Cell locomotion: New research tests old ldeas on membrane and cytoskeletal flow

Heath, Julian P.; Holifield, B.

doi:10.1002/cm.970180402

Cited by 120 publications

(58 citation statements)

References 105 publications

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“…Another possibility is that bead structures may represent precursors of cortical actin filaments. Active assembly of a cortical sheath of actin and myosin is known to take place in the region immediately behind the lamellipodia (Giuliano and Taylor, 1990;Heath and Holifield, 1991), in addition to the assembly of actin filaments at the leading edge. This process is coupled to a continuous, long-range flow of cortex toward the perinuclear region.…”

Section: Discussionmentioning

confidence: 99%

“…M ANY motile activities of noumuscle cells, including cytokinesis, cell locomotion, and growth cone extension are associated with the reorganization of actin filaments and the formation of new actin-containing structures (Satterwhite and Pollard, 1992;Heath and Holifield, 1991;Mitchison and Kirschner, 1988). At least some of these processes, most notably cell locomotion, have been shown to involve the de novo polymerization of actin filaments (Wang, 1985;Theriot and Mitchison, 1991).…”

mentioning

confidence: 99%

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Localization and dynamics of nonfilamentous actin in cultured cells [published erratum appears in J Cell Biol 1993 Nov;123(3):following 767]

Cao¹

1993

The Journal of Cell Biology

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Abstract. Although the distribution of filamentous actin is well characterized in many cell types, the distribution of nonfilamentous actin remains poorly understood. To determine the relative distribution of filamentous and nonfilamentous actin in cultured NRK cells, we have used a number of labeling agents that differ with respect to their specificities toward the filamentous or nonfilamentous form, including monoclonal and polyclonal anti-actin antibodies, vitamin D-binding protein (DBP), and fluorescent phalloidin. Numerous punctate structures were identified that bind poorly to phalloidin but stain positively with several anti-actin antibodies. These bead structures also stain with DBP, suggesting that they are enriched in nonfilamentous actin. Similar punctate structures were observed after the microinjection of fluorescently labeled actin into living cells, allowing us to examine their dynamics in living cells. The actin-containing punctate structures were observed predominantly in the region behind lamellipodia, particularly in spreading cells induced by wounding confluent monolayers. Time-lapse recording of cells injected with fluorescent actin indicated that they form continuously near the leading edge and move centripetally toward the nucleus. Our results suggest that at least part of the unpolymerized actin molecules are localized at discrete sites, possibly as complexes with monomer sequestering proteins. These structures may represent transient storage sites of G-actin within the cell which can be transformed rapidly into actin filaments upon stimulation by specific signals.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Localization and dynamics of nonfilamentous actin in cultured cells [published erratum appears in J Cell Biol 1993 Nov;123(3):following 767]

Cao¹

1993

The Journal of Cell Biology

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“…Membrane ruffles are specialized plasma membrane ultrastructures of cells, which are thought to have roles in growth, development, and locomotion (Heath and Holifield, 1991). Being associated with cell motility, membrane ruffling may be important in determining the metastatic potential of cells.…”

Section: Akt Can Influence Membrane Ruffling In Mcf-7 Cellsmentioning

confidence: 99%

Effect of estradiol on estrogen receptor-α gene expression and activity can be modulated by the ErbB2/PI 3-K/Akt pathway

