Developmental expression of murine β-trace in embryos and adult animals suggests a function in maturation and maintenance of blood-tissue barriers

Hoffmann, Andrea; Bächner, Dietmar; Betat, Nicole; Lauber, Jörg; Groß, Gerhard

doi:10.1002/(sici)1097-0177(199611)207:3<332::aid-aja10>3.0.co;2-6

Cited by 54 publications

(42 citation statements)

References 29 publications

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“…Only the leptomeninges showed robust levels of recombination, confirming the specificity of this promoter for the arachnoid (data not shown). The low levels of recombination in the brain and spinal cord samples is consistent with previous published data (Hoffmann et al, 1996), and may indicate the presence of contaminating leptomeninges in these tissue samples. Recombination was also detected in testis and ovary, suggesting germline Cre Figure 1 Spatial and temporal PGDS expression pattern.…”

Section: Resultssupporting

confidence: 90%

Identification of a progenitor cell of origin capable of generating diverse meningioma histological subtypes

et al. 2011

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Meningiomas are among the most common primary central nervous system tumours in adults. Studies focused on the molecular basis for meningioma development are hampered by a lack of information with regard to the cell of origin for these brain tumours. Herein, we identify a prostaglandin D synthase-positive meningeal precursor as the cell of origin for murine meningioma, and show that neurofibromatosis type 2 (Nf2) inactivation in prostaglandin D2 synthase (PGDS) ( þ ) primordial meningeal cells, before the formation of the three meningeal layers, accounts for the heterogeneity of meningioma histological subtypes. Using a unique PGDSCre strain, we define a critical embryonic and early postnatal developmental window in which biallelic Nf2 inactivation in PGDS ( þ ) progenitor cells results in meningioma formation. Moreover, we identify differentially expressed markers that characterize the two major histological meningioma subtypes both in human and mouse tumours. Collectively, these findings establish the cell of origin for these common brain tumours as well as a susceptible developmental period in which signature genetic mutations culminate in meningioma formation.

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Section: Resultssupporting

confidence: 90%

Identification of a progenitor cell of origin capable of generating diverse meningioma histological subtypes

et al. 2011

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“…Recently PGDS expression in testis and heart has been reported (16,17). PGDS mRNA is detected by in situ hybridization in mouse embryonic mesenchymal cells destined to become arachnoid cells and later in the developing testis (18).…”

Section: Discussionmentioning

confidence: 99%

“…Recently, it was reported that multipotent mesenchymal stem cells were isolated from adult bone marrow, and they were induced to differentiate into a variety of mesenchymal tissues (22,23). In situ hybridization studies by Hoffmann et al (18) showed cellular localization of PGDS mRNA during embryonic development of mice. Initially, at 14.5 days postconception, PGDS mRNA was found to be condensed only in the leptomeningeal cells of the brain and spinal cord.…”

Section: Discussionmentioning

confidence: 99%

Prostaglandin D Synthase (β-Trace) in Meningeal Hemangiopericytoma

et al. 2001

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The level of prostaglandin D synthase (PGDS), a major protein constituent of cerebrospinal fluid (CSF), is altered in various brain diseases, including meningitis. However, its role in the brain remains unclear. PGDS is mainly synthesized in the arachnoid cells, the choroid plexus and oligodendrocytes in the central nervous system. Among brain tumors, meningiomas showed intense immunoreactivity to PGDS in the perinuclear region. Thus, PGDS has been considered a specific cell marker of meningioma. In this study, we examined 25 meningeal hemangiopericytomas (HPCs) and found that 16 of the tumors (64%) showed immunoreactivity for PGDS in the perinuclear region. For comparison, 15 meningiomas, 14 soft-tissue HPCs, 1 mesenchymal chondrosarcoma, 3 choroid plexus papillomas, and 7 oligodendrogliomas were also examined. Meningiomas showed positive immunoreactivity for PGDS in 13 cases (80%). Except for one case located at the sacrum, none of the other soft-tissue HPCs showed immunostaining for PGDS. Mesenchymal chondrosarcoma arises in the bones of the skull, and its histological pattern resembles that of HPC; however, it showed no immunoreactivity for PGDS. Neither choroid plexus papillomas nor oligodendrogliomas were immunopositive for PGDS. These findings suggest that meningeal HPCs may have a unique molecular phenotype that is distinct from that of the soft-tissue HPCs. The origin of meningeal HPCs may be more closely related to the arachnoid cells.

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“…The structural similarity between ␤TP and other lipocalin transporters provides indirect support for a role in lipid transport. Further support for the role of ␤TP in transport processes has recently been provided by the work of Hoffmann et al (60) who, in a careful in situ analysis of ␤TP expression in the developing mouse, have observed ␤TP expression at or near a number of blood-tissue barriers, hinting at a role for ␤TP in transport across these barriers.…”

Section: Figmentioning

confidence: 94%

β-Trace Gene Expression Is Regulated by a Core Promoter and a Distal Thyroid Hormone Response Element

White¹,

Takeda

DeGroot

et al. 1997

Journal of Biological Chemistry

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We isolated and characterized the human ␤-Trace protein (␤TP) gene promoter. ␤TP, also known as prostaglandin D 2 synthase, is a lipocalin secreted from the choroid plexus and meninges into cerebrospinal fluid. Basal transcription of the ␤TP gene is directed from a core promoter found within the first 325 bases of the 5-flanking sequence. The ␤TP gene promoter is responsive to thyroid hormone (3,3,5-triiodothyronine, T 3 ) and efficiently repressed by unliganded human thyroid hormone receptor ␤ (TR␤). Functional analysis of the ␤TP promoter in TE671 cells revealed that responsiveness to T 3 occurs in sequences 2.5 kilobase pairs 5 of the start site. Within the hormone-responsive region we identified a thyroid hormone response element (TRE) located from ؊2576 to ؊2562 base pairs relative to the transcription start site. The ␤TP TRE is composed of two directly repeated consensus half-sites separated by a 3-base pair space (DR3). The ␤TP TRE forms specific complexes with TR␤. We have shown that a gene active in the choroid plexus and meninges is responsive to T 3 . T 3 may play a role in the regulated transport of substances into the cerebrospinal fluid and ultimately the brain.

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Developmental expression of murine β-trace in embryos and adult animals suggests a function in maturation and maintenance of blood-tissue barriers

Cited by 54 publications

References 29 publications

Identification of a progenitor cell of origin capable of generating diverse meningioma histological subtypes

Identification of a progenitor cell of origin capable of generating diverse meningioma histological subtypes

Prostaglandin D Synthase (β-Trace) in Meningeal Hemangiopericytoma

β-Trace Gene Expression Is Regulated by a Core Promoter and a Distal Thyroid Hormone Response Element

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