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At least 685 records · Page 38Linked to original sources

PubMed1999

Colocalization of phospholipase D1 and GTP-binding-defective mutant of ADP-ribosylation factor 6 to endosomes and lysosomes.

Phospholipase D (PLD) is involved in various aspects of cellular function. Two isoforms, PLD1 and PLD2, have been identified. PLD1, which has two splicing variants, is regulated by various factors, including ADP-ribosylation factor (ARF). We here show that both variants of PLD1 are predominantly localized to late endosomes and lysosomes, but not to the Golgi apparatus or endoplasmic reticulum in contrast to earlier studies. Furthermore, PLD1s show significant colocalization with an ARF6 mutant defective in GTP binding. The data suggest that PLD1, under the regulation of ARF6, plays a role in the function of endosomes and lysosomes.

ADP-Ribosylation Factor 6↗

PubMed2002

Expression of transcriptional repressor ATF3/LRF1 in human atherosclerosis: colocalization and possible involvement in cell death of vascular endothelial cells.

Vascular endothelial cell death contributes to the progression of atherosclerotic lesion, and several transcriptional regulators are involved in the process. Activating transcription factor 3/liver regenerating factor-1 (ATF3/LRF-1), a stress-inducible transcriptional repressor, was shown to be highly expressed in vascular endothelial cells and macrophages of human atherosclerotic lesions by immunohistological assay. The expression was colocalized in these cells which were positive for TdT-mediated dUTP nick-end labeling (TUNEL) and annexin V. Treatment of human umbilical vein endothelial cells (HUVECs) by tumor necrosis factor (TNF)-alpha, oxidized low density lipoprotein (oxLDL), and lysophosphatidylcholine (LPC) rapidly induced ATF3/LRF-1, which showed an increased DNA binding to the consensus ATF/CRE sequence by supershift of gel shift assay. Flow cytometry analysis and immunostaining analysis with TUNEL assay showed that ATF3/LRF-1 was highly expressed in cell death induced by these agents. Moreover, antisense ATF3/LRF-1 cDNA partly suppressed the cell death induced by TNF-alpha, oxLDL, and LPC. From these results, it is indicated that ATF3/LRF-1 is one of the immediate early response genes in vascular endothelial cells in response to atherogenic stimuli, and may play a role in the endothelial cell death associated with atherogenesis.

Activating Transcription Factor 3↗

PubMed1998

Colocalization of iron and ceroid in human atherosclerotic lesions.

The presence of ceroid, a complex of protein associated with oxidized lipids, is commonly observed in human atherosclerotic lesions. When the human aortic walls were examined by Perls' staining, it was found that the iron deposits were evident in aortas with atherosclerosis. The extent of iron deposition was associated with the severity of the lesion. Furthermore, the iron deposits appeared to be colocalized with ceroids either extracellularly or intracellularly in foam cell-like macrophages or smooth muscle cells. Electron microscopy and X-ray microanalysis revealed that some of the extracellular iron aggregates were present within the ceroids. Likewise, some of the subcellular iron aggregates were found to be located near the lipid droplets or within the ceroids of foam cells. Collectively, these observations support the theory that the lipid oxidation occurring in lipid-laden cells of aortic lesions is facilitated by iron-overload in these cells.

Adult↗

PubMed1995

Immunocytochemical colocalizations of serotonin, aromatic L-amino acid decarboxylase and polypeptide hormones in A- and PP-cells of the chicken endocrine pancreas.

The colocalization of serotonin and aromatic L-amino acid decarboxylase (AADC) in the avian pancreatic polypeptide-containing PP-cells and glucagon-storing A-cells of the chicken endocrine pancreas was investigated using combined pre-embedding immuno-peroxidase and post-embedding immunogold electron microscopic immunocytochemistry. The avian pancreatic polypeptide-immunoreactive cells manifested by the labeling of immunogold particles on secretory granules were also immunoreactive with antisera directed against serotonin and AADC, an enzyme involved in the synthesis of serotonin. In PP-cells immunoreactivity against the anti-serotonin serum was stronger in secretory granules than in the cytoplasmic matrix, whereas immunoreaction with the anti-AADC serum was observed to be more intense in the cytoplasmic matrix. Immunoreactions with the serotonin and AADC antisera were also found in secretory granules of glucagon-storing A-cells. These results indicate that serotonin is co-stored within secretory granules of both A- and PP-cells, and that AADC is localized within secretory granules of A-cells, and may be present in the cytoplasmic matrix of PP-cells. It is probable that serotonin is synthesized and released simultaneously with secretory granules from both A- and PP-cells of the chicken endocrine pancreas.

