Induced expression of syndecan in healing wounds.

Elenius, Klaus; Vainio, Seppo; Laato, Matti; Salmivirta, Markku; Thesleff, Irma; Jalkanen, Markku

doi:10.1083/jcb.114.3.585

Cited by 228 publications

(133 citation statements)

References 53 publications

(68 reference statements)

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“…Most studies report enhanced immune cell infiltration in Sdc-1 2/2 mice, which has been correlated with enhanced extravasation from postcapillary venules because of effects ranging from modulation of integrin activity and interaction with cell adhesion molecules (14,15) to modulation of cytokine and chemokine gradients (16). Yet, the expression of syndecan-1 on endothelium and immune cells in vivo is difficult to detect, with the notable exception of B lymphocytes, which may be partially because of its dynamic regulation (9,(17)(18)(19).…”

mentioning

confidence: 99%

Syndecan-1, a Cell Surface Proteoglycan, Negatively Regulates Initial Leukocyte Recruitment to the Brain across the Choroid Plexus in Murine Experimental Autoimmune Encephalomyelitis

Zhang¹,

Wu²,

Song³

et al. 2013

The Journal of Immunology

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The cell surface heparan sulfate proteoglycan, syndecan-1, has been reported to be a negative regulator of various inflammatory processes, but its precise mode of action is poorly defined. In this study, we use the murine model of the 35–55 peptide of myelin oligodendrocyte glycoprotein–induced experimental autoimmune encephalomyelitis (EAE), a T lymphocyte–mediated inflammation where the steps in disease development and recovery are well characterized, to decipher how syndecan-1 impacts on the inflammatory reaction. Syndecan-1 knockout (Sdc-1−/−) mice show enhanced disease severity and impaired recovery. The use of bone marrow chimeric mice reveals that both an immune cell and a CNS-resident source of syndecan-1 contribute to this phenotype. Epithelial cells of the choroid plexus, where initial CCL20-induced leukocyte recruitment to the brain occurs, are identified as the predominant site of syndecan-1 expression. Syndecan-1 is lost from this site during the course of EAE by shedding into the cerebrospinal fluid, which correlates with loss of epithelial cell surface–bound CCL20 and is associated with the upregulation of IL-6 expression. In Sdc-1−/− mice, early leukocyte recruitment via the choroid plexus is enhanced, and IL-6 is elevated, which collectively results in higher numbers of the disease inducing Th17 cells in the CNS, thereby contributing to enhanced disease severity. Furthermore, Sdc-1−/− mice have intrinsically elevated plasma cell numbers and higher myelin oligodendrocyte glycoprotein–specific Ab levels during EAE, which we propose contributes to impaired recovery. Our data identify the choroid plexus epithelium as a novel source of IL-6 in EAE and demonstrate that its expression negatively correlates with syndecan-1 expression at this site.

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mentioning

confidence: 99%

Syndecan-1, a Cell Surface Proteoglycan, Negatively Regulates Initial Leukocyte Recruitment to the Brain across the Choroid Plexus in Murine Experimental Autoimmune Encephalomyelitis

Zhang¹,

Wu²,

Song³

et al. 2013

The Journal of Immunology

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“…Before reacting with the decorin-specific antiserum LF-30, the sections were treated with 0.05 U/ml chondroitin ABC lyase (Seikagaku Co., Tokyo, Japan) in enriched Tris buffer for 3 hours at 37°C. 20 After rinses with PBS, a biotin-conjugated secondary antibody was applied and incubated for 10 minutes at room temperature. The slides were washed twice with PBS, and thereafter incubated with streptavidin-conjugated horseradish peroxidase for 10 minutes.…”

Section: 13mentioning

confidence: 99%

Decorin Is Produced by Capillary Endothelial Cells in Inflammation-Associated Angiogenesis

Nelimarkka

Salminen

Kuopio

et al. 2001

The American Journal of Pathology

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Decorin is a small extracellular chondroitin/dermatan sulfate proteoglycan that has previously been shown to be involved in the angiogenesis-like behavior of endothelial cells (ECs) in vitro. There is also evidence that decorin plays a role in angiogenesis in vivo. In this study we sought to further explore the involvement of decorin in angiogenesis in vivo, especially in that associated with inflammation. We found by CD31 immunostaining of ECs that in giant cell arteritis there are capillary blood vessels not only in the adventitia as in uninvolved temporal artery wall, but also in the media and the external zone of the thickened intima. Localization of decorin by antiserum LF-30 in adjacent sections showed that in normal temporal artery wall decorin resides mainly in the media and the adventitia, whereas in inflamed temporal artery wall decorin is distributed throughout the vessel wall including the intima. Furthermore, the most intense reaction for decorin was evident in ECs of capillary neovessels within the media and the thickened intima of inflamed temporal artery wall. Decorin was also found in capillary ECs in certain pathological and physiological conditions in which the pivotal role of angiogenesis is more generally accepted. Pyogenic granulomas, granulation tissue of healing dermal wounds, and ovaries at different phases of follicle and corpus luteum formation all contained widely distributed CD31-positive capillaries. Decorin, on the other hand, was found in capillary ECs in pyogenic granulomas and granulation tissue, but not in those in the ovaries. The assessment of the degree of inflammation in the specimens with the presence of CD68-positive macrophages showed that the pyogenic granuloma, granulation tissue, and giant cell arteritis specimens were rich in macrophages around the decorin-positive capillaries. In contrast, the ovarian specimens were populated with fewer macrophages and even they were not located in close vicinity of capillaries negative for decorin. Our results confirm that decorin is involved in angiogenesis in vivo and, particularly, in conditions in which the inflammatory component is dominant.

