Induction of neuronal apoptosis by Semaphorin3A-derived peptide

Shirvan, Anat; Shina, Ronit; Ziv, Ilan; Melamed, Eldad; Barzilai, Ari

doi:10.1016/s0169-328x(00)00198-4

Cited by 37 publications

(30 citation statements)

References 51 publications

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“…3D). Collectively, these effects are reminiscent of the previously reported collapse of oligodendrocyte processes and death of neural precursors induced by secreted SEMA-3A, a brain-derived semaphorin (12)(13)(14).…”

Section: Cd100-producing T Cells Dramatically Affect Neural Precursorsupporting

confidence: 52%

“…In fact, CD100 (also known as semaphorin 4D (SEMA-4D)) 4 and SEMA-4A, two immune semaphorins, are expressed constitutively in T cells (5,6), function as soluble ligand to regulate the humoral and cellular immune responses (7)(8)(9), and are suspected to be involved in autoimmune diseases such as experimental autoimmune encephalitis (EAE) (6,10). SEMA-3A acts in axonal guidance, apoptosis of neural precursors or neurons, and oligodendrocyte alteration (11)(12)(13)(14), and inhibits the chemokine-induced migration of human immune cells similarly to CD100 (15). Neuropilin-1, a component of SEMA-3A receptor in brain, is also expressed in immune cells and plays a role in the establishment of contacts between naive T lymphocytes and dendritic cells (16).…”

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confidence: 99%

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Semaphorin CD100 from Activated T Lymphocytes Induces Process Extension Collapse in Oligodendrocytes and Death of Immature Neural Cells

Giraudon¹,

Vincent²,

Vuaillat³

et al. 2004

The Journal of Immunology

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An inappropriate cross talk between activated T lymphocytes infiltrating the CNS and neural cells can sustain the onset and progression of demyelination and axonal degeneration in neuroinflammatory diseases. To mimic this deleterious cross talk, we designed an experimental paradigm consisting of transient cocultures of T lymphocytes chronically activated by retrovirus infection (not virus productive) with human multipotent neural precursors or primary oligodendrocytes from rat brain. We showed that activated T lymphocytes induced apoptotic death of multipotent neural progenitors and immature oligodendrocytes after a progressive collapse of their process extensions. These effects were reminiscent of those induced by brain semaphorin on neural cells. Blockade by specific Abs of soluble CD100 (sCD100)/semaphorin 4D released by activated T cells, or treatment with rsCD100, demonstrated that this immune semaphorin has the ability to collapse oligodendrocyte process extensions and to trigger neural cell apoptosis, most likely through receptors of the plexin family. The specific presence of sCD100 in the cerebrospinal fluid and of CD100-expressing T lymphocytes in the spinal cord of patients suffering with neuroinflammatory demyelination pointed to the potential pathological effect of sCD100 in the CNS. Thus, our results show that CD100 is a new important element in the deleterious T cell-neural cell cross talk during neuroinflammation and suggest its role in demyelination or absence of remyelination in neuroinflammatory diseases including multiple sclerosis and human T lymphotropic virus type 1-associated myelopathy.

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Section: Cd100-producing T Cells Dramatically Affect Neural Precursorsupporting

confidence: 52%

mentioning

confidence: 99%

Semaphorin CD100 from Activated T Lymphocytes Induces Process Extension Collapse in Oligodendrocytes and Death of Immature Neural Cells

Giraudon¹,

Vincent²,

Vuaillat³

et al. 2004

The Journal of Immunology

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“…These findings accord with prior observations by Bachelder et al that NP-1 supports a VEGF signaling pathway that is critical for breast carcinoma cell survival (32) and that VEGF and SEMA3A are antagonistic NP-1 ligands that regulate breast carcinoma cell migration (33). Also, SEMA3A induces apoptosis in neurons (38,39), competes with VEGF-A binding on porcine aortic endothelial, medulloblastoma, and human embryonic kidney 293 cells, and affects cell survival and migration (27)(28)(29). Recent research also shows SEMA3F (whose gene is located Ϸ70 kb telomeric of SEMA3B in the same 3p21.3 region) and VEGF as having opposing effects on cell attachment and motility in breast cancer lines MCF-7 and C100 (40).…”