Animals↗

PubMed1996

Immunocytochemical colocalizations of insulin, aromatic L-amino acid decarboxylase, dopamine beta-hydroxylase, S-100 protein and chromogranin A in B-cells of the chicken endocrine pancreas.

The colocalization of aromatic L-amino acid decarboxylase (AADC), dopamine beta-hydroxylase (DBH), S-100 protein and chromogranin A (CgA) in the insulin-containing B-cells of the chicken endocrine pancreas was investigated by using light microscopic immunohistochemistry and combined pre-embedding immunoperoxidase and post-embedding immunogold electron microscopic immunocytochemistry. Using the post-embedding method, immunoreactivity against the anti-insulin serum by protein A-gold technique was observed in the core of all types of B-cell granules. Immunoreaction with anti-S-100 protein serum was detected in the core of all types of B-cell granules. Immunoreaction with anti-S-100 protein serum was detected in the core of all types of B-cell granules from non-osmicated tissues even by post-embedding method, but immunoreactivities against the anti-AADC, DBH and CgA sera were only demonstrable in crystalloid granules of B-cells by pre-embedding method. Immunoreaction with the anti-CgA serum was also detected in the cytoplasmic matrix around crystalloid granules and also in the dense bodies showing immunonegative with anti-insulin serum. From these results, it seems likely that S-100 protein co-stored all types of B-cell granules involved in the maturation of granules, and AADC, DBH and CgA are related to the synthesis of noradrenaline in crystalloid granules of B-cells.

Animals↗

PubMed1997

Colocalization of calretinin and glucagon in rat pancreatic A cells.

Calretinin is a calcium-binding protein whose major functions are assumed to be buffering, transport of Ca2+, regulation of various enzyme systems and cellular protection. Moreover, calretinin does not seem to be a specific marker for any particular cell since it has been discovered in various mammalian and avian organs. In order to give clue to its function(s), we investigate its distribution in the rat pancreas using immunocytochemistry and transmission electron microscopy. We have found calretinin immunoreactive cells in rat pancreas only in the islets of Langerhans. These cells correspond to A cells producing glucagon. The colocalization of calretinin and glucagon was confirmed with double-labelling immunofluorescence. Nevertheless, the role of calretinin and its relationship with the production and/or the exocytosis of glucagon granules remains to be elucidated.

Animals↗

PubMed1998

Partner of Numb colocalizes with Numb during mitosis and directs Numb asymmetric localization in Drosophila neural and muscle progenitors.

During mitosis of multiple types of precursor cells in Drosophila, Numb is asymmetrically distributed between the two daughter cells and confers distinct daughter cell fates. Here we report the identification of a novel gene product, Partner of Numb (PON), based on its physical interaction with Numb. PON is asymmetrically localized during mitosis and colocalizes with Numb. Loss of pon function disrupts Numb localization in muscle progenitors and delays Numb crescent formation in neural precursors. Moreover, ectopically expressed PON responds to the apical-basal polarity of epithelial cells and is sufficient to localize Numb basally. We propose that PON is one component of a multimolecular machinery that localizes Numb by responding to polarity cues conserved in neural precursors and epithelial cells.

Amino Acid Sequence↗

PubMed1997

Protection of nitrergic neurotransmission by and colocalization of neural nitric oxide synthase with copper zinc superoxide dismutase.

