Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q9UIJ5 (Rec)
 58,342 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Following intravenous injection, cytochrome c traverses the capillary endothelium of the rat choroid plexus and permeates the perivascular space and the extracellular space between epithelial cells. The tracer is incorporated into pinocytotic vesicles adjacent to the lateral and basal plasmalemmas. Thereafter, cytochrome c is incorporated into multivesicular and dense bodies. Tracerladen vesicles were not found to fuse with the apical plasmalemma and cytochrome c was not discharged into the cerebral ventricles. Acid phosphatase activity of the choroidal epithelium after the administration of cytochrome c was greatly increased and localized in the same intracellular sites shown for cytochrome c. These data suggest that cytochrome c and possibly other proteins that penetrate the choroidal stroma are taken up by the choroidal epithelium and subsequently degraded in lysosomal vesicles. This heterolytic mechanism may be an important means for preventing the entry of certain substances such as proteins into CSF and subsequently into nervous tissue.
Anat Rec 1975 Apr
PMID:The blood-brain barrier of the rat choroid plexus. 16 40

Effects of colony-stimulating factors M-CSF, GM-CSF, G-CSF, and IL-3 were assessed on cells of macrophage lineage present in organ cultured 14-day prenatal rat lungs. Treatment groups were compared between one another and against control lungs grown on standard medium containing 40% fetal bovine serum without added factors, where a monoculture of macrophages rapidly develops from precursors present at explantation, leading to appearance of a large mature population on the pleural surface outside the lungs. Studies were carried out in living cultures and by light and electron microscopy using peroxidase-coupled isolectin B4 of Griffonia simplicifolia to identify macrophages and their precursors. In the first experiment, 14-day prenatal lung explants (14 + 0 days) containing macrophage precursors but not matured cells were exposed to individual CSFs for 7 days in an attempt to determine whether precursors are committed irrevocably to the macrophage line or can be altered by exposure to factors promoting significant granulocyte development. In succeeding experiments, 4- and 7-day-old cultures (14 + 4, 14 + 7 days) containing matured macrophages were targeted to see whether macrophage survival can be extended beyond expectations in controls and whether mitotic activity is stimulated. Recombinant CSFs were used at dosage levels known to promote colony formation in vitro (200-1,000 CFU/ml). Cultures exposed from prenatal day 14 to M-, GM-, G-CSF, or IL-3 yielded a monoculture of macrophages without exception. Populations developed in the presence of M- or GM-CSF were much larger than in controls or cultures grown with the other blood factors. GM-CSF-exposed cultures produced by far the largest macrophages, among them many multinucleate giant cells. Macrophages developed in the presence of G-CSF were also significantly larger than controls. Growth of the mature macrophage population was greatly stimulated by exposure to M-CSF or GM-CSF but not by IL-3 or G-CSF. Mitotic figures were noted in the coronas of emerged cells surrounding stimulated cultures, compared to none in the controls. Ultrastructurally, macrophages stimulated by M-CSF retained a mature appearance like macrophages in control, IL-3, and G-CSF treatment groups, whereas many in the GM-CSF group became less differentiated. As to long-term survival, a single 14-day explant was grown for 8 days on standard medium (the equivalent date for birth), then placed in a soft agar medium containing M-CSF.(ABSTRACT TRUNCATED AT 400 WORDS)
Anat Rec 1992 Jul
PMID:Macrophage development: IV. Effects of blood factors on macrophages from prenatal rat lung cultures. 160 73

"Naturally activated" (NA) and "small resting" (SR) T lymphocytes were stimulated with anti-CD3 or anti-thy 1 monoclonal antibodies (mAbs). Both proliferation and secreted IL-2, IL-3/GM-CSF activities were found in NA T cell, but not in SR T cell cultures. SR T cells could be fully activated by anti-CD3 only if PMA or IL-2 was added to the cultures. NA T cell proliferation induced with anti-CD3 was blocked with anti-IL-2 or anti-IL-2R mAbs. The combination of anti-CD3 and rec IL-4 was not effective in promoting SR T cell proliferation. IL-4 plays a minor role in NA T cell activation with anti-CD3, as assayed with neutralizing anti IL-4 mAbs. No differences in the proliferative and secretory activities were found when NA or SR T cells were stimulated with Con A. Both NA and SR T cells responded when stimulated with the calcium ionophone A23187 plus PMA. Only NA T cells responded to A23187 alone. The mechanisms and the possible physiologic relevance of this differential responsiveness behavior are discussed.
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PMID:Naturally activated and resting T cells differ in their activation requirements for growth and secretory activities. 213 15

