The Vertebrate Epidermal Chalone

Bullough, W. S.; Laurence, Edna B.; Iversen, Ole‐Jan; Elgjo, Kjell

doi:10.1038/214578a0

Cited by 130 publications

(18 citation statements)

References 12 publications

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“…It is well known that IGF-1 functions as an extrinsic growth factor for promoting muscle development. However, as organ size is tightly controlled, intrinsic cell type-specific mitotic inhibitors, also known as "chalones," are expected (49). Our current findings suggest that myostatin may be an IGF-1-induced chalone produced locally by skeletal muscle cells that function to limit the skeletal muscle growth stimulated by growth-promoting factors, such as IGF-1.…”

Section: Discussionmentioning

confidence: 78%

Myostatin Induces Cyclin D1 Degradation to Cause Cell Cycle Arrest through a Phosphatidylinositol 3-Kinase/AKT/GSK-3β Pathway and Is Antagonized by Insulin-like Growth Factor 1

Yang

Zhang

et al. 2007

Journal of Biological Chemistry

195

158

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Myostatin is a transforming growth factor ␤ superfamily member and is known as an inhibitor of skeletal muscle cell proliferation and differentiation. Exposure to myostatin induces G 1 phase cell cycle arrest. In this study, we demonstrated that myostatin down-regulates Cdk4 activity via promotion of cyclin D1 degradation. Overexpression of cyclin D1 significantly blocked myostatin-induced proliferation inhibition. We further showed that phosphorylation at threonine 286 by GSK-3␤ was required for myostatin-stimulated cyclin D1 nuclear export and degradation. This process is dependent upon the activin receptor IIB and the phosphatidylinositol 3-kinase/ Akt pathway but not Smad3. Insulin-like growth factor 1 (IGF-1) treatment or Akt activation attenuated the myostatin-stimulated cyclin D1 degradation as well as the associated cell proliferation repression. In contrast, attenuation of IGF-1 signaling caused C2C12 cells to undergo apoptosis in response to myostatin treatment. The observation that IGF-1 treatment increases myostatin expression through a phosphatidylinositol 3-kinase pathway suggests a possible feedback regulation between IGF-1 and myostatin. These findings uncover a novel role for myostatin in the regulation of cell growth and cell death in concert with IGF-1.

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Section: Discussionmentioning

confidence: 78%

Myostatin Induces Cyclin D1 Degradation to Cause Cell Cycle Arrest through a Phosphatidylinositol 3-Kinase/AKT/GSK-3β Pathway and Is Antagonized by Insulin-like Growth Factor 1

Yang

Zhang

et al. 2007

Journal of Biological Chemistry

195

158

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“…This implies possible roles for locally produced factors in both positive-and negative-feedback mechanisms and the maintenance of homeostasis in the epidermis and dermis. Autocrine regulators previously identified in epidermal cells (chalones) have been found to be potent inhibitors of epidermal cell proliferation (11,12). This led to the belief that epidermal cell growth is regulated by negative feedback.…”

Section: Discussionmentioning

confidence: 99%

Growth regulation of skin cells by epidermal cell-derived factors: implications for wound healing.

Eisinger

Sadan

Silver

et al. 1988

Proc. Natl. Acad. Sci. U.S.A.

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Epidermal cell-derived factors (EDF), present in extracts and supernatant fluids of cultured epidermal cells, were found to stimulate the proliferation of keratinocytes but to inhibit fibroblasts. In vitro, the effect of EDF on epidermal cells resulted in an increased number of rapidly proliferating colonies composed mainly of basal keratinocytes. Control cultures grown in the absence of EDF had a high proportion of terminally differentiated cells. In fibroblast cultures EDF inhibited the ability of fibroblasts to cause contraction of collagen sponges by 90%. Epidermal growth factor, basic fibroblast growth factor, platelet-derived growth factor, transforming growth factor P, nerve growth factor, and extracts of WI-38 cells (human embryonic lung fibroblasts) did not have this inhibitory activity. Application of EDF to surgical wounds stimulated extensive migration and proliferation of keratinocytes from remnants of glands, hair follicles, and wound edges. The restoration of complete epidermal coverage of wounds treated with EDF occurred twice as rapidly as that of control wounds. In addition, regenerating dermis in the EDF-treated wounds contained 1/5th to 1/15th as many cells as wounds treated with epidermal growth factor, urogastrone, transforming growth factor, or phosphatebuffered saline. The use of EDF to enhance re-epithelization and to prevent scar formation is proposed.

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“…The apparently central role played by the glycopeptide complex in the promotion of swarming is puzzling. This class of compound is believed to influence cell division (Bullough et al, 1967) and possibly the long forms and rafts of long forms that are consistently present in monolayers are incompletely divided organisms that exhibit their characteristic helical swarming movement by virtue of their rich endowment with flagella. The alternative hypothesis (Lominski and Lendrum) that production of toxic metabolites promotes swarming would seem to implicate amino acids and vitamins as the limiting factors in the induction of swarming.…”

Section: Discussionmentioning

confidence: 99%

The Swarming Of Proteus On Semisynthetic Media

Brogan¹,

Nettleton

Reid

1971

Journal of Medical Microbiology

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PLATES I-IVSWARMING by proteus on solid medium has been the subject of investigation since it was first described by Hauser (1885), as it is a phenomenon that does not occur to the same degree with other Gram-negative rods. Lominski and Lendrum (1947) suggested that swarming is a reaction by the organisms to toxic products of their own metabolism, a view supported by the work of Hughes (1957), who demonstrated that the forms in a swarm are morphologically indistinguishable from those produced by the damaging action of penicillin. A relation exists between the ability of proteus to swarm on a solid medium and the composition of the medium. It is common knowledge that the presence of bile salts inhibits swarming and a variety of toxic substances as diverse as chloral hydrate (Kramer and Koch, 1931) and sulphonamides (Holman, 1957) inhibit swarming when added to media. Naylor (1960) devised a medium that did not promote swarming of proteus, by omitting sodium chloride from the conventional formula of nutrient agar. Jones and Park (1967) found that growth but not swarming occurred on a solid medium based on the minimal medium of Fildes (1938), but these workers also claimed that swarming on this medium was promoted by the addition of various amino compounds.The present investigation is an attempt to define the components of solid media that are responsible for the promotion of swarming by proteus. MATERIALS AND METHODSOrganisms Proteus mirabilis NCTC5887 and 1 1 wild strains of Proteus mirabilis variously isolated from urinary infections, wounds, ulcers and rectal swabs were studied in the present investigation; the wild strains were identified as Proteus mirabilis by the criteria of Cowan and Steel (1965). The organisms were maintained in Robertson's cooked-meat broth at room temperature and were subcultured at monthly intervals. Before testing, the organisms were brought into the log phase of growth by inoculating them into 5 ml of nutrient broth and incubating for 5 hr at 37°C.

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The Vertebrate Epidermal Chalone

Cited by 130 publications

References 12 publications

Myostatin Induces Cyclin D1 Degradation to Cause Cell Cycle Arrest through a Phosphatidylinositol 3-Kinase/AKT/GSK-3β Pathway and Is Antagonized by Insulin-like Growth Factor 1

Myostatin Induces Cyclin D1 Degradation to Cause Cell Cycle Arrest through a Phosphatidylinositol 3-Kinase/AKT/GSK-3β Pathway and Is Antagonized by Insulin-like Growth Factor 1

Growth regulation of skin cells by epidermal cell-derived factors: implications for wound healing.

The Swarming Of Proteus On Semisynthetic Media

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