This study examined in the rat anococcygeus muscle the tissue distribution of copper zinc superoxide dismutase, the activity of CuZn SOD, and the role of CuZn SOD in protecting nitric oxide from destruction by superoxide anion. Immunohistochemical studies revealed intense staining for CuZn SOD in neuronal nitric oxide synthase-containing nerves. Muscle strips contained 1081 +/- 300 units SOD g-1 wet tissue (mean +/- S.E.M., n = 5). Diethyldithiocarbamate (2 mM) inhibited CuZn SOD activity in supernatant fractions of muscle homogenates by 34% (P < 0.01, n = 5), an effect reversed by CuCl2 (2 mM). In control conditions, electrical field stimulation of nitrergic inhibitory nerves evoked a 61.5 +/- 10.5% (n = 10) relaxation against guanethidine (30 microM)-induced tone. Relaxation evoked by nitrergic inhibitory nerves was neither potentiated by exogenous CuZn SOD (10-1000 U ml-1) nor reduced by the O-2-generator, pyrogallol (30 microM). When diethyldithiocarbamate (2 mM) was present, stimulation of nitrergic inhibitory nerves evoked a 51.7 +/- 10.8% (P < 0.05, n = 10) relaxation against guanethidine (30 microM)-induced tone. Addition of pyrogallol (30 microM) to diethyldithiocarbamate-treated (2 mM for 30 min) muscle strips further reduced nerve-evoked relaxation to 30.7 +/- 7.6% (P < 0.01, n = 10). The inhibitory effect of pyrogallol was reversed by exogenous CuZn SOD (100 U ml-1). Diethyldithiocarbamate (2 mM) had no effect on relaxation evoked by exogenous NO (1 microM). The data indicate that CuZn SOD is present in rat anococcygeus muscle, that it is colocalized with nNOS in the nitrergic nerves, and that it protects NO from destruction by O-2.

Animals↗

PubMed1998

The UL112/113 gene products of human cytomegalovirus which colocalize with viral DNA in infected cell nuclei are related to efficient viral DNA replication.

The UL112/113 gene products of human cytomegalovirus (HCMV) were shown by transient complementation ori Lyt-dependent DNA replication assay to be early viral proteins required for efficient viral DNA synthesis. By immunofluorescence analysis followed by fluorescence in situ hybridization, we showed that UL112/113 gene products of HCMV are colocalized with viral DNA prior to and during viral DNA replication in infected cell nuclei. We have used an anti-sense RNA approach for functional analysis of the UL112/113 gene in HCMV. The astrocytoma cell line U373-MG was used for permanent expression of the anti-sense UL112/113 gene. Expression of the anti-sense RNA in this cell line significantly blocked expression of UL112/113 gene products and viral DNA replication, indicating that the UL112/113 gene products are related to efficient viral DNA replication.

Cell Line↗

PubMed2000

Colocalization of the mu-opioid receptor and calcium/calmodulin-dependent kinase II in distinct pain-processing brain regions.

The mu-opioid receptor (MOR1) mediates the main analgesic effects of morphine and several other opioids. However, the clinical benefit of these drugs is limited by the development of tolerance and dependence. In vitro the mu-opioid receptor undergoes a rapid homologous desensitization during prolonged agonist exposure. We have recently identified the serine residues, Ser(261) and Ser(266), within the third intracellular loop as two consensus calcium/calmodulin-dependent protein kinase II (CaMKII) sites required for agonist-induced phosphorylation and desensitization of the mu-opioid receptor in HEK 293 cells. Since the specific pattern of mu-opioid receptor regulation in vivo is thought to depend on the cell- and tissue-specific complement of protein kinases, we examined the spatial relation between MOR1 and CaMKII in rat brain using specific antibodies. We found that MOR1 and CaMKII alpha which is a major CaMKII isoform expressed in the central nervous system co-exist in distinct pain-processing brain regions including the superficial layers of the spinal cord dorsal horn and dorsal root ganglia. At high power magnification it was evident that virtually all MOR1-expressing nociceptive spinal cord neurons also co-contain CaMKII. In naive or saline-treated animals the mu-opioid receptor was almost exclusively confined to the plasma membrane, while CaMKII was localized to vesicle-like structures throughout the cytoplasm. After subcutaneous administration of the mu-opioid receptor agonist, etorphine, a large proportion of the mu-opioid receptor proteins redistributed from the plasma membrane into the cytosol where it was frequently co-localized with CaMKII. Together, we identify CaMKII as a potential protein kinase, which by virtue of its colocalization with MOR1 may be in a position to phosphorylate the mu-opioid receptor and may thus contribute to the development of tolerance to opioid analgesics.

