Expression of mRNA encoding neurotrophins and neurotrophin receptors in human granulocytes and bone marrow cells—enhanced neurotrophin-4 expression induced by LTB4

Laurenzi, Maria Assunta; Beccari, Tommaso; Stenke, Leif; Sjölinder, Mikael; Stinchi, Sofia; Lindgren, Jan

doi:10.1002/jlb.64.2.228

Cited by 35 publications

(18 citation statements)

References 53 publications

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“…Various types of immune cells (Laurenzi et al 1998;Besser and Wank 1999;Braun et al 1999;Kerschensteiner et al 1999;Moalem et al 2000;Ziemssen et al 2002), including activated mouse macrophages (Braun et al 1999;Barouch et al 2001a) have been shown to produce TrkB ligands. In contrast, it seems less probable that blood-borne NTs act on splenic macrophages bearing TrkB receptors, as no significant levels of BDNF have been detected in mouse serum (Radka et al 1996).…”

Section: Discussionmentioning

confidence: 99%

TrkB mRNA and protein in mouse spleen: structure of the spleen of functionally deficient TrkB mice

Pérez-Pérez

García‐Suárez

Blanco-Gelaz

et al. 2004

Cell and Tissue Research

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Whereas it is nowadays clear that neurotrophins are involved in the regulation of various aspects of the functioning of immune system, knowledge of their actual immunomodulatory roles is still fragmentary and incomplete. In this respect, knock-out mouse models remain particularly unexplored. In the present study, the expression of the TrkB neurotrophin receptor in murine spleen was addressed at the mRNA (reverse transcription/polymerase chain reaction) and protein (Western blot) levels. Once the presence of TrkB at both levels was demonstrated, the age-dependent changes in the pattern of expression of the receptor were analyzed and quantified, and TrkB-positive cells were identified by immunohistochemistry. TrkB-immunoreactive cells, identified as red pulp macrophages, were detected in the spleen throughout postnatal development and adult life; their numbers peaked at the age of 15 days. The absence of functional TrkB did not appear to result in morphological changes as assessed by light and electron microscopy of spleens from 15-day-old mice knockout for the trkB gene. The present results support the idea that, in the murine spleen, TrkB and its ligands are involved in macrophage physiology in a developmentally regulated fashion, but they do not seem to be essential for macrophage survival.

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Section: Discussionmentioning

confidence: 99%

TrkB mRNA and protein in mouse spleen: structure of the spleen of functionally deficient TrkB mice

Pérez-Pérez

García‐Suárez

Blanco-Gelaz

et al. 2004

Cell and Tissue Research

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“…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. 35,36,43,47 In human blood monocytes, trkA expression has been shown to decrease during macrophage differentiation 22 and was absent in monocytic (U937 and THP1) cell lines.…”

Section: Discussionmentioning

confidence: 99%

“…Bone marrow tissues were decalcified by electrolysis in decalcifying buffer (Bayer Diagnostics, Puteaux, France) for 2 hours and embedded in paraffin. 37 TrkB In pAb is raised in chickens against a mouse TrkB intracellular domain corresponding to amino acids 482-501. The anti-TrkC NC2 is directed against a peptide corresponding to the exon B of the rat TrkC TK Ϫ receptors ic158 and ic143.…”

Section: Patients and Bone Marrow Samplesmentioning

confidence: 99%

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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“…BMSCs constitutively secrete soluble factors, including growth factors that regulate the proliferation and differentiation of hematopoietic stem/progenitor cells (Eaves et al, 1991;Moore, 1991). BMSCs produce NGF (Caneva et al, 1995;Laurenzi et al, 1998;Labouyrie et al, 1999). In the present study, we employed a mouse EAE model to mimic MS and investigated the long-term (45 weeks after clinical onset) efficacy of BMSC therapy to test whether BMSCs alter axonal degeneration in EAE mice.…”

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confidence: 99%

Bone marrow stromal cells reduce axonal loss in experimental autoimmune encephalomyelitis mice

Zhang¹,

Li²,

Lü

et al. 2006

J of Neuroscience Research

138

101

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We investigated the ability of human bone marrow stromal cell (hBMSC) treatment to reduce axonal loss in experimental autoimmune encephalomyelitis (EAE) mice. EAE was induced in SJL/J mice by injection with proteolipid protein (PLP). Mice were injected intravenously with hBMSCs or PBS on the day of clinical onset, and neurological function was measured daily (score 0-5) until 45 weeks after onset. Mice were sacrificed at week 1, 10, 20, 34, and 45 after clinical onset. Bielshowsky silver was used to identify axons. Immunohistochemistry was performed to measure the expression of nerve growth factor (NGF) and MAB1281, a marker of hBMSCs. hBMSC treatment significantly reduced the mortality, the disease severity, and the number of relapses in EAE mice compared with PBS treatment. Axonal density and NGF(+) cells in the EAE brain were significantly increased in the hBMSC group compared with the PBS group at 1, 10, 20, 34, and 45 weeks. Disease severity was significantly correlated with decreased axonal density and decreased NGF, and increased axonal density was significantly correlated with reduced loss of NGF expression after hBMSC treatment. Most of the NGF(+) cells are brain parenchymal cells. Under 5% of MAB1281(+) cells colocalized with NG2(+), a marker of oligodendrocyte progenitor cells. Nearly 10% of MAB1281(+) cells colocalized with GFAP, a marker of astrocytes, and MAP-2, a marker of neurons. Our findings indicate that hBMSCs improve functional recovery and may provide a potential therapy aimed at axonal protection in EAE mice, in which NGF may play a vital role.

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Expression of mRNA encoding neurotrophins and neurotrophin receptors in human granulocytes and bone marrow cells—enhanced neurotrophin-4 expression induced by LTB4

Cited by 35 publications

References 53 publications

TrkB mRNA and protein in mouse spleen: structure of the spleen of functionally deficient TrkB mice

TrkB mRNA and protein in mouse spleen: structure of the spleen of functionally deficient TrkB mice

Expression of Neurotrophins and their Receptors in Human Bone Marrow

Bone marrow stromal cells reduce axonal loss in experimental autoimmune encephalomyelitis mice

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