Nerve growth factor suppresses apoptosis of murine neutrophils

Kannan, Yukiko; Usami, Kaori; Okada, Mitsuhiro; Shimizu, Shinya; Matsuda, Hiroshi

doi:10.1016/0006-291x(92)90853-d

Cited by 74 publications

(41 citation statements)

References 25 publications

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“…25 Third, the pattern of NT receptor expression may also change after cellular isolation or stimulation, thus accounting for some discrepancies. Whereas NGF promotes survival and functional properties of murine neutrophils and eosinophils, 45,46 NT receptor transcripts were not detected in human peripheral blood granulocytes. 37 However, the myeloid (TF1 and KG1) cells and some leukemia cell lines have been shown to express trkA transcripts.…”

Section: Discussionmentioning

confidence: 90%

Expression of Neurotrophins and their Receptors in Human Bone Marrow

Labouyrie

Dubus

Groppi

et al. 1999

The American Journal of Pathology

164

104

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The expression of neurotrophins and their receptors, the low-affinity nerve growth factor receptor (p75 LNGFR ) and the Trk receptors (TrkA , TrkB, and TrkC) , was investigated in human bone marrow from 16 weeks fetal age to adulthood. Using reverse transcription-polymerase chain reaction , all transcripts encoding for catalytic and truncated human TrkB or TrkC receptors were detected together with trkAI transcripts , whereas trkAII transcripts were found only in control nerve tissues. Transcripts for the homologue of the rat truncated TrkC(ic113) receptor were identified for the first time in human tissue. Stromal adventitial reticular cells were found immunoreactive for all neutrophin receptors. In contrast, hematopoietic cell types were not immunoreactive for p75 LNGFR Nerve growth factor (NGF) 1 is the prototype of a family of related neurotrophic factors known as neurotrophins (NT), which also includes brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and neurotrophin-4 (NT-4, also called neurotrophin-5 or NT-5 in humans) (reviewed in Lindsay et al 2 ). NT are trophic factors for the growth, differentiation, and survival of specific subsets of neurons in the developing and mature nervous system. 2 NT can interact with two classes of receptors with distinct ligand affinity and specificity. The low-affinity nerve growth factor receptor, p75 LNGFR , binds all known NT. 3,4 Tyrosine kinase receptors of the Trk family are essential components of NT high-affinity binding sites that trigger neuronal survival, growth, and differentiation. 5 TrkA is the preferred receptor for NGF 6,7 but has a lower efficiency for NT-3 or NT-4/5. TrkB is bound by BDNF and NT-4 and, to a lesser extent, by 9 TrkC is characterized by a unique ligand, NT-3. 10 In some cell lines, TrkA is sufficient to form high-affinity binding sites through homodimerization, 7 whereas p75 LNGFR potentiates TrkA activation by NGF in the PC12 cell line. 11 Variants of tyrosine kinase receptors (TK ϩ ) with insertions in either the extracellular domain (ECD) or the tyrosine kinase domain have been identified for trkA 12,13 and trkC [13][14][15][16] in both human and rat.Truncated receptors lacking the kinase domain (TK Ϫ ) have been described for TrkB and TrkC but not for TrkA. [15][16][17][18] These receptors may function as dominant negative isoforms or immunoadhesins. 13,19,20 Both TK ϩ and TK Ϫ receptors have been detected in neurons while only truncated TrkB and TrkC isoforms have been detected primarily in nonneuronal cells. [15][16][17][18]21 The expression of functional NGF receptors has been detected in several bone marrow-derived cells such as monocytes, 22 mastocytes, 23,24 and B or T cell clones. [25][26][27][28] Among its pleiotropic effects, NGF induces platelet shape changes, 29 triggers monocyte cytotoxic activity, 22 and induces basophilic cell differentiation 30 -32 and mast cell development and degranulation. 24,33 However, NGF receptors have not been consistently detected on bone marrow cells. Although trkA and p75 L...