Analgesics, Opioid↗

PubMed2002

LRP and senile plaques in Alzheimer's disease: colocalization with apolipoprotein E and with activated astrocytes.

The low density lipoprotein receptor-related protein (LRP) is a multifunctional receptor which is present on senile plaques in Alzheimer's disease (AD). It is suggested to play an important role in the balance between amyloid beta (Abeta) synthesis and clearance mechanisms. One of its ligands, apolipoprotein E (apoE), is also present on senile plaques and has been implicated as a risk factor for AD, potentially affecting the deposition, fibrillogenesis and clearance of Abeta. Using immunohistochemistry we show that LRP was present only on cored, apoE-containing senile plaques, in both PDAPP transgenic mice and human AD brains. We detected strong LRP staining in neurons and in reactive astrocytes, and immunostaining of membrane-bound LRP showed colocalization with fine astrocytic processes surrounding senile plaques. LRP was not present in plaques in young transgenic mice or in plaques of APOE-knockout mice. As LRP ligands associated with Abeta deposits in AD brain may play an important role in inducing levels of LRP in both neurons and astrocytes, our findings support the idea that apoE might be involved in upregulation of LRP (present in fine astrocytic processes) and act as a local scaffolding protein for LRP and Abeta. The upregulation of LRP would allow increased clearance of LRP ligands as well as clearance of Abeta/ApoE complexes.

Aged↗

PubMed2003

Distribution and colocalization of NGF and GDNF family ligand receptor mRNAs in dorsal root and nodose ganglion neurons of adult rats.

To understand the dependence of primary sensory neurons on neurotrophic factors, we examined the distribution and colocalization of mRNAs for receptors of nerve growth factor (NGF) and glial cell line-derived neurotrophic factor (GDNF) family ligands in dorsal root ganglion (DRG) and nodose ganglion (NG) neurons of adult rats by in situ hybridization (ISH) histochemistry using serial sections. About 35, 10, and 20% of the lumbar DRG neurons expressed trkA, trkB and trkC mRNAs, respectively. Messenger RNA signals for c-ret, a common signaling receptor of GDNF family ligands, were seen in about 60% of DRG neurons, and some of these neurons expressed trkA, trkB, or trkC mRNAs. Most (97%) of the DRG neurons observed were positive to at least one of these four mRNAs. About 50, 20, and 20% of DRG neurons expressed GDNF family receptor alpha1 (GFR alpha1), GFR alpha2, and GFR alpha3 mRNAs, respectively, and most of these neurons were positive to c-ret mRNA. Interestingly, GFR alpha2 and GFR alpha3 mRNA signals were frequently seen in the same neurons, which lack GFR alpha1 mRNA signals. On the other hand, 98% of NG neurons expressed trkB mRNA and 30-40% of NG neurons co-expressed c-ret and GFR alpha1 mRNAs. However, mRNA signals for other receptors (TrkA, TrkC, GFR alpha2, GFR alpha3) were seen in only a few NG neurons. These findings suggest that all the DRG neurons in adult rats depend on at least one of the NGF and GDNF family ligands, and that some DRG neurons depend on two ligands or more. In contrast, NG neurons were suggested to be divided into two major groups; one group depends on brain-derived neurotrophic factor (BDNF)/neurotrophin-4/5 (NT-4/5), and the other depends on both BDNF/NT-4/5 and GDNF.

Age Factors↗

PubMed2003

Embryonic expression of cholesterogenic genes is restricted to distinct domains and colocalizes with apoptotic regions in mice.