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“…Expression of the four members of the syndecan family is regulated in diverse tissues at critical periods of development or remodelling (Elenius et al, 1991;Bemfield et al, 1992;Kim et al, 1994). To assess the potential contribution of the syndecan family to the complex epithelial-mesenchymal interactions during morphogenesis of the intestine, we analysed the expression of syndecan gene family members in intestinal models.…”

Section: Discussionmentioning

confidence: 99%

“…Syndecan-1 levels have been reported to be regulated at the transcriptional, post-transcriptional (Sanderson et al, 1992;Vainio Effect of malignant transformation on syndecan-1…”

Section: Transcript Levels In Developing Rat Intestine and Intestinalmentioning

confidence: 99%

Syndecan-1 is up-regulated in ras-transformed intestinal epithelial cells

Wong

Choo²,

Li³

et al. 1998

Br J Cancer

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Summary The syndecans, a family of cell-surface heparan sulphate proteoglycans, have been proposed to mediate cellular interactions with extracellular effector molecules, such as growth factors and components of the extracellular matrix, during critical phases of development.Transcripts of all four syndecans are expressed at varying levels in the developing rat intestine and in a series of immature rat intestinal epithelial cell lines. In addition, we report the novel finding that, in the intestinal epithelial cell lines, expression of syndecan-1 transcript is up-regulated by transformation with activated H-ras. This is in contrast to other cell lines in which ras transformation is associated with a decrease in syndecan-1 levels. The observed increase in the syndecan-1 occurs as a result of increased transcription and can be correlated with the degree of transformation of the IEC-18 cells. Transformation is also associated with a decrease in apparent molecular weight and increased shedding of the proteoglycan into the culture medium. Increased shedding of syndecan-1 into the culture medium after transformation with H-ras may contribute to the disruption of proteoglycan interactions with the extracellular matrix, leading to alterations in cell adhesion and organization.Keywords: proteoglycan; syndecan; ras transformation; intestinal epithelial cell In the rat intestine, dramatic changes over the last few days of gestation result in the reorganization of a tubular structure into the mature crypt-villus structure in which the mesenchyme is lined by a simple columnar epithelium (Moog, 1979;Trier and Moxey, 1979;Madara et al, 1981). Underlying this morphogenesis and the maintenance of the adult crypt-villus structure are reciprocal interactions between the epithelium and mesenchyme (Kedinger et al, 1986) that involve recognition phenomena between cell-surface molecules and components of the pericellular environment. Membrane-bound proteoglycans contribute to the regulation of cell behaviour through interactions with extracellular matrix components or by acting as co-receptors for biologically active peptides (Klagsbrun and Baird, 1991;Rapraeger et al, 1991;Yayon et al, 1991;Aviezer et al, 1994).Two gene families encoding cell-surface heparan sulphate proteoglycans (HSPG) have been identified on the basis of sequence similarities between their core proteins: the glypicanrelated integral membrane proteoglycans (PGs) and syndecan-like integral membrane PGs (David, 1993). We have reported that OCI-5, a glypican-related HSPG (Filmus et al, 1995), is involved in intestinal development (Filmus et al, 1988). Although syndecans-1 and -4 have been detected in the adult intestine (Kim et al, 1994), the involvement of the syndecan family in intestinal development or differentiation is largely unknown. The role of syndecan-1 in epithelial-mesenchymal interactions during morphogenesis of a variety of tissues raises the possibility of a similar role in the developing intestine. The recent cloning of the four members of the syndecan...

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Induced expression of syndecan in healing wounds.

Cited by 228 publications

References 53 publications

Syndecan-1, a Cell Surface Proteoglycan, Negatively Regulates Initial Leukocyte Recruitment to the Brain across the Choroid Plexus in Murine Experimental Autoimmune Encephalomyelitis

Syndecan-1, a Cell Surface Proteoglycan, Negatively Regulates Initial Leukocyte Recruitment to the Brain across the Choroid Plexus in Murine Experimental Autoimmune Encephalomyelitis

Decorin Is Produced by Capillary Endothelial Cells in Inflammation-Associated Angiogenesis

Syndecan-1 is up-regulated in ras-transformed intestinal epithelial cells

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