Role of epidermal growth factor-induced membrane depolarization and resulting calcium influx in osteoblastic cell proliferation

Loza, J.; Marzec, N.; Simasko, Steven M.; Dziak, Rosemary

doi:10.1016/0143-4160(95)90076-4

Cited by 14 publications

(15 citation statements)

References 18 publications

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“…Several physiological situations of nonexcitable cells that require dramatic reorganizations of the cytoskeleton are accompanied by modifications in the PMP. For instance, it has been shown that plasma membrane depolarization occurs and may participate in cell proliferation [Loza et al, 1995;Bianchi et al, 1998;MacFarlane and Sontheimer, 2000;Platoshyn et al, 2000;Milovanova et al, 2006;Raffaghello et al, 2006;Seo et al, 2006], cell differentiation [Greenwood et al, 1996;Gu et al, 2001;Koegel and Alzheimer, 2001], cell migration [Rao et al, 2002], and wound healing [Chifflet et al, 2005]. Moreover, it is well documented that malignant cells from different tissues are depolarized in relation to control tissues and that this depolarization may be related to the higher mitotic rate exhibited by these cells [Marino et al, 1994;Bianchi et al, 1998;Sun et al, 2003].…”

Section: Discussionmentioning

confidence: 95%

“…Thus, to obtain noticeable modifications in the cytoskeleton, both for the experimental PMP depolarization [Chifflet et al, 2003[Chifflet et al, , 2004 and hyperpolarization (this study), sustained treatments lasting at least several minutes were required. Significantly, actual observations reveal that the PMP changes that take place during or preceding differentiation and migration last from several minutes to hours [Loza et al, 1995]. Concerning the physiological stimuli that could determine PMP modifications in nonexcitable cells, some first messengers have been shown to produce changes in PMP in epithelia [Koegel and Alzheimer, 2001].…”

Section: Discussionmentioning

confidence: 97%

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Hyperpolarization of the plasma membrane potential provokes reorganization of the actin cytoskeleton and increases the stability of adherens junctions in bovine corneal endothelial cells in culture

Nin

Hernández

Chifflet

2009

Cell Motil. Cytoskeleton

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In previous works we showed that the depolarization of the plasma membrane potential (PMP) determines a reorganization of the cytoskeleton of diverse epithelia in culture, consisting mainly of a reallocation of peripheral actin toward the cell center, ultimately provoking intercellular disruption. In view of this evidence, we explored in this study the possible effects of membrane potential hyperpolarization on the cytoskeletal organization and adherens junction (AJ) morphology and the stability of confluent bovine corneal endothelial cells in culture. For this purpose, hyperpolarization was achieved by substitution of extracellular sodium by nondiffusible cations or via the incorporation of valinomycin to the control solution. Actin compactness at the cell periphery was assessed by quantitative analysis of fluorescence microscopy images. The stability of the AJ was challenged by calcium deprivation or temperature decrease. Our results showed that plasma membrane hyperpolarization provokes a compaction of AJ-associated actin filaments toward the plasma membrane and an increase in the stability of the AJs. We also observed that the hyperpolarizing procedures determined similar modifications in the actin cytoskeleton of endothelial cells in whole bovine corneas. Together with our previous work, the results of this study contribute to the idea that modifications in the PMP of nonexcitable cells participate in cellular adaptive responses involving reorganization of cytoskeletal components.

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Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 97%

Hyperpolarization of the plasma membrane potential provokes reorganization of the actin cytoskeleton and increases the stability of adherens junctions in bovine corneal endothelial cells in culture

Nin

Hernández

Chifflet

2009

Cell Motil. Cytoskeleton

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“…In these cells, IGF-1 or IGF-2 increased Ca 21 uptake via a calcium-permeable cation channel only when these fibroblasts were primed with epidermal growth factor (EGF), but not in quiescent or proliferating BALB/c 3T3 fibroblasts. Since EGF acts on several intracellular signal tranduction pathways [Loza et al, 1995;Peppelenbosch et al, 1991Peppelenbosch et al, , 1992Casabiell et al, 1993;Cerpovicz and Ochs, 1992;Dean and Boyton, 1995;Dunlop and Clark, 1993;Yeo and Exton, 1995] and there are crosstalks between these signaling pathways, two mechanisms may be responsible for the apparent effect of IGF-1 or IGF-2 on intracellular calcium in EGF-primed BALB/c 3T3 fibroblasts and may explain the apparent lack in cells not primed with EGF. One is that protein kinase C (PKC) activation by EGF may exert a negative feedback control on phosphatidylinositol 4,5 bisphosphate hydrolysis [Loza et al, 1995;Peppelenbosch et al, 1991], masking a possible effect of IGF-1 or IGF-2 on PLC and on the mobilization of Ca 21 from intracellular Ca 21 stores.…”

