causing or linked with chromaffin differentiation) reduced NPY mRNA accumulation (P < 0:05). These data show that the regulation pattern of NPY mRNA expression in cultured human pheochromocytoma cells is different from that previously described in rat pheochromocytoma PC12 cells. Regulation of NPY mRNA expression in primary cultures by these differentiating factors suggests that the expression of NPY mRNA in pheochromocytoma tissues may be associated with the neuronal differentiation of the tumor cells affected by multiple factors.

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Section: Discussionmentioning

confidence: 99%

Regulation of neuropeptide Y mRNA expression in cultured human pheochromocytoma cells

Liu

Kahri

Heikkilä

et al. 1999

European Journal of Endocrinology

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“…Exposure of PC12 cells to STS has been studied extensively to investigate either neuronal differentiation by application of low concentrations (range of 10 nM) (Demeneix et al, 1990;Rasouly et al, 1996) or induced apoptosis when applied at high concentrations (up to 1 pM) (Xia et al, 1995). In response to nerve growth factor (NGF), PC12 cells differentiate into neuronal cells with neurite extensions (Greene, 1978).…”

Section: Vector-based Rbm3 Over-expression Mimics the Protective Effementioning

confidence: 99%

The RNA-binding protein RBM3 is involved in hypothermia induced neuroprotection

Chip

Zelmer

Ogunshola

et al. 2011

Neurobiology of Disease

119

110

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Induced hypothermia is the only therapy with proven efficacy to reduce brain damage after perinatal asphyxia. While hypothermia down-regulates global protein synthesis and cell metabolism, low temperature induces a small subset of proteins that includes the RNA-binding protein RBM3 (RNA-binding motif protein 3), which has recently been implicated in cell survival. Here, immunohistochemistry of the developing postnatal murine brain revealed a spatio-temporal neuronal RBM3 expression pattern very similar to that of doublecortin, a marker of neuronal precursor cells. Mild hypothermia (32°C) profoundly promoted RBM3 expression and rescued neuronal cells from forced apoptosis as studied in primary neurons, PC12 cells, and cortical organotypic slice cultures. Blocking RBM3 expression in neuronal cells by specific siRNAs significantly diminished the neuroprotective effect of hypothermia while vector-driven RBM3 over-expression reduced cleavage of PARP, prevented internucleosomal DNA fragmentation, and LDH release also in the absence of hypothermia. Together, neuronal RBM3 up-regulation in response to hypothermia apparently accounts for a substantial proportion of hypothermia-induced neuroprotection. Together, neuronal RBM3 up-regulation in response to hypothermia apparently accounts for a substantial proportion of hypothermia-induced neuroprotection.

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“…Similarly, rat pheochromocytoma PC12 cells exhibit neurite outgrowth after stimulation with staurosporine (Rasouly et al, 1994;Rasouly et al, 1996). Although the signaling pathways underlying these phenomena are not defined, there may be a common mechanism that also controls the formation of cellular extensions in keratinocytes.…”

Section: Introductionmentioning

confidence: 99%

Glycogen synthase kinase-3 regulates formation of long lamellipodia in human keratinocytes

Koivisto

Alavian

Häkkinen

et al. 2003

Journal of Cell Science

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During wound healing, keratinocytes initiate migration from the wound edge by extending lamellipodia into a fibronectin-rich provisional matrix. While lamellipodia-like structures are also found in cultured keratinocytes exposed to epidermal growth factor (EGF), the signaling pathway that regulates the formation of these structures is not defined. In cultured human keratinocytes seeded on fibronectin, we found that protein-serine/threonine kinase inhibitors including staurosporine, induced concentration-dependent formation of extended lamellipodia (E-lams). The formation of E-lams was inhibited by the proteintyrosine kinase inhibitors herbimycin A and genistein and augmented by the protein-tyrosine phosphatase inhibitor sodium orthovanadate. Staurosporine treatment induced relocation of tyrosine phosphorylated phospholipase C-γ1 (PLC-γ1) to the tips of lamellipodia where actin assembly was initiated. Consistent with an involvement of PLC-γ1 in E-lam formation, intracellular free calcium (Ca2+) was elevated during the formation of E-lams and conversely, E-lam formation was blocked by intracellular Ca2+ chelation with BAPTA/AM, but not by extracellular reduction of Ca2+ by EGTA. Notably, glycogen synthase kinase-3α/β (GSK-3α/β) was activated by staurosporine as evidenced by reduced phosphorylation on Ser-21/9. Suppression of GSK-3 activity by LiCl2 or by a specific chemical inhibitor, SB-415286, blocked E-lam formation but without altering cell spreading. Furthermore, GSK-3 inhibitors blocked both staurosporine- and EGF-induced keratinocyte migration in scratch-wounded cultures. We propose that GSK-3 plays a crucial role in the formation of long lamellipodia in human keratinocytes and is potentially a central regulatory molecule in epithelial cell migration during wound healing.

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Staurosporine induces neurite outgrowth in neuronal hybrids (PC12EN) lacking NGF receptors

Cited by 9 publications

References 12 publications

Regulation of neuropeptide Y mRNA expression in cultured human pheochromocytoma cells

Regulation of neuropeptide Y mRNA expression in cultured human pheochromocytoma cells

The RNA-binding protein RBM3 is involved in hypothermia induced neuroprotection

Glycogen synthase kinase-3 regulates formation of long lamellipodia in human keratinocytes

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