Tenascin: a modulator of cell growth

End, Peter; Panayotou, George; Entwistle, Alan; Waterfield, Michael D.; Chiquet, Matthias

doi:10.1111/j.1432-1033.1992.tb17380.x

Cited by 85 publications

(39 citation statements)

References 63 publications

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“…In light of the tenascin-C mitogenic effects for several cell types [30], we expected to find higher tenascin-C transcript levels in tissues from fast growing fetuses [31] than in adults, especially those from 42-month-old females. Actually, only a few fetal tissues expressed higher transcription levels of both genes compared to the corresponding tissues from adults.…”

Section: Discussionmentioning

confidence: 99%

Distinct Tissue Distribution in Pigs of Tenascin‐X and Tenascin‐C Transcripts

Geffrotin

Garrido

Tremet

et al. 1995

European Journal of Biochemistry

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-EJB 95 0444/2Tenascin-X and tenascin-C glycoproteins are phylogenetically conserved components of the extracellular matrix, although their specific roles remain to be determined. cDNA probes were produced from pig tenascin-X and tenascin-C genes and were used to examine the tissue distribution of the transcripts in 28 tissues from Large-White pigs, 4.5-42-months old (called adults) and 17 tissues from 87-day-old fetuses. The hybridization of Northern blots with tenascin-X probes revealed, in most tissues, a complex pattern of bands including a major band of about 13 kb, assumed to correspond to the main tenascin-X transcript. Hybridization with the tenascin-C probe showed two transcripts of 6.8 kb and 8.2 kb. The data from the ribonuclease-protection technique showed that both genes displayed large variations in the transcription levels among the tissues analysed. Overall, the tenascin-X gene was significantly expressed in two thirds of the tissues, and the tenascin-C gene in about 50% of them. The highest tenascin-X signals were observed in tendons, ligaments and, unexpectedly, in peripheral nerves. Other tissues, including colon, dermis, skin, heart, uterus, stomach, jejunum, placentae, aorta, lung, mammary and adrenal glands also exhibited significant signal intensities. In fetuses, mainly testes and skeletal muscle showed higher transcription levels than the adult counterparts. The tenascin-C gene was predominantly transcribed in the ligament, tendon, adrenal gland and colon, and more weakly in the stomach, jejunum, lung and spinal cord. In fetuses, the tenascin-C signal in the brain was higher than the signal in the brain of adult, whereas the reverse was true for the adrenal gland and the colon. Within a given tissue, the level of tenascin-X and tenascin-C transcripts varied greatly, indicating independent tenascin-X and tenascin-C transcription regulation mechanisms; this was particularly obvious in adult and fetal nerves but also in the dermis, skin, heart, uterus, placentae and aorta, where tenascin-X RNA molecules were much more abundant than those of tenascin-C. In addition, similar differences were observed in the skeletal muscle and adrenal gland of fetuses. In contrast, the amount of tenascin-C transcripts in the fetal brain and adult spinal cord was higher than those for tenascin-X. Our results draw attention to a possible specific role of tenascin-X in the peripheral nerve physiology.

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Section: Discussionmentioning

confidence: 99%

Distinct Tissue Distribution in Pigs of Tenascin‐X and Tenascin‐C Transcripts

Geffrotin

Garrido

Tremet

et al. 1995

European Journal of Biochemistry

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“…Two recent studies report contradictory results on how TN-C can affect the mitogenic response of cells. End et al (1992) reported that TN-C was mitogenic for several cell types and that this activity was associated with a region in the fibronectin type III domains. In contrast, Crossin (1991) reported that TN-C inhibited the mitogenic response of 3T3 fibroblasts stimulated by growth factors.…”

Section: Introductionmentioning

confidence: 99%

Mitogenesis, cell migration, and loss of focal adhesions induced by tenascin-C interacting with its cell surface receptor, annexin II.

Chung

Murphy-Ullrich

Erickson

1996

MBoC

193

124

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In a previous study we demonstrated that the alternatively spliced region of tenascin-C, TNfnA-D, bound with high affinity to a cell surface receptor, annexin II. In the present study we demonstrate three changes in cellular activity that are produced by adding intact tenascin-C or TNfnA-D to cells, and we show that all three activities are blocked by antibodies against annexin II. 1) TNfnA-D added to confluent endothelial cells induced loss of focal adhesions. 2) TNfnA-D produced a mitogenic response of confluent, growth-arrested endothelial cells in 1% serum. TNfnA-D stimulated mitogenesis only when it was added to cells before or during exposure to other mitogens, such as basic fibroblast growth factor or serum. Thus the effect of TNfnA-D seems to be to facilitate the subsequent response to growth factors. 3) TNfnA-D enhanced cell migration in a cell culture wound assay. Antibodies to annexin II blocked all three cellular responses to TNfnA-D. These data show that annexin II receptors on endothelial cells mediate several cell regulatory functions attributed to tenascin-C, potentially through modulation of intracellular signalling pathways.

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“…Tn-C is mitogenic for some cell types [17]. In this study, only Tn-190 and Tn-ADC+ stimulated proliferation of CEWB cells.…”

Section: Discussionmentioning

confidence: 43%

Tenascin‐C induced stimulation of chondrogenesis is dependent on the presence of the C‐terminal fibrinogen‐like globular domain

et al. 2000

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The relationship between structure of tenascin-C (Tn-C), a multi-domain extracellular matrix protein, and its stimulation of chondrogenesis was examined using recombinant Tn-C isoforms (full length or with specific domains deleted) as substrata for undifferentiated chicken mesenchymal cells. Of the Tn-C variants tested, only Tn-C lacking the fibrinogen-like domain or Tn-C comprised solely of fibrinogen-like domains failed to stimulate chondrogenesis. The ability of variants to stimulate chondrogenesis was not dependent on their ability to support adhesion or stimulate proliferation. These results demonstrate that the fibrinogen-like domain of Tn-C is necessary but not sufficient for induction of chondrogenesis. ß

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Tenascin: a modulator of cell growth

Cited by 85 publications

References 63 publications

Distinct Tissue Distribution in Pigs of Tenascin‐X and Tenascin‐C Transcripts

Distinct Tissue Distribution in Pigs of Tenascin‐X and Tenascin‐C Transcripts

Mitogenesis, cell migration, and loss of focal adhesions induced by tenascin-C interacting with its cell surface receptor, annexin II.

Tenascin‐C induced stimulation of chondrogenesis is dependent on the presence of the C‐terminal fibrinogen‐like globular domain

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