Ascorbic acid mediates acetylcholine receptor increase induced by brain extract on myogenic cells.

Knaack, David; Podleski, Thomas R.

doi:10.1073/pnas.82.2.575

Cited by 37 publications

(30 citation statements)

References 42 publications

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“…Our findings that all of the analogs of ascorbic acid tested were active in promoting SC differentiation are attributable to the ability of the analogs to be convertexl enzymatically to ascorbic acid within the cell (dehydroascorbic acid, Tolbert and Ward, 1982; L-ascorbic acid 2-sulfate, Benitez and Halver, 1982) or to directly substitute for ascorbic acid as an enzymatic cofactor (D-isoascorbic acid; Hutton et al, 1967;Kutnink et al, 1969). The relative activities of the analogs in stimulating basal lamina and myelin formation by SCs were similar to those reported for functions of other cell types (Murad et al, 1983;Knaack and Podleski, 1985).…”

Section: Discussionsupporting

confidence: 60%

“…In the absence of serum, ascorbic acid predominantly causes SCs to migrate into aggregates (curved arrows), but also promotes the formation of occasional short myelin segments (arrowheads). Bar (DeClerck and Jones, 1980), and an increase in the number of acetylcholine receptors on myogenic L5 cells (Knaack and Podleski, 1985). Our findings that nonascorbic acid reducing agents had no activity in promoting either aspect of SC differentiation studied mean that it is unlikely that ascorbic acid is required simply as a general source of reducing activity.…”

Section: Discussionmentioning

confidence: 62%

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Differentiation of axon-related Schwann cells in vitro. I. Ascorbic acid regulates basal lamina assembly and myelin formation.

Eldridge¹,

Bunge²,

Bunge³

et al. 1987

The Journal of Cell Biology

382

301

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Abstract. Rat Schwann cells cultured with dorsal root ganglion neurons in a serum-free defined medium fail to ensheathe or myelinate axons or assemble basal laminae. Replacement of defined medium with medium that contains human placental serum (HPS) and chick embryo extract (EE) results in both basal lamina and myelin formation. In the present study, the individual effects of HPS and EE on basal lamina assembly and on myelin formation by Schwann cells cultured with neurons have been examined, Some batches of HPS were unable to promote myelin formation in the absence of EE, as assessed by quantitative evaluation of cultures stained with Sudan black; such HPS also failed to promote basal lamina assembly, as assessed by immunofluorescence using antibodies against laminin, type IV collagen, and heparan sulfate proteoglycan. The addition of EE or L-ascorbic acid with such HPS led to the formation of large quantities of myelin and to the assembly of basal laminae. Pretreatment of EE with ascorbic acid oxidase abolished the EE activity, whereas trypsin did not. Other batches of HPS were found to promote both basal lamina and myelin formation in the absence of either EE or ascorbic acid. Ascorbic acid oxidase treatment or dialysis of these batches of HPS abolished their ability to promote Schwann cell differentiation, whereas the subsequent addition of ascorbic acid restored that ability. Ascorbic acid in the absence of serum was relatively ineffective in promoting either basal lamina or myelin formation. Fetal bovine serum was as effective as HPS in allowing ascorbic acid (and several analogs but not other reducing agents) to manifest its ability to promote Schwann cell differentiation. We suggest that ascorbic acid promotes Schwann cell myelin formation by enabling the Schwann cell to assemble a basal lamina, which is required for complete differentiation.

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Section: Discussionsupporting

confidence: 60%

Section: Discussionmentioning

confidence: 62%

Differentiation of axon-related Schwann cells in vitro. I. Ascorbic acid regulates basal lamina assembly and myelin formation.