A Golgi study of the floor of the caudal fourth ventricle in the developing and adult rabbit brain stem revealed the presence of several clusters of tanycytes. These tanycytes possessed ciliated apical surfaces and basal shafts extending into the substance of the medulla and pons where they intermingled with specific neuronal fields. These shafts ended in the serotonergic nuclei raphe obscurus and pallidus, and the noradrenergic locus coeruleus and nucleus intercalatus (group A2). The tanycyte shafts extended into the medullary midline early in ontogeny (day 18 of gestation), following which the neurons of the raphe began to sprout neurites. These shafts then formed the underlying structure for a large medullary dendrite bundle. These shafts developed extensive spines during early neonatal ontogeny, which then diminished in number through adulthood. the tanycyte shafts extending into locus coeruleus and nucleus intercalatus developed later in ontogeny than the midline shafts, just before birth. These shafts also persisted into adulthood in close relationship with the monoamine neurons. We suggest that the tanycytes on the floor of the fourth ventricle may take up substances from the CSF and transport them to the region of the monoamine nuclei where the shafts terminate, in a manner similar to median eminence tanycytes. The early development of shafts from fourth ventricular tanycytes suggests a possible regulatory role for these cells over the neuritic sprouting and maturation of the monoaminergic nuclei.
Anat Rec 1981 Jul
PMID:Ontogeny of caudal fourth ventricular tanycytes in the rabbit brain: a Golgi study. 616 13

Granulocyte-macrophage colony-stimulating factor (GM-CSF), a cytokine secreted by lymphohaemopoietic and other cell lineages, is known to influence ovarian cyclicity and embryo development. The aim of this study was to examine the effect of GM-CSF on ovarian follicular cell function using GM-CSF-deficient (GM -/-) mice. Immature GM -/- and GM +/+ mice were stimulated with eCG, and cumulus-oocyte complexes and mural granulosa cells were collected 48 h later. Expression of GM-CSF receptor (GM-CSFR) alpha and beta mRNA subunits by cumulus-oocyte complexes and mural granulosa cells was examined using RT-PCR. Cumulus-oocyte complexes from both genotypes were found to express mRNA for the GM-CSFRalpha-subunit only, while the mural granulosa cells expressed both the alpha and beta receptor subunits. Cumulus-oocyte complexes recovered from GM -/- mice had approximately twice the number of cumulus cells per cumulus-oocyte complex than did those of GM +/+ mice (P < 0.05), even though the growth-promoting activity of denuded GM -/- oocytes was found to be equivalent to that of wild-type oocytes. GM-CSF deficiency was associated with marginally increased DNA synthesis in cumulus cells and significantly (P < 0.05) lower progesterone production by mural granulosa cells recovered from GM -/- compared with those recovered from GM +/+ mice. The addition of rec-mGM-CSF in vitro did not affect DNA synthesis in either cell type or progesterone production by mural granulosa cells, irrespective of GM-CSF status. There was no effect of GM-CSF deficiency on the capacity of FSH and insulin-like growth factor I to stimulate DNA synthesis in cumulus-oocyte complexes (approximately 15- and threefold, respectively) and in mural granulosa cells (approximately two- and threefold, respectively). Taken together, these data show that GM-CSF influences events associated with follicular maturation in mice. The effects of GM-CSF are not exerted directly in granulosa or cumulus cells, but appear to be mediated indirectly, perhaps through the agency of steroidogenesis-regulating secretions of local macrophage populations residing in the theca.
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PMID:Effect of granulocyte-macrophage colony-stimulating factor deficiency on ovarian follicular cell function. 1105 44

The differentiation and functions of osteoclasts (OCs) are regulated by osteoblast-derived factors. Receptor activator of NFkB ligand (RANKL) is one of the key regulatory molecules in OC formation. Osteoprotegerin (OPG) is a novel secreted member of the TNF receptor superfamily that negatively regulates osteoclastogenesis and binds to RANKL. We examined the biological actions of macrophage-colony-stimulating factor (M-CSF), RANKL, and OPG on the differentiation of OCs isolated from cocultures of mouse osteoblastic cells and bone marrow cells. Preosteoclasts (pOCs) and OCs were characterized by their ultrastructure and the expression of OC markers such as tartrate-resistant acid phosphatase (TRAP) and vacuolar-type H(+)-ATPase. pOCs formed without any additives expressed TRAP, but showed little resorptive activity on cocultured dentine slices. TRAP-positive pOCs treated with M-CSF began to fuse with each other, but lacked a ruffled border (RB) and showed almost no resorptive activity. pOCs treated with RANKL became TRAP-positive multinucleated cells, which expressed intense vacuolar-type H(+)-ATPase along the RB membranes and exhibited prominent resorptive activity. Such effects of RANKL on pOCs were completely inhibited by the addition of OPG. OPG inhibited RB formation in mature OCs and reduced their resorptive activity, and also induced apoptosis of some OCs. These results suggest that 1) RANKL induces differentiation of functional OCs from pOCs, 2) M-CSF induces macrophage-like multinucleated cells, but not OCs, 3) OPG inhibits RB formation and resorptive activity in mature OCs, 4) OPG also induces apoptosis of OCs, and 5) RANKL and OPG are, therefore, important regulators of not only the terminal differentiation of OCs but also their resorptive function.
Anat Rec 2002 Oct 01
PMID:Regulation of osteoclast differentiation and function by receptor activator of NFkB ligand and osteoprotegerin. 1222 20