et al. 2003

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Epidermal growth factor (EGF), insulin-like growth factor-I (IGF-I), and heregulin-b1 (HRG-b1), can modulate the expression and activity of the estrogen receptor-a (ER-a) via the phosphatidylinositol 3-kinase (PI 3-K)/Akt pathway in the ER-a-positive breast cancer cell line, MCF-7. Estradiol can also rapidly activate PI 3-K/Akt in these cells (nongenomic effect). The recent study examines whether Akt is involved in the ER-a regulation by estradiol (genomic effect). Stable transfection of parental MCF-7 cells with a dominant-negative Akt mutant, as well as the PI 3-K inhibitors wortmannin and LY 294,002, blocked the effect of estradiol on ER-a expression and activity by 70-80 and 55-63%, respectively. Stable transfection of MCF-7 cells with a constitutively active Akt mimicked the effect of estradiol. The changes in ER-a expression and activity were abrogated in response to estradiol by an arginine to cysteine mutation in the pleckstrin homology (PH) domain of Akt (R25C), suggesting the involvement of this amino acid in the interaction between Akt and ER-a. Experiments employing selective ErbB inhibitors demonstrate that the effect of estradiol on ER-a expression and activity is mediated by ErbB2 and not by EGFR. Moreover, anchorage-dependent and -independent growth assays, cell cycle and membrane ruffling analyses showed that Akt exerts estrogen-like activity on cell growth and membrane ruffling and that a selective ErbB2 inhibitor, but not anti-ErbB2 antibodies directed to the extracellular domain, can block these effects. In the presence of constitutively active Akt, tamoxifen only partially inhibits cell growth. In contrast, in cells stably transfected with either a dominant-negative Akt or with R25C-Akt, as well as in parental cells in the presence of a selective ErbB2 inhibitor, the effect of estradiol on anchorage-dependent and -independent cell growth was inhibited by 50-75 and 100%, respectively. Dominant-negative Akt inhibited membrane ruffling by 54%; however, R25C-Akt did not have any effect, suggesting that kinase activity plays an important role in this process. Scatchard analysis demonstrated a 67% reduction in estrogen-binding capacity in cells transfected with constitutively active Akt. No change in binding affinity of estradiol to the receptor was observed upon transfection with either Akt mutant. Taken together, our results suggest that estradiol treatment results in binding to membrane ER-a and interaction with a heterodimer containing ErbB2, leading to tyrosine phosphorylation. This results in the activation of PI 3-K and Akt. Akt, in turn, may interact with nuclear ER-a, altering its expression and activity.

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“…This cycle includes the turnover of adhesion sites, formed at the front and broken at the rear, to facilitate forward movement [33][34][35][36]. Vinculin (117 kDa, 1,066 amino acids) is a ubiquitous highly conserved cytoskeletal protein that was localized in both cell-cell and cell-extracellular matrix junctions [37].…”

Section: Introductionmentioning

confidence: 99%

Low‐energy laser irradiation increases endothelial cell proliferation, migration, and eNOS gene expression possibly via PI3K signal pathway

2008

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Background and Objectives: The purpose of this study, therefore, was to determine the mechanisms by which lowenergy laser irradiation (LELI) may exert some of its angiogenic effects via the PI3 kinase/eNOS signaling pathway and induce endothelial cell migration and neovascularization, an important and necessary part of wound healing. Study Design/Materials and Methods: The possible molecular mechanism of helium-neon (He-Ne) laser irradiation on endothelial cells was proposed. He-Ne laser at 632.5 nm was used to stimulate human umbilical vein endothelial cell (HUVEC), and its effect on cell proliferation, nitric oxide secretion, and cell migration was determined. Results: Irradiation enhanced endothelial nitric oxidase synthase (eNOS) protein expression, and irradiation of less than 0.26 J/cm 2 enhanced eNOS gene expression in HUVEC. The cell migration ability was promoted for HUVEC irradiated with 0.26 J/cm 2 . This agreed with the vinculin protein expression induced by irradiation. In addition, the angiogenesis was promoted. The induced eNOS expression was inhibited by LY294002, indicating that the effect of laser on EC could be attributed to the upregulation of eNOS expression through PI3K pathway at the cellular and molecular levels as a result of the He-Ne laser. Conclusions: The study has shown that LELI increased endothelial cell proliferation, migration, NO secretion, and identified that activation of PI3K/Akt pathway was a critical step for the elevated for eNOS expression upon LELI.

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Cell locomotion: New research tests old ldeas on membrane and cytoskeletal flow

Cited by 120 publications

References 105 publications

Localization and dynamics of nonfilamentous actin in cultured cells [published erratum appears in J Cell Biol 1993 Nov;123(3):following 767]

Localization and dynamics of nonfilamentous actin in cultured cells [published erratum appears in J Cell Biol 1993 Nov;123(3):following 767]

Effect of estradiol on estrogen receptor-α gene expression and activity can be modulated by the ErbB2/PI 3-K/Akt pathway

Low‐energy laser irradiation increases endothelial cell proliferation, migration, and eNOS gene expression possibly via PI3K signal pathway

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