Section: Sema3b Induces Apoptosis Of H1299 Lung Carcinoma Cells and Vmentioning

confidence: 99%

Semaphorin 3B (SEMA3B) induces apoptosis in lung and breast cancer, whereas VEGF ₁₆₅ antagonizes this effect

Castro-Rivera

Ran

Thorpe

et al. 2004

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

178

148

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Semaphorin 3B (SEMA3B) is a secreted member of the semaphorin family, important in axonal guidance. We and others have shown that SEMA3B can act as a tumor suppressor by inducing apoptosis either by reexpression in tumor cells or applied as a soluble ligand. The common method of inactivation of SEMA3B is by allele loss and tumor-acquired promoter methylation. We studied the mechanism of SEMA3B-induced tumor cell apoptosis and found that vascular endothelial growth factor (VEGF) 165 significantly decreased the proapoptotic and antimitotic effect of transfected or secreted SEMA3B on lung and breast cancer cells. VEGF 165 binds to neuropilin, receptors for SEMA3B, and we found that SEMA3B competed for binding of 125 I-VEGF165 to lung and breast cancer cells. We also found that small interfering RNA knockdown of tumor-produced VEGF-A or the use of an anti-VEGF neutralizing antibody (Ab) significantly inhibited tumor cell growth in vitro. By contrast, VEGF 121, a VEGF variant that lacks binding to neuropilin (NP)-1 or NP-2 receptors, was not expressed in tumor cells and had no effect on SEMA3B growth-suppressing activities. In conclusion, we hypothesize that VEGF 165, produced by tumor cells, acts as an autocrine survival factor and that SEMA3B mediates its tumor-suppressing effects, at least in part, by blocking this VEGF autocrine activity.

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“…Sympathetic innervation can also be modulated by neuro-inhibitory factors such as interferongamma (IFNG), leukemia inhibitory factor (LIF), and Semaphorin 3c (Shirvan, Shina et al 2000;Kim, Beck et al 2002;Ng, He et al 2003). However, none of those factors showed a stress-induced decrease that might permissively favor lymph node hyper-innervation.…”

Section: Molecular Mechanismsmentioning

confidence: 99%

Stress-induced remodeling of lymphoid innervation

Sloan¹,

Capitanio

Cole³

2008

Brain, Behavior, and Immunity

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Lymphoid organs have long been known to harbor neural fibers from the sympathetic division of the autonomic nervous system, but recent studies suggest a surprising degree of plasticity in the density of innervation. This review summarizes data showing that behavioral stress can increase the density of catecholaminergic neural fibers within lymphoid organs of adult primates. Stress-induced neural densification is associated with increased expression of neurotrophic factors, and functional consequences include alterations in lymph node cytokine expression and increased replication of a lymphotropic virus. The finding that behavioral stress can tonically alter lymph node neural structure suggests that behavioral factors could exert long-term regulatory influences on the initiation, maintenance, and resolution of immune responses.

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Induction of neuronal apoptosis by Semaphorin3A-derived peptide

Cited by 37 publications

References 51 publications

Semaphorin CD100 from Activated T Lymphocytes Induces Process Extension Collapse in Oligodendrocytes and Death of Immature Neural Cells

Semaphorin CD100 from Activated T Lymphocytes Induces Process Extension Collapse in Oligodendrocytes and Death of Immature Neural Cells

Semaphorin 3B (SEMA3B) induces apoptosis in lung and breast cancer, whereas VEGF ₁₆₅ antagonizes this effect

Stress-induced remodeling of lymphoid innervation

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Induction of neuronal apoptosis by Semaphorin3A-derived peptide

Cited by 37 publications

References 51 publications

Semaphorin CD100 from Activated T Lymphocytes Induces Process Extension Collapse in Oligodendrocytes and Death of Immature Neural Cells

Semaphorin CD100 from Activated T Lymphocytes Induces Process Extension Collapse in Oligodendrocytes and Death of Immature Neural Cells

Semaphorin 3B (SEMA3B) induces apoptosis in lung and breast cancer, whereas VEGF 165 antagonizes this effect

Stress-induced remodeling of lymphoid innervation

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Semaphorin 3B (SEMA3B) induces apoptosis in lung and breast cancer, whereas VEGF ₁₆₅ antagonizes this effect