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Section: Discussionmentioning

confidence: 90%

Expression of Neurotrophins and their Receptors in Human Bone Marrow

Labouyrie

Dubus

Groppi

et al. 1999

The American Journal of Pathology

164

104

View full text Add to dashboard Cite

show abstract

“…NGF-trkA interaction, for example, modulates several functional properties of monocytes, such as triggering the respiratory burst activity (29). Similarly, it has been demonstrated that NGF prevents apoptosis in rat peritoneal mast cells through the p140 trkA tyrosine kinase receptor (57).…”

Section: Discussionmentioning

confidence: 99%

“…Other than its effect on neuronal system, NGF is able to regulate immune responses through direct and͞or indirect effects on a number of immunocompetent cells (23)(24)(25)(26)(27)(28)(29). In addition, NGF potently affects several functions of M͞M, such as differentiation, cytokine production, phagocytosis, and antimicrobial activity (30,31).…”

mentioning

confidence: 99%

Nerve growth factor is an autocrine factor essential for the survival of macrophages infected with HIV

Garaci

Caroleo

Aloe

et al. 1999

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

118

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Nerve growth factor (NGF) is a neurotrophin with the ability to exert specific effects on cells of the immune system. Human monocytes͞macrophages (M͞M) infected in vitro with HIV type 1 (HIV-1) are able to produce substantial levels of NGF that are associated with enhanced expression of the high-affinity NGF receptor (p140 trkA) on the M͞M surface. Treatment of HIVinfected human M͞M with anti-NGF Ab blocking the biological activity of NGF leads to a marked decrease of the expression of p140 trkA high-affinity receptor, a concomitant increased expression of p75 NTR low-affinity receptor for NGF, and the occurrence of apoptotic death of M͞M. Taken together, these findings suggest a role for NGF as an autocrine survival factor that rescues human M͞M from the cytopathic effect caused by HIV infection.

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“…In prior studies, we have demonstrated that NGF promotes not only granulocyte differentiation from human PBMC and murine bone marrow cells (12,13), but also differentiation of connective tissue-type mast cells from murine bone marrow cells and bone marrow-derived culture mast cells (14). NGF is capable of supporting survival of neutrophils (15), eosinophils (16), and mast cells (9) by preventing apoptosis, and enhancing functional properties of neutrophils, eosinophils, macrophages, and mast cells: phagocytosis, superoxide production, matrix metalloproteinase-9 production, and chemotaxis (11, 12, 16 -20). These experimental findings strongly support a possibility that NGF acts as a cytokine that is capable of modulating inflammatory responses and tissue repair.…”

Section: N Erve Growth Factor (Ngf)mentioning

confidence: 98%

Nerve Growth Factor Activates Mast Cells Through the Collaborative Interaction with Lysophosphatidylserine Expressed on the Membrane Surface of Activated Platelets

Kawamoto

Aoki

Tanaka

et al. 2002

The Journal of Immunology

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Effect of nerve growth factor (NGF) on platelet-associated mast cell activation was investigated. Although neither NGF alone nor platelets alone induced significant 5-hydroxytriptamine (5-HT) release from rat peritoneal mast cells, marked 5-HT release was detected when costimulated with NGF and calcium ionophore-activated platelets. This response reached maximal levels as early as 5 min after the initiation of the coincubation and was completely blocked by anti-NGF Ab or by an inhibitor for a tyrosine kinase of the trkA NGF receptor. Paraformaldehyde-fixed platelets activated with either calcium ionophore or thrombin exhibited the collaborative ability, suggesting the possible involvement of some membrane molecules expressed on activated platelets in mast cell activation. Because activation of platelets induced expression of phosphatidylserine (PS) and/or lysoPS on membrane surface, and since lysoPS, unlike PS, initiated the NGF-induced 5-HT release, lysoPS expressed on activated platelets may be involved in the mast cell activation. Moreover, intradermal injection of NGF and activated platelets into the rat skin increased local vascular permeability. These findings suggested that NGF collaboratively worked with membrane lysoPS of activated platelets to induce mast cell activation. Thus, NGF released in response to inflammatory stimuli may contribute to mast cell activation in collaboration with locally activated platelets in the process of inflammations and tissue repair.

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Nerve growth factor suppresses apoptosis of murine neutrophils

Cited by 74 publications

References 25 publications

Expression of Neurotrophins and their Receptors in Human Bone Marrow

Expression of Neurotrophins and their Receptors in Human Bone Marrow

Nerve growth factor is an autocrine factor essential for the survival of macrophages infected with HIV

Nerve Growth Factor Activates Mast Cells Through the Collaborative Interaction with Lysophosphatidylserine Expressed on the Membrane Surface of Activated Platelets

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