Thy-1 molecule associates with protein tyrosine kinase(s) in rat mesangial cells

Narisawa‐Saito, Mako; Yamanashi, Yuji; Morioka, Tetsuo; Oite, Takashi; Shimizu, Fujio

doi:10.1046/j.1365-2249.1996.d01-800.x

Cited by 20 publications

(20 citation statements)

References 30 publications

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“…Thy-1 also may function as an adhesion molecule in other cells, including T cells [41]. We previously showed that Thy-1.1-mediated signal transduction via the Src-mediated protein tyrosine kinase and phosphatidylinositol turnover is triggered differentially by 1-22-3 and OX7 [13, 14]. The epitopes or domains of Thy-1.1 molecule important in different aspects of mesangial cell function, such as cell adhesion, migration, and differentiation, remain to be determined.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, we have recently demonstrated a physical association of protein tyrosine kinases, p59 fyn and p56/53 lyn, with Thy-1.1 molecule in cultured rat mesangial cells, and the activities were observed to be higher than those in mAb OX7 precipitates [13]. We have also reported the two to three times higher inositol triphosphate production and a greater response in Thy-1.1-mediated increase in intracellular free calcium concentration by 1-22-3-treated than OX7-treated mesangial cells [14].…”

Section: Introductionmentioning

confidence: 99%

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Comparative Nephritogenicity of Two Monoclonal Antibodies That Recognize Different Epitopes ofRat Thy-1.1 Molecule

Nakayama

Oite²,

Kawachi³

et al. 1998

Nephron

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The pathophysiological role of the Thy-1.1 molecule expressed on rat mesangial cells with regard to mesangial cell dysfunction and injury remains unknown. The mechanism of Thy-1.1-associated injury has now been investigated with two monoclonal antibodies, 1-22-3 and OX7, that recognize different epitopes of Thy-1.1. Mesangiolysis and mesangial cell proliferation were more marked in rats injected with 1-22-3 than in those treated with OX7. Immunostaining for rat complement component C3 and also C9 was similar in the kidneys of rats 1 h after injection of either antibody. Alpha smooth muscle actin was first detected 3 days after injection of 1-22-3 and peaked on day 5; type I collagen staining showed a mesangial pattern on days 5 and 10. The staining for alpha smooth muscle actin and type I collagen was less intense in OX7-treated rats than in the 1-22-3-injected rats. The amounts of mRNAs encoding collagen types I and III peaked 5 days after injection of 1-22-3 and 10 days after injection of OX7. Rats injected with 1-22-3 developed proteinuria that was already marked on day 1 and peaked at 150 mg/day on day 3, whereas OX7 induced a low grade of proteinuria with large interindividual variability on day 3. Immunostaining for rat C3 in the normal rat kidneys, incubated in vitro with 1-22-3 or OX7 followed by incubation with normal rat fresh serum as a complement source, as well as the levels of serum complement activity, CH50, 30 min after injection of 1-22-3 or OX7 were similar, suggesting that the difference in the nephritogenicity of these two antibodies is not attributable to a difference in their complement-fixing activities, but rather may result from the difference in epitope specificities. The epitope recognized by 1-22-3 thus appears to be important in the initiation and progression of antibody-induced nephritis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Comparative Nephritogenicity of Two Monoclonal Antibodies That Recognize Different Epitopes ofRat Thy-1.1 Molecule

Nakayama

Oite²,

Kawachi³

et al. 1998

Nephron

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“…Thy-1 has been co-immunoprecipitated with the SFK Fyn from noncaveolar rafts in PC 12 cells and with active Fyn and Lyn SFKs in mesangial cells (34,35). Two models have been described for Thy-1-SFK interaction.…”

Section: Thy-1 Required For Tsp-1-mediated Focal Adhesion Disassemblymentioning

confidence: 99%

Thrombospondin-1-induced Focal Adhesion Disassembly in Fibroblasts Requires Thy-1 Surface Expression, Lipid Raft Integrity, and Src Activation

Barker

Pallero

MacEwen

et al. 2004

Journal of Biological Chemistry

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The hep I peptide of thrombospondin-1 is known to induce the disassembly of focal adhesions, a critical step in regulating cellular adhesive changes needed for cell motility. Fibroblasts that are heterogeneous with respect to the surface expression of Thy-1 differ markedly in morphology, cytoskeletal organization, and migration, suggesting differential regulation of focal adhesion dynamics. Here we demonstrate that disassembly of focal adhesions mediated by both full-length thrombospondin-1 and the hep I peptide in fibroblasts requires the expression of Thy-1, although it does not appear to function as a stable member of the hep I receptor complex. Consistent with a known function of Thy-1 in regulating lipid raft-associated signaling, intact lipid rafts are necessary for hep I-mediated focal adhesion disassembly. Furthermore, we establish Src family kinase (SFK) activation as a novel component required for hep I-induced signaling leading to focal adhesion disassembly. hep I induces transient phosphorylation of SFKs in Thy-1-expressing fibroblasts only. Therefore, we conclude that Thy-1 surface expression is required for thrombospondin-1-induced focal adhesion disassembly in fibroblasts through an SFK-dependent mechanism. This represents a novel role for Thy-1 in the regulation of fibroblast-matrix interactions critical to tissue homeostasis and remodeling.

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“…Apoptosis induced via triggering of Thy-1 has previously been demonstrated for mouse thymocytes, which could be inhibited by addition of the tyrosine kinase inhibitor herbimycin. Interestingly, in rat mesangial cells, Thy-1 was shown to be associated with tyrosine kinases as well [19], and mAb-mediated triggering of mesangial Thy-1 induced an increase in the intracellular calcium concentration that could be blocked by herbimycin [20]. …”

Section: Cross-linking Of Thy-1 Induces Apoptosis In Cultured Mesangimentioning

confidence: 99%

Induction of Renal Cell Apoptosis by Antibodies and Complement

Roos

Sato²,

Maier³

et al. 2001

Nephron Exp Nephrol

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Renal diseases are in many cases associated with the presence of increased numbers of apoptotic cells in the kidney. Apoptosis has been proposed as an important mechanism involved in the resolution of a proliferative response. Furthermore, recent studies indicate its possible involvement in progression of renal disease, leading to sclerosis. Moreover, in an experimental model of acute mesangioproliferative glomerulonephritis in the rat, induced via antibodies directed to Thy-1, evidence was obtained for the occurrence of apoptosis coinciding with the very early induction of mesangial injury. The present review is focused on apoptosis in relation to this model, and discusses recent findings concerning direct involvement of triggering of Thy-1 as well as deposition of terminal complement complexes in the induction of mesangial cell apoptosis.

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Thy-1 molecule associates with protein tyrosine kinase(s) in rat mesangial cells

Cited by 20 publications

References 30 publications

Comparative Nephritogenicity of Two Monoclonal Antibodies That Recognize Different Epitopes ofRat Thy-1.1 Molecule

Comparative Nephritogenicity of Two Monoclonal Antibodies That Recognize Different Epitopes ofRat Thy-1.1 Molecule

Thrombospondin-1-induced Focal Adhesion Disassembly in Fibroblasts Requires Thy-1 Surface Expression, Lipid Raft Integrity, and Src Activation

Induction of Renal Cell Apoptosis by Antibodies and Complement

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