Identification of Human Semaphorin E Gene Expression in Rheumatoid Synovial Cells by mRNA Differential Display

Mangasser-Stephan, Kerstin; Dooley, Steven; Welter, Cornelius; Mutschler, Wolf; Hanselmann, R.

doi:10.1006/bbrc.1997.6607

Cited by 39 publications

(24 citation statements)

References 22 publications

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“…There may be a link between the regulation of neurite growth and cell survival mechanisms. Mangasser-Stephan et al (40) reported that a 493-bp cDNA fragment, identical to part of H-sema E, hybridized with a gene that was overexpressed in synovial cells from patients with rheumatoid arthritis. The cell deathresistant activity of semaphorin E may be involved in the irreversible destructive growth of synovial cells in this disease (41).…”

Section: Discussionmentioning

confidence: 99%

Identification of semaphorin E as a non-MDR drug resistance gene of human cancers

Yamada¹,

Endo²,

Gotoh³

et al. 1997

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

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To improve cancer chemotherapy, a better understanding of the molecular mechanisms of drug resistance is essential. To identify the molecules responsible for drug resistance that is unrelated to MDR1 or MRP gene products, a eukaryotic expression cDNA library of cisdiamminedichloroplatinum(II) (CDDP)-resistant ovarian cancer TYKnuR cells was introduced into Cos-7 cells. After repeated CDDP selection, cDNA homologous to murine semaphorin E was isolated from surviving cells. Human semaphorin E (H-sema E) was overexpressed in CDDP-resistant cell lines and was readily induced not only by diverse chemotherapeutic drugs but also by x-ray and UV irradiation. Transfection of H-sema E conferred a drug-resistant phenotype to CDDP-sensitive cells. In addition, the aberrant expression of H-sema E protein was detected immunohistochemically in 14 of 42 (33.3%) recurrent squamous cell carcinomas removed at autopsy after extensive radiochemotherapy. Recently, another member of the semaphorin family, CD100, was shown to significantly improve the viability of B lymphocytes. These results suggest the involvement of semaphorins in diverse cell survival mechanisms.

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Section: Discussionmentioning

confidence: 99%

Identification of semaphorin E as a non-MDR drug resistance gene of human cancers

Yamada¹,

Endo²,

Gotoh³

et al. 1997

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

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“…7); its co-receptor neuropilin-2 was also identified. The expression of semaphorin 3C (sema E) in rheumatoid synovial cells has suggested that it may serve an immunosuppressive role (82). Alternatively semaphorin 3C has been shown to inhibit axon growth of sympathetic nerves, decreasing norepinephrine and thereby playing a pro-inflammatory role by enhancing TNF-␣ production (83).…”

Section: Matrix Degradation and Synthesis In Response To Injurious Comentioning

confidence: 99%

Mechanical Injury and Cytokines Cause Loss of Cartilage Integrity and Upregulate Proteins Associated with Catabolism, Immunity, Inflammation, and Repair

Stevens

Wishnok

White

et al. 2009

Molecular & Cellular Proteomics

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The objectives of this study were to perform a quantitative comparison of proteins released from cartilage explants in response to treatment with IL-1␤, TNF-␣, or mechanical compression injury in vitro and to interpret this release in the context of anabolic-catabolic shifts known to occur in cartilage in response to these insults in vitro and their implications in vivo. Bovine calf cartilage explants from 6 -12 animals were subjected to injurious compression, TNF-␣ (100 ng/ml), IL-1␤ (10 ng/ml), or no treatment and cultured for 5 days in equal volumes of medium. The pooled medium from each of these four conditions was labeled with one of four iTRAQ labels and subjected to nano-2D-LC/MS/MS on a quadrupole time-of-flight instrument. Data were analysed by ProQuant for peptide identification and quantitation. k-means clustering and biological pathways analysis were used to identify proteins that may correlate with known cartilage phenotypic responses to such treatments. IL-1␤ and TNF-␣ treatment caused a decrease in the synthesis of collagen subunits (p < 0.05) as well as increased release of aggrecan G2 and G3 domains to the medium (p < 0.05). MMP-1, MMP-3, MMP-9, and MMP-13 were significantly increased by all treatments compared with untreated samples (p < 0.10). Increased release of proteins involved in innate immunity and immune cell recruitment were noted following IL-1␤ and TNF-␣ treatment, whereas increased release of intracellular proteins was seen most dramatically with mechanical compression injury. Proteins involved in insulin-like growth factor and TGF-␤ superfamily pathway modulation showed changes in pro-anabolic pathways that may represent early repair signals. At the systems level, two principal components were sufficient to describe 97% of the covariance in the data. A strong correlation was noted between the proteins released in response to IL-1␤ and TNF-␣; in contrast, mechanical injury resulted in both similarities and unique differ-

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“…Thus, some genes preferentially expressed in cultured RA synovial fibroblasts have been identified using differential display (DD) (7) and representational difference analysis (RDA) (8). In addition, attempts have started to directly examine the mRNA expression profiles of synovial tissue specimens using cDNA array techniques (9,10).…”

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confidence: 99%

Expression of ID Family Genes in the Synovia from Patients with Rheumatoid Arthritis

Sakurai

Yamaguchi

Tsuchiya³

et al. 2001

Biochemical and Biophysical Research Communications

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Identification of Human Semaphorin E Gene Expression in Rheumatoid Synovial Cells by mRNA Differential Display

Cited by 39 publications

References 22 publications

Identification of semaphorin E as a non-MDR drug resistance gene of human cancers

Identification of semaphorin E as a non-MDR drug resistance gene of human cancers

Mechanical Injury and Cytokines Cause Loss of Cartilage Integrity and Upregulate Proteins Associated with Catabolism, Immunity, Inflammation, and Repair

Expression of ID Family Genes in the Synovia from Patients with Rheumatoid Arthritis

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