Section: Discussionmentioning

confidence: 96%

Different mechanisms are involved in intracellular calcium increase by insulin-like growth factors 1 and 2 in articular chondrocytes: Voltage-gated calcium channels, and/or phospholipase C coupled to a pertussis-sensitive G-protein

et al. 1997

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This study describes the mechanisms involved in the IGF-1 and IGF-2-induced increases in intracellular calcium concentration [Ca2+]i in cultured chondrocytes and the involvement of type 1 IGF receptors. It shows that IGF-1, IGF-2, and insulin increased the cytosolic free calcium concentration [Ca2+]i in a dose-dependent manner, with a plateau from 25 to 100 ng/ml for both IGF-1 and IGF-2 and from 1 to 2 micrograms/ml for insulin. The effect of IGF-1 was twice as great as the one of IGF-2, and the effect of insulin was 40% lower than IGF-1 effect. Two different mechanisms are involved in the intracellular [Ca2+]i increase. 1) IGF-1 and insulin but not IGF-2 involved a Ca2+ influx through voltage-gated calcium channels: pretreatment of the cells by EGTA and verapamil diminished the IGF-1 or insulin-induced [Ca2+]i but did not block the effect of IGF-2. 2) IGF-1, IGF-2, and insulin also induced a Ca2+ mobilization from the endoplasmic reticulum: phospholipase C (PLC) inhibitors, neomycin, or U-73122 partially blocked the intracellular [Ca2+]i increase induced by IGF-1 and insulin and totally inhibited the effect of IGF-2. This Ca2+ mobilization was pertussis toxin (PTX) dependent, suggesting an activation of a PLC coupled to a PTX-sensitive G-protein. Lastly, preincubation of the cells with IGF1 receptor antibodies diminished the IGF-1-induced Ca2+ spike and totally abolished the Ca2+ influx, but did not modify the effect of IGF-2. These results suggest that IGF-1 action on Ca2+ influx involves the IGF1 receptor, while part of IGF-1 and all of IGF-2 Ca2+ mobilization do not implicate this receptor.

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“…However, the current work is the first demonstration that targeted expression of PV can be used to examine the effects of Ca 2ϩ in distinct subcellular regions. EGF-mediated increases in Ca cyt 2ϩ have been suggested to mediate processes such as mitogenesis, proliferation, and gene expression (82)(83)(84)(85)(86)(87). However, the role specifically for Ca nuc 2ϩ in EGF signaling has yet to be defined.…”

Section: Discussionmentioning

confidence: 99%

Epidermal Growth Factor-mediated Activation of the ETS Domain Transcription Factor Elk-1 Requires Nuclear Calcium

Pusl¹,

Wu²,

Zimmerman³

et al. 2002

Journal of Biological Chemistry

104

109

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Cytosolic and nuclear Ca2؉ have been shown to differentially regulate transcription. However, the impact of spatially distinct Ca 2؉ signals on mitogen-activated protein kinase-mediated gene expression remains unknown. Here we investigated the role of nuclear and cytosolic Ca 2؉ signals in epidermal growth factor (EGF)-induced transactivation of the ternary complex factor Elk-1 using a GAL4-Elk-1 construct. EGF increased Ca

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Role of epidermal growth factor-induced membrane depolarization and resulting calcium influx in osteoblastic cell proliferation

Cited by 14 publications

References 18 publications

Hyperpolarization of the plasma membrane potential provokes reorganization of the actin cytoskeleton and increases the stability of adherens junctions in bovine corneal endothelial cells in culture

Hyperpolarization of the plasma membrane potential provokes reorganization of the actin cytoskeleton and increases the stability of adherens junctions in bovine corneal endothelial cells in culture

Different mechanisms are involved in intracellular calcium increase by insulin-like growth factors 1 and 2 in articular chondrocytes: Voltage-gated calcium channels, and/or phospholipase C coupled to a pertussis-sensitive G-protein

Epidermal Growth Factor-mediated Activation of the ETS Domain Transcription Factor Elk-1 Requires Nuclear Calcium

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