Early in development, the behavior of neuroepithelial cells is controlled by several factors, which act in a developmentally regulated manner. Diffusible factors are secreted locally by the neuroepithelium itself, although other nearby structures may also be involved. Evidence suggests a physiological role for the cerebrospinal fluid in the development of the brain. Here, using organotypic cultures of chick embryo neuroepithelial explants from the mesencephalon, we show that the neuroepithelium in vitro is not able to self-induce cell survival, replication, and neurogenesis. We also show that the embryonic cerebrospinal fluid (E-CSF) promotes neuroepithelial stem cell survival and induces proliferation and neurogenesis in mesencephalic explants. These data strongly suggest that E-CSF is involved in the regulation of neuroepithelial cells behavior, supporting the hypothesis that this fluid plays a key role during the early development of the central nervous system.
Anat Rec A Discov Mol Cell Evol Biol 2005 May
PMID:Embryonic cerebrospinal fluid regulates neuroepithelial survival, proliferation, and neurogenesis in chick embryos. 1580 75

It has been clearly established that osteoclasts, which play a crucial role in bone resorption, differentiate from hematopoietic cells belonging to the monocyte/macrophage lineage in the presence of macrophage-colony stimulating factor (M-CSF) and receptor activator of NF-kappaB ligand (RANKL). We have here investigated the M-CSF- and RANKL-induced osteoclastic differentiation of two distinct clones of the murine monocytic/macrophagic RAW 264.7 cell line, known as TIB-71 and CRL-2278, the latter cell clone being defective for the expression of the inducible nitric oxide synthase isoform in response to interferon-gamma or lipopolysaccharide. CRL-2278 cells demonstrated a more rapid osteoclastic differentiation than TIB-71 cells, as documented by morphology, tartrate-resistant acid phosphatase positivity, and bone resorption activity. The enhanced osteoclastic differentiation of CRL-2278 was accompanied by a higher rate of cells in the S/G2-M phases of cell cycle as compared to TIB-71. The analysis of nitric oxide synthase (NOS) isoforms clearly demonstrated that only neuronal NOS was detectable at high levels in CRL-2278 but not in TIB cells under all tested conditions. Moreover, the broad inhibitor of NOS activity L-NAME significantly inhibited osteoclastic differentiation of CRL-2278 cells. Altogether, these results demonstrate that a basal constitutive neuronal NOS activity positively affects the RANKL/M-CSF-related osteoclastic differentiation.
Anat Rec A Discov Mol Cell Evol Biol 2005 Oct
PMID:Different levels of the neuronal nitric oxide synthase isoform modulate the rate of osteoclastic differentiation of TIB-71 and CRL-2278 RAW 264.7 murine cell clones. 1614 87

It has been clearly established that receptor activator of nuclear factor kappa B ligand (RANKL) is a key cytokine involved in the differentiation of osteoclastic precursors of the monocytic/macrophagic lineage. However, relatively little information is available on the ability of RANKL to modulate the expression of genes controlling cell survival/apoptosis and proliferation in human osteoclastic cells in comparison to macrophages. For this purpose, CD14+ human peripheral blood mononuclear cells, which express the cognate high affinity receptor activator of nuclear factor kappa B (RANK), were differentiated along the macrophagic or osteoclastic lineage by adding macrophage-colony stimulating factor (M-CSF) or M-CSF plus RANKL in culture for 12 days. RANKL up-regulated the expression of the chemokine MIP1alpha, which potentiates osteoclastic differentiation and simultaneously activated both anti-apoptotic (Bcl-2) and pro-apoptotic (CIDEB, PYCARD, and BAK-1) genes. Moreover, RANKL markedly up-regulated cylin D2, while it significantly decreased the levels of cyclin A, cyclin-dependent kinase 2, and other cyclin-dependent kinases, in keeping with the notion that end-stage osteoclasts are nondividing cells. Finally, a long-term exposure of RANKL up-regulated the adaptor protein TRAF3 but not TRAF6.
Anat Rec (Hoboken) 2007 Jul
PMID:Receptor activator of nuclear factor kappa B ligand (RANKL) modulates the expression of genes involved in apoptosis and cell cycle in human osteoclasts. 1750 59

Samples of uncontaminated cerebrospinal fluid (csf) were collected from the cisterna magna of 20 healthy laboratory rabbits and 21 pet rabbits with vestibular disease and/or paresis due to clinically suspected encephalitozoonosis. In the healthy rabbits' csf the leucocyte count was <or=4 leucocytes/microl (median 1.5 microl) and the concentration of protein ranged from 0.13 to 0.31 g/l (median 0.24 g/l). In the diseased rabbits, the number of leucocytes ranged from 1 to 87/microl (median 15/microl; P<0.001), and the concentration of protein ranged from 0.31 to 1.54 g/l (median 0.79 g/l; P<0.001); a cytological evaluation showed that they had greater numbers of lymphocytes and monocytes. It was concluded that encephalitozoonosis in rabbits is characterised by lymphomonocytic pleocytosis in CSF.
Vet Rec 2008 May 10
PMID:Analysis of cerebrospinal fluid in healthy rabbits and rabbits with clinically suspected encephalitozoonosis. 1848 21


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