Cytoskeleton-disrupting drugs enhance effect of growth factors and hormones on initiation of DNA synthesis.

Otto, Angela M.; Zumbe, Albert; Gibson, Lianne; Kubler, Anne‐Marie; Asúa, Luis Jiménez de

doi:10.1073/pnas.76.12.6435

Cited by 79 publications

(39 citation statements)

References 15 publications

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“…Gammaactin mRNA synthesis reached a peak level at 6 h after serum stimulation and then declined rapidly (Fig. 4) (12,24,29), an observation which is consistent with the above notion. Maness …”

supporting

confidence: 86%

Cell-cycle-specific and serum-dependent expression of gamma-actin mRNA in Swiss mouse 3T3 cells.

Masibay¹,

Qasba²,

Sengupta³

et al. 1988

Mol. Cell. Biol.

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We isolated cDNA tiones that represent genes whose expression is enhanced when resting Swiss mouse 3T3 cells are stimulated to proliferate with serum. Two clones (designated pME1 and pMR6) were analyzed further. A partial sequence analysis of the pM1:1 insert DNA indicated that it contained a 104-base-pair stretch with extensive homology to the 3' untranslated region of ganmma actin. Similar analysis of the insert DNA from the pMR6 clone indicated that it did not correspond to any previously reported gene sequence. We used the pME1 clone as a probe to determine the level of gamma actin-specific transcript in 3T3 cells under a variety of conditions. The level of gamma actiil-specific mRNA began to increase in resting cells upon serum stimulation and reached a peak at 6 h. Thereafter its level declined, and by 24 h it was hardly detectable. In contrast, pMR6-specific transcript was detectable in resting cells but remained elevated even at 24 h poststimulation. The level of gamma-actin mRNA was elevated in resting cells by 12-0-tetradecanoylphorbol-13-acetate, calcium ionophore A23187, and bombesin and to a lesser extent by cholera toxin, fibroblast-derived growth factor, and dibutyryl cyclic AMP. However, insulin, vasopressin, or epidermal growth factor failed to enhance gammaactin mRNA levels in resting cells. Inhibitors of transcription diminished the induction of gamma-actin mRNA. Gamma-actin gene was superinduced in serum-stimulated cells by cycloheximide, an inhibitor of translation. Analysis of proteins frdm serum-stimulated cells by two-dimensional gel electrophoresis indicated that enhanced transcription of gamma-actin mRNA resulted in a concomitant increase in the corresponding actin protein. The possible role of gamma actin, a component of the cytoskeleton, in the regulation of cell growth is discussed.

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supporting

confidence: 86%

Cell-cycle-specific and serum-dependent expression of gamma-actin mRNA in Swiss mouse 3T3 cells.

Masibay¹,

Qasba²,

Sengupta³

et al. 1988

Mol. Cell. Biol.

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“…We have speculated that CB may act by increasing the level of specific receptors on cells (9). This role is supported by the observations that CB enhances the in vitro stimulatory effect of growth factors (22) and melanocyte-stimulating hormone (23) on their specific target cells, and can inhibit the release ofspecific membrane components (24). Hence, via increasing the numbers of the relevant receptors, CB may enhance the stimulatory influence of a serum factor on corneal epithelial cells, resulting in production of stimulator, and similarly enhance the influence of stimulator(s) on stromal cells, resulting in production of collagenase.…”

Section: Chromatography Of Conditioned Mediummentioning

confidence: 82%

Regulation of connective tissue collagenase production: stimulators from adult and fetal epidermal cells.