Eldridge¹,

Bunge²,

Bunge³

et al. 1987

The Journal of Cell Biology

382

301

View full text Add to dashboard Cite

show abstract

“…Quantification of the amount of 125-I-BTX binding by using gamma counting has been described in several previous publications Knaack and Podleski, 1985;Neugebauer et al, 1985, Knaack et al, 1986. Briefly, 6 of the 24 wells on 1 multiwell plate were used for any 1 treatment.…”

Section: Assay Of 125-i-btx Binding By Gamma Countingmentioning

confidence: 99%

Acetylcholine receptor clustering and triton solubility: Neural effect

Podleski

Salpeter

1988

J. Neurobiol.

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Previous studies by Prives et al. (1980, 1982a and b) have shown that acetylcholine receptors (AchRs) are extracted from muscle cells in vitro by Triton X-100 at different rates, and that clustered receptors extract most slowly. The present study was aimed at comparing the relative extractability of receptors in clusters with those in intercluster regions and the role of neural factors in regulating this extractability. Using primary rat muscle cells in vitro we confirmed that receptor extraction with Triton X-100 does not fit a single exponential but has more than one rate, and that in control cells clustered receptors extract more slowly than do receptors in intercluster regions. The major new observation in this study was that neural extract lowered the overall Triton extraction rate of intercluster receptors to that of clustered receptors. Additional new observations include the findings that (1) both clustered and intercluster receptors show multiphasic extraction rates; (2) stabilization of AchRs against Triton extraction increases with time in the surface membrane; (3) the effect of neural extract on Triton extractability of AChR is dependent on factors that control RNA synthesis, cytoskeletal elements, and collagen; (4) fixation and/or buffer washes accelerate receptor extraction only in cells that are treated with Triton, but not in control cells; (5) in control cells (not exposed to neural factors) Triton X-100 causes new clusters to form. From experiments using Con A we suggest that the Triton-induced new clusters may not be formed by a redistribution of receptors but are, most likely, due to the presence of groups of intercluster receptors with extraction rates lower than those of surrounding receptors.

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“…Ascorbic acid is an essential cofactor for prolyl lysyl hydroxylase (33,35,36), a key enzyme in collagen biosynthesis. In addition, ascorbic acid is necessary for the differentiation of many mesenchymal-derived cell types, including adipocytes (43), osteoblasts (3,9,26,40,42), myoblasts (15,18), and chondrocytes (12,21). In ATDC5 cells, ascorbic acid has been shown to enhance the differentiation process in the presence of high-dose insulin (2).…”

mentioning

confidence: 99%

The mechanism of ascorbic acid-induced differentiation of ATDC5 chondrogenic cells

Temu

Gruppuso

et al. 2010

American Journal of Physiology-Endocrinology and Metabolism

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The ATDC5 cell line exhibits a multistep process of chondrogenic differentiation analogous to that observed during endochondral bone formation. Previous investigators have induced ATDC5 cells to differentiate by exposing them to insulin at high concentrations. We have observed spontaneous differentiation of ATDC5 cells maintained in ascorbic acid-containing alpha-MEM. A comparison of the differentiation events in response to high-dose insulin vs. ascorbic acid showed similar expression patterns of key genes, including collagen II, Runx2, Sox9, Indian hedgehog, and collagen X. We took advantage of the action of ascorbic acid to examine signaling events associated with differentiation. In contrast to high-dose insulin, which downregulates both IGF-I and insulin receptors, there were only minimal changes in the abundance of these receptors during ascorbic acid-induced differentiation. Furthermore, ascorbic acid exposure was associated with ERK activation, and ERK inhibition attenuated ascorbic acid-induced differentiation. This was in contrast to the inhibitory effect of ERK activation during IGF-I-induced differentiation. Inhibition of collagen formation with a proline analog markedly attenuated the differentiating effect of ascorbic acid on ATDC5 cells. When plates were conditioned with ATDC5 cells exposed to ascorbic acid, ATDC5 cells were able to differentiate in the absence of ascorbic acid. Our results indicate that matrix formation early in the differentiation process is essential for ascorbic acid-induced ATDC5 differentiation. We conclude that ascorbic acid can promote the differentiation of ATDC5 cells by promoting the formation of collagenous matrix and that matrix formation mediates activation of the ERK signaling pathway, which promotes the differentiation program.

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Ascorbic acid mediates acetylcholine receptor increase induced by brain extract on myogenic cells.

Cited by 37 publications

References 42 publications

Differentiation of axon-related Schwann cells in vitro. I. Ascorbic acid regulates basal lamina assembly and myelin formation.

Differentiation of axon-related Schwann cells in vitro. I. Ascorbic acid regulates basal lamina assembly and myelin formation.

Acetylcholine receptor clustering and triton solubility: Neural effect

The mechanism of ascorbic acid-induced differentiation of ATDC5 chondrogenic cells

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