IGF-I and vasoactive intestinal peptide (VIP) regulate cAMP-response element-binding protein (CREB)-dependent transcription via the mitogen-activated protein kinase (MAPK) pathway in pituitary cells: requirement of Rap1

Fernández, Miriam; Sánchez‐Franco, Franco; Palacios, Nuria; Sánchez, Israel M.; Cacicedo, Lucinda

doi:10.1677/jme.1.01703

Cited by 28 publications

(20 citation statements)

References 59 publications

(29 reference statements)

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“…4B), reflecting the targeted activation of Star gene expression in response to the peptidergic stimulation. This observation may mirror the pituitary, where previously published observations showed that VIP could strongly induce the phosphorylation of CREB (Fernandez et al, 2005). This data pairs well with the results from our real time PCR and promoter activity data indicating that incubation of KK1 and primary granulosa cells with VIP strongly induced Star promoter activity, resulting in mRNA levels comparable to those observed in response to dbcAMP.…”

Section: Discussionsupporting

confidence: 64%

Vasoactive intestinal peptide (VIP)-mediated expression and function of steroidogenic acute regulatory protein (StAR) in granulosa cells

Kowalewski

Dyson

Boos

et al. 2010

Molecular and Cellular Endocrinology

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Summary VIP is a peptide hormone capable of activating the cAMP/PKA pathway and modifying gonadal steroidogenic capacity. Less is known about the molecular mechanisms of VIP-mediated steroidogenesis and its role in regulating the steroidogenic acute regulatory protein (STAR). We examined the impact of VIP on STAR expression and function in immortalized (KK1) and primary mouse granulosa cells, where VIP strongly upregulated STAR expression and steroidogenesis. Inhibitors of the PKA and PKC pathways suggested that both are activated by VIP. VIP did not efficiently phosphorylate STAR (P-STAR); however, VIP together with cAMP-analogs that activate Type II PKA increased P-STAR and further increased steroidogenesis. Our results suggest that VIP-induced STAR expression and function in granulosa cells result from the preferential activation of Type I PKA. Furthermore, the PKA and PKC pathways appear to converge at regulating VIP-mediated Star transcription and translation.

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Section: Discussionsupporting

confidence: 64%

Vasoactive intestinal peptide (VIP)-mediated expression and function of steroidogenic acute regulatory protein (StAR) in granulosa cells

Kowalewski

Dyson

Boos

et al. 2010

Molecular and Cellular Endocrinology

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“…These active integrin subunits then signal to the Rho family of GTPases leading to actin reorganization [168]. Chemokines such as stromal derived factor-1 (SDF-1) and insulin-like growth factor-1 (IGF-I) stimulate Rap1 activation and integrin-mediated binding to endothelial cells [169,170]. In endothelial cells, Rap1 is involved in the maintenance of junctions and decreased Rap1 activation leads to retraction of VE-cadherin and junction disassembly [171,172].…”

Section: Rho Gtpases In Extravasationmentioning

confidence: 99%

Stepping out of the flow: capillary extravasation in cancer metastasis

Miles

Pruitt

Golen

et al. 2007

Clin Exp Metastasis

229

221

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In order for cancer cells to successfully colonize a metastatic site, they must detach from the primary tumor using extracellular matrix-degrading proteases, intravasate and survive in the circulation, evade the immune response, and extravasate the vasculature to invade the target tissue parenchyma, where metastatic foci are established. Though many of the steps of metastasis are widely studied, the precise cellular interactions and molecular alterations associated with extravasation are unknown, and further study is needed to elucidate the mechanisms inherent to this process. Studies of leukocytes localized to inflamed tissue during the immune response may be used to elucidate the process of cancer extravasation, since leukocyte diapedesis through the vasculature involves critical adhesive interactions with endothelial cells, and both leukocytes and cancer cells express similar surface receptors capable of binding endothelial adhesion molecules. Thus, leukocyte extravasation during the inflammatory response has provided a model for transendothelial migration (TEM) of cancer cells. Leukocyte extravasation is characterized by a process whereby rolling mediated by cytokine-activated endothelial selectins is followed by firmer adhesions with beta1 and beta2 integrin subunits to an activated endothelium and subsequent diapedesis, which most likely involves activation of Rho GTPases, regulators of cytoskeletal rearrangements and motility. It is controversial whether such selectin-mediated rolling is necessary for TEM of cancer cells. However, it has been established that similar stable adhesions between tumor and endothelial cells precede cancer cell transmigration through the endothelium. Additionally, there is support for the preferential attachment of tumor cells to the endothelium and, accordingly, site-specific metastasis of cancer cells. Rho GTPases are critical to TEM of cancer cells as well, and some progress has been made in understanding the specific roles of the Rho GTPase family, though much is still unknown. As the mechanisms of cancer TEM are elucidated, new approaches to study and target metastasis may be utilized and developed.

