Induction of TrkA receptor by retinoic acid in leukaemia cell lines

Xie, Ping; Cheung, Wmw; Ip, Fanny Chun Fun; Ip, Nancy Y.; Leung, Mun-Fai

doi:10.1097/00001756-199703240-00001

Cited by 22 publications

(21 citation statements)

References 5 publications

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“…The meninges presumably influence the brain via the synthesis of growth factors such as TGF␤, IGFII, and BMP-6 and -7 (Pelton et al, 1990;Sullivan and Feldman, 1994;Charytoniuk et al, 2000). RA can also be added to this list in its role as a transcriptional regulator that can itself induce expression of many growth factors (Braunhut et al, 1989;Glick et al, 1989;Lowe et al, 1992;Matsumoto et al, 1992) as well as growth factor and neurotrophin receptors (Joh et al, 1992;Kaplan et al, 1993;Afink et al, 1995;Wan et al, 1995;Xie et al, 1997;Sizemore et al, 1998;Yoshizawa et al, 1998).…”

Section: Discussionmentioning

confidence: 99%

The Meninges Is a Source of Retinoic Acid for the Late-Developing Hindbrain

et al. 2003

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One general function for retinoic acid (RA) is pattern organization in the CNS. This regulatory factor has an essential role in spinal cord motor neuron and early posterior hindbrain development. In the anterior CNS, however, there is only a limited number of foci of RA synthesis, and less attention has been placed on regions such as the anterior hindbrain where RA synthesizing enzymes are absent. This study shows that a rich source of RA lies around the hindbrain from the RA synthetic enzyme retinaldehyde dehydrogenase-2 (RALDH2) present in the surrounding meninges and mesenchyme by embryonic day 13. RALDH2 is not distributed uniformly throughout the meninges but is restricted to territories over the developing hindbrain, suggesting that RA signaling may be localized to those regions. Further regulation of RA signaling is provided by the presence of a RA sink in the form of the CYP26B1 RA catabolic enzyme expressed in deeper regions of the brain. As a guide to the neural anatomy of hindbrain RA signaling, we used a mouse transgenic for a lacZ reporter gene driven by a RA response element (RAREhsplacZ) to identify regions of RA signaling. This reporter mouse provides evidence that RA signaling in the hindbrain after embryonic day 13 occurs in the regions of the cerebellum and precerebellar system adjacent to sources of RA, including the inferior olive and the pontine nuclei.

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Section: Discussionmentioning

confidence: 99%

The Meninges Is a Source of Retinoic Acid for the Late-Developing Hindbrain

et al. 2003

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“…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. 35,36 However, NGF triggers phagocytosis, parasite killing, and interleukin-1␤ production by macrophages through activation of the TrkA receptor, 48 whose expression can be enhanced by several inflammatory molecules.…”

Section: Discussionmentioning

confidence: 99%

“…43 The constitutive expression of several NT in certain leukemia cell lines and in human cord blood-derived mast cells also suggests an autocrine role for NT on hematopoietic cells. 24,47 The cellular source of NT within the bone marrow needs to be further characterized by cellular separation or in situ hybridization studies. The wide distribution of NT receptors in the bone marrow suggests that NT may play an important role during the onset of hematopoiesis and on the differentiation of specific hematopoietic progenitors and precursors throughout life.…”

Section: Discussionmentioning

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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“…In addition, a direct relationship between RA and neurogenesis in these brain areas has been demonstrated (Jacobs et al, 2006 andBonnet et al, 2008, for hippocampus;Wang et al, 2005, andZhang et al, 2006, for the subventricular zone). In this regard, although RA is not alone in inducing the different steps in neuronal differentiation, it may act as a master control in certain regions of the central nervous system by inducing the expression of a variety of factors that control differentiation (Joh et al, 1992;Kaplan et al, 1993;Afink et al, 1995;Xie et al, 1997;Sizemore et al, 1998;Yoshizawa et al, 1998;Maden, 2002;Duester, 2008). Consequently, the knowledge of the mechanisms involved in neurogenesis activation from neural precursors in both embryonic and adult brain, may be a hidden key to developing neuro-regenerative strategies based on the expansion and differentiation of neural precursor populations in the adult brain.…”

Section: Ra Is Involved In Neurogenesis Induced By E-csfmentioning

confidence: 99%

Cerebrospinal fluid control of neurogenesis induced by retinoic acid during early brain development

Alonso

Martín

Carnicero

et al. 2011

Developmental Dynamics

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Embryonic‐cerebrospinal fluid (E‐CSF) plays crucial roles in early brain development including the control of neurogenesis. Although FGF2 and lipoproteins present in the E‐CSF have previously been shown to be involved in neurogenesis, the main factor triggering this process remains unknown. E‐CSF contains all‐trans‐retinol and retinol‐binding protein involved in the synthesis of retinoic acid (RA), a neurogenesis inducer. In early chick embryo brain, only the mesencephalic‐rombencephalic isthmus (IsO) is able to synthesize RA. Here we show that in chick embryo brain development: (1) E‐CSF helps to control RA synthesis in the IsO by means of the RBP and all‐trans‐retinol it contains; (2) E‐CSF has retinoic acid activity, which suggests it may act as a diffusion pathway for RA; and (3) the influence of E‐CSF on embryonic brain neurogenesis is to a large extent due to its involvement in RA synthesis. These data help to understand neurogenesis from neural progenitor cells. Developmental Dynamics 240:1650–1659, 2011. © 2011 Wiley‐Liss, Inc.

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Induction of TrkA receptor by retinoic acid in leukaemia cell lines

Cited by 22 publications

References 5 publications

The Meninges Is a Source of Retinoic Acid for the Late-Developing Hindbrain

The Meninges Is a Source of Retinoic Acid for the Late-Developing Hindbrain

Expression of Neurotrophins and their Receptors in Human Bone Marrow

Cerebrospinal fluid control of neurogenesis induced by retinoic acid during early brain development

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