Johnson-Wint¹,

Gross²

1984

The Journal of Cell Biology

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We have examined the ability of primary adult rabbit skin cells to regulate collagenase production in vitro. Dermal cells constitutively produce collagenase in culture, and enzyme production by these cells can be influenced by epithelial cells. Co-culture with skin epidermal cells resulted in more enzyme production by dermal cells, whereas co-culture with corneal epithelial cells yielded less enzyme activity . Connective tissue cells from a different source, cornea, also produced collagenase when co-cultured with skin epidermal cells, although the stromal cells alone made no enzyme .The drug cytochalasin B had very little influence on collagenase production by dermal cells, either alone or in co-culture with epidermal cells, but did significantly potentiate enzyme production by corneal stromal cells responding to epidermal effector molecules .Epidermal-cell-conditioned medium from both fetal and adult rabbit skin was a potent source of stimulators (apparent mol wt 20,500 and 55,000) of connective-tissue-cell Collagenase production . Stimulator production by epidermal cultures was cell density dependent . Optimal production of stimulators occurred in adult cultures containing 106 epidermal cells/ ml of medium, and in fetal cultures containing 105 cells/ml . Inhibitors of connective tissue cell enzyme production were not detected in conditioned medium from either adult or fetal epidermal cells .A growing body of evidence suggests that fibroblast behavior in situ may be regulated by neighboring cells over relatively short distances via secreted effector molecules called cytokines. Both mononuclear cells and epidermal cells produce cytokines (1). One ofthese molecules has been shown to be a fibroblast mitogen when derived from either monocytes (2, 3), macrophages (4), or epithelial cells (5, 6), and another molecule, mononuclear cell factor, stimulates collagenase production by fibroblasts (7) . Some of these effector molecules may be interleukin 1 (2, 3, 5-7).We are interested in cellular interactions that regulate collagenase production, and have previously shown that production of this enzyme by stromal cells from the adult rabbit cornea can be regulated in vitro by cell products from the epithelium of the same tissue (8, 9). Consistent with the observation that no enzyme is present in normal adult corneal tissue (10), we found that primary cultures of stromal or epithelial cells, or the two cell types mixed, made no collagenase . Indeed, conditioned-medium experiments demonstrated that the corneal epithelium made inhibitors (apparent mol wt 19,000 and 7,000) of stromal cell enzyme production. When, 90BARBARA JOHNSON-WINT and JEROME GROSS The Developmental Biology Laboratory, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114 however, we added cytochalasin B (CB)' to corneal cell cultures, their behavior changed . Under the in vitro influence of CB, adult corneal epithelial cells secreted substances (apparent mol wt 19,000 and 54,000) that stimu...

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“…They are an essential component of the mitotic spindle needed for cell division and are required for maintaining cell shape and a variety of other cellular activities, such as motility, anchorage, transport between cellular organelles, extracellular secretory processes (1), modulation of the interactions of growth factors with cell surface receptors, and intracellular signal transduction (2)(3)(4)(5). Furthermore, microtubules probably play a critical regulatory role in cell replication, as both the c-mos oncogene and CDC-2-kinase, which regulate entry into mitosis, bind to and phosphorylate tubulin (6,7) and the product of both the tumor suppressor gene p53 and the T-antigen of simian virus 40 bind tubulin in a ternary complex (8).…”

Section: Introductionmentioning

confidence: 99%

Taxol inhibits neointimal smooth muscle cell accumulation after angioplasty in the rat.

Sollott¹,

Cheng²,

Pauly³

et al. 1995

J. Clin. Invest.

239

150

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Despite significant improvements in the primary success rate of the medical and surgical treatments for atherosclerotic disease, including angioplasty, bypass grafting, and endarterectomy, secondary failure due to late restenosis continues to occur in 30-50% of individuals. Restenosis and the later stages in atherosclerotic lesions are due to a complex series of fibroproliferative responses to vascular injury involving potent growth-regulatory molecules (such as platelet-derived growth factor and basic fibroblast growth factor) and resulting in vascular smooth muscle cell (VSMC) proliferation, migration, and neointimal accumulation. We show here, based on experiments with both taxol and deuterium oxide, that microtubules are necessary for VSMCs to undergo the multiple transformations contributing to the development of the neointimal fibroproliferative lesion. Taxol was found to interfere both with platelet-derived growth factor-stimulated VSMC migration and with VSMC migration and with VSMC proliferation, at nanomolar levels in vitro. In vivo, taxol prevented medial VSMC proliferation and the neointimal VSMC accumulation in the rat carotid artery after balloon dilatation and endothelial denudation injury. This effect occurred at plasma levels approximately two orders of magnitude lower than that used clinically to treat human malignancy (peak levels achieved in this model were -50-60 nM). Taxol may therefore be of therapeutic value in preventing human restenosis with minimal toxicity. (J. Clin. Invest. 1995Invest. . 95:1869Invest. -1876

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Cytoskeleton-disrupting drugs enhance effect of growth factors and hormones on initiation of DNA synthesis.

Cited by 79 publications

References 15 publications

Cell-cycle-specific and serum-dependent expression of gamma-actin mRNA in Swiss mouse 3T3 cells.

Cell-cycle-specific and serum-dependent expression of gamma-actin mRNA in Swiss mouse 3T3 cells.

Regulation of connective tissue collagenase production: stimulators from adult and fetal epidermal cells.

Taxol inhibits neointimal smooth muscle cell accumulation after angioplasty in the rat.

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