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“…Plasmids pRL-TK, which contains a cDNA coding for Renilla, was used to monitor transfection efficiency. The reporter constructs used were: pNIS-2.8-Luc, which contains a 2.854-bp DNA fragment of the rat NIS promoter (33), hTGenh/prm-Luc, which contains the human Tg promoter/enhancer (64), and 3xCRE-Luc, which contains three CREs in tandem (65). Nterminal FLAG-tagged human G-protein ␤1 subunit and Nterminal HA-tagged human G-protein ␥2 subunit, cloned into pcDNA3.1ϩ, were obtained from the Guthrie cDNA Resource Center (Sayre, PA).…”

Section: Fig 9 G␤␥ Effect On Pax8 Localizationmentioning

confidence: 99%

Gβγ Dimers Released in Response to Thyrotropin Activate Phosphoinositide 3-Kinase and Regulate Gene Expression in Thyroid Cells

Zaballos

García

Santisteban

2008

Molecular Endocrinology

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Signaling by TSH through its receptor leads to the dissociation of trimeric G proteins into Galpha and Gbetagamma. Galphas activates adenylyl cyclase, which increases cAMP levels that induce several effects in the thyroid cell, including transcription of the sodium-iodide symporter (NIS) gene through a mechanism involving Pax8 binding to the NIS promoter. Much less is known about the function of Gbetagamma in thyroid differentiation, and therefore we studied their role in TSH signaling. Gbetagamma overexpression inhibits NIS promoter activation and reduces NIS protein accumulation in response to TSH and forskolin. Conversely, inhibition of Gbetagamma-dependent pathways increases NIS promoter activity elicited by TSH but does not modify forskolin-induced activation. Gbetagamma dimers are being released from the Gs subfamily of proteins, because cholera toxin mimics the effects elicited by TSH, whereas pertussis toxin has no effect on NIS promoter activity. We also found that TSH stimulates Akt phosphorylation in a phosphoinositide 3-kinase (PI3K)-dependent and cAMP-independent manner. This is mediated by Gbetagamma, because its overexpression or specific sequestration, respectively, increased or reduced phosphorylated Akt levels upon TSH stimulation. Gbetagamma sequestration increases NIS protein levels induced by TSH and Pax8 binding to the NIS promoter, which is also increased by PI3K inhibition. This is, at least in part, caused by Gbetagamma-mediated Pax8 exclusion from the nucleus that is attenuated when PI3K activity is blocked. These data unequivocally demonstrate that Gbetagamma released by TSH action stimulate PI3K, inhibiting NIS gene expression in a cAMP-independent manner due to a decrease in Pax8 binding to the NIS promoter.

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IGF-I and vasoactive intestinal peptide (VIP) regulate cAMP-response element-binding protein (CREB)-dependent transcription via the mitogen-activated protein kinase (MAPK) pathway in pituitary cells: requirement of Rap1

Cited by 28 publications

References 59 publications

Vasoactive intestinal peptide (VIP)-mediated expression and function of steroidogenic acute regulatory protein (StAR) in granulosa cells

Vasoactive intestinal peptide (VIP)-mediated expression and function of steroidogenic acute regulatory protein (StAR) in granulosa cells

Stepping out of the flow: capillary extravasation in cancer metastasis

Gβγ Dimers Released in Response to Thyrotropin Activate Phosphoinositide 3-Kinase and Regulate Gene Expression in Thyroid Cells

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