Immunolocalization of epimorphin in skin

Butt, Khalid Iqbal; Manabe, Motomu; Yaguchi, Hirohisa; Tsuboi, Ryoji; Ogawa, Hideoki

doi:10.1016/s0923-1811(96)00534-8

Cited by 7 publications

(5 citation statements)

References 12 publications

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“…For example, epimorphin mRNA has been shown to be present in ameloblasts, which are epithelium-derived cells (31). Also, immunohistochemical analyses have also yielded variable results, since the epimorphin antibody cross-reacts with syntaxin 1 (7). Our data agree with those reported originally by Hirai et al (22), describing epimorphin as a mesenchymal skin and lung protein in fetal tissues.…”

Section: Discussionsupporting

confidence: 87%

Characterization of rat epimorphin/syntaxin 2 expression suggests a role in crypt-villus morphogenesis

Goyal¹,

Singh

Swietlicki

et al. 1998

American Journal of Physiology-Gastrointestinal and Liver Physi

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The rodent intestinal mucosa undergoes a remarkable morphogenesis as the crypt-villus axis is formed. Endoderm-mesenchymal interactions play a critical role in this process. Epimorphin is a mesenchymal protein postulated to play a role in lung and skin morphogenesis. The rat homologue, syntaxin 2, belongs to a family of integral membrane proteins that function in vesicle docking and fusion. To clarify its role in fetal gut morphogenesis, epimorphin expression was examined during ontogeny, in an isograft model of ischemic injury and mucosal repair, and during intestinal adaptation after small bowel resection. Epimorphin/syntaxin 2 mRNA levels were increased in fetal gut during lumen formation and villus morphogenesis. mRNA levels remained elevated in the first 2 wk after birth and then declined at weaning. In situ hybridization showed epimorphin/syntaxin 2 mRNA in gestational day 14( G14) and G15 intestinal mesenchymal cells and in the mucosal lamina propria during villus formation. Epimorphin/syntaxin 2 mRNA expression increased during villus repair in the isograft. In contrast, in the early stages of intestinal adaptation after small bowel resection, epimorphin/syntaxin 2 mRNA expression was suppressed in the adapting gut. We conclude the cell-specific and temporal patterns of epimorphin expression in the models used in this study suggest a role in the morphogenesis of the crypt-villus axis.

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Section: Discussionsupporting

confidence: 87%

Characterization of rat epimorphin/syntaxin 2 expression suggests a role in crypt-villus morphogenesis

Goyal¹,

Singh

Swietlicki

et al. 1998

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…The gene that encodes EPM also encodes syntaxin-2, a protein that has been shown to function during targeting/ fusion of intracellular vesicles with the plasma membrane (Bennett et al, 1993;Pelham, 1993). Although syntaxins have been shown to act at the cytoplasmic face of membranes (Brose, 1993;Pelham, 1993;Rothman, 1994;Wheeler et al, 1996;Jagadish et al, 1997), the subcellular localization of syntaxins can be modulated through various mechanisms (Hui et al, 1997;Jagadish et al, 1997;Rodger et al, 1998;Quiñones et al, 1999), and syntaxins have been found at the cell surface at least transiently (Hirai et al, 1993(Hirai et al, , 1998Smirnova et al, 1993a,b;Butt et al, 1996;Nagamatsu et al, 1997;Guo et al, 1998). Evidently, these complex and versatile proteins can perform multiple functions, and it will be a considerable challenge to discover how these diverse roles are related.…”

Section: Epm Is a Member Of The Syntaxin Familymentioning

confidence: 99%

Epimorphin Mediates Mammary Luminal Morphogenesis through Control of C/EBPβ

Hirai

Radisky

Boudreau

et al. 2001

The Journal of Cell Biology

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We have shown previously that epimorphin (EPM), a protein expressed on the surface of myoepithelial and fibroblast cells of the mammary gland, acts as a multifunctional morphogen of mammary epithelial cells. Here, we present the molecular mechanism by which EPM mediates luminal morphogenesis. Treatment of cells with EPM to induce lumen formation greatly increases the overall expression of transcription factor CCAAT/enhancer binding protein (C/EBP)β and alters the relative expression of its two principal isoforms, LIP and LAP. These alterations were shown to be essential for the morphogenetic activities, since constitutive expression of LIP was sufficient to produce lumen formation, whereas constitutive expression of LAP blocked EPM-mediated luminal morphogenesis. Furthermore, in a transgenic mouse model in which EPM expression was expressed in an apolar fashion on the surface of mammary epithelial cells, we found increased expression of C/EBPβ, increased relative expression of LIP to LAP, and enlarged ductal lumina. Together, our studies demonstrate a role for EPM in luminal morphogenesis through control of C/EBPβ expression.

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“…Nevertheless, some antibodies to syntaxin 1A react with living cultured cells ( Inoue et al, 1992 ) and syntaxin 1B functions as a glutamic acid receptor at the cell surface in addition to its intracellular function ( Smirnova et al, 1993 a , b ). Analogous to syntaxin 1A and B, epimorphin is localized both in the cytoplasm and at the extracellular surface of the plasma membrane ( Hirai, 1994 ; Butt et al, 1996 ). Some isoforms of epimorphin might be anchored in the plasma membrane by a putative membrane-spanning region, the expression of which is modulated by alternative splicing ( Bennett et al, 1993 ; Hirai, 1993 ).…”

mentioning

confidence: 99%

Epimorphin Functions as a Key Morphoregulator for Mammary Epithelial Cells

Hirai

Lochter

Galosy

et al. 1998

The Journal of Cell Biology

137

188

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Hepatocyte growth factor (HGF) and EGF have been reported to promote branching morphogenesis of mammary epithelial cells. We now show that it is epimorphin that is primarily responsible for this phenomenon. In vivo, epimorphin was detected in the stromal compartment but not in lumenal epithelial cells of the mammary gland; in culture, however, a subpopulation of mammary epithelial cells produced significant amounts of epimorphin. When epimorphin-expressing epithelial cell clones were cultured in collagen gels they displayed branching morphogenesis in the presence of HGF, EGF, keratinocyte growth factor, or fibroblast growth factor, a process that was inhibited by anti-epimorphin but not anti-HGF antibodies. The branch length, however, was roughly proportional to the ability of the factors to induce growth. Accordingly, epimorphin-negative epithelial cells simply grew in a cluster in response to the growth factors and failed to branch. When recombinant epimorphin was added to these collagen gels, epimorphin-negative cells underwent branching morphogenesis. The mode of action of epimorphin on morphogenesis of the gland, however, was dependent on how it was presented to the mammary cells. If epimorphin was overexpressed in epimorphin-negative epithelial cells under regulation of an inducible promoter or was allowed to coat the surface of each epithelial cell in a nonpolar fashion, the cells formed globular, alveoli-like structures with a large central lumen instead of branching ducts. This process was enhanced also by addition of HGF, EGF, or other growth factors and was inhibited by epimorphin antibodies. These results suggest that epimorphin is the primary morphogen in the mammary gland but that growth factors are necessary to achieve the appropriate cell numbers for the resulting morphogenesis to be visualized.

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Immunolocalization of epimorphin in skin

Cited by 7 publications

References 12 publications

Characterization of rat epimorphin/syntaxin 2 expression suggests a role in crypt-villus morphogenesis

Characterization of rat epimorphin/syntaxin 2 expression suggests a role in crypt-villus morphogenesis

Epimorphin Mediates Mammary Luminal Morphogenesis through Control of C/EBPβ

Epimorphin Functions as a Key Morphoregulator for Mammary Epithelial Cells

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