Cholesterol biosynthesis has been assumed to be an ubiquitous process in vertebrate organisms. Here we present data demonstrating that expression of key enzymes of cholesterol biosynthesis is restricted to specific tissues during embryonic development. Distinct expression starts in the dorsal neural tube at embryonic day 8 and is later detected in dorsal root and cephalic ganglia, in the pharyngeal pouches and limb buds. In the limb, expression becomes progressively restricted to interdigital regions during differentiation. Caspase3 whole mount immunostaining revealed that cholesterol biosynthesis colocalizes with apoptotic regions that are targets of the morphogenic signal Sonic hedgehog. This expression pattern correlates closely with the shared phenotypic features of cholesterol biosynthesis and hedgehog mutants.

Animals↗

PubMed1998

Interleukin-6 expression in chronic sinusitis: colocalization of gene transcripts to eosinophils, macrophages, T lymphocytes, and mast cells.

Chronic sinusitis in allergic (ACS) and nonallergic (NCS) patients is characterized by persistent inflammation and subepithelial fibrosis of the sinus mucosa. The inflammatory infiltrate is rich in T lymphocytes, monocyte/macrophages, plasma cells, and eosinophils. Th2-type cytokines are thought to regulate inflammatory cell recruitment, activation, survival, and the release of tissue-damaging mediators. Interleukin-6 is a proinflammatory Th2-type cytokine that stimulates fibroblast proliferation and collagen synthesis. Expression of interleukin-6 has been reported in pulmonary fibrosis and a number of other conditions associated with fibrotic tissue changes. In vitro studies have indicated that interleukin-6 is produced by macrophages, T cells, eosinophils, mast cells, and other cell types. Here we examined interleukin-6 messenger RNA and immunoreactivity in the sinus epithelium and subepithelium of subjects with ACS and NCS by in situ hybridization and immunocytochemistry, performed on sinus biopsy and polyp sections obtained from patients. Nasal turbinate biopsy specimens from normal volunteers were used as controls. Interleukin-6 messenger RNA and immunoreactivity were expressed by a significantly greater proportion of epithelial and subepithelial cells in ACS and NCS subjects than in normal controls. There was no difference in epithelial or subepithelial interleukin-6 expression between ACS and NCS patients. Colocalization studies revealed that macrophages, T cells, eosinophils, and mast cells are sources of interleukin-6 messenger RNA in ACS and NCS. The numbers of interleukin-6 messenger RNA-positive cells coexpressing immunoreactivity for the mast-cell marker were significantly greater in ACS than in NCS subjects. The results of this study suggest a role for interleukin-6 in the inflammatory response of chronic sinusitis.

Adult↗

PubMed2002

Distribution of urocortin in the rat's gastrointestinal tract and its colocalization with tyrosine hydroxylase.

Urocortin (Ucn), a newly identified member of the corticotropin-releasing factor (CRF) family, is not only expressed in the brain, but also abundantly present in the peripheral tissues, especially in the gastrointestinal tract (GI) as determined by radioimmuoassay. In order to determine the precise localization of urocorin in the GI, we mapped the distribution of urocortin-like immunoreactivity (ir) in the GI of the rat using an immunofluorescence histochemical technique. Ucn, both in the brain and the peripheral tissues, is involved in the regulatory control of host-defense mechanism during stress. In order to study the possible involvement of the sympathetic system in the expression of GI urocortin in response to stress, we examined the effect of chemical sympathectomy on urocortin-ir and its colocalization with tyrosine hydroxylase (TH). UCn was expressed in all parietal cells of the stomach, myenteric and submucosal plexuses as well as in cells in Lieberkühn crypts of the small and large intestine. Most of the acid secreting parietal cells contained both Ucn and TH. Chemical sympathectomy did not affect Ucn immunoreactivity of parietal cells.

Animals↗

PubMed1998

Colocalization of inhibitory mediators, NO, VIP and galanin, in canine enteric nerves.

The colocalization of three putative inhibitory mediators of enteric nerves, vasoactive intestinal peptide (VIP), galanin (GAL) and nitric oxide synthase (nNOS), was examined in the myenteric plexus of canine antrum, intestine and colon. Many ileal and colonic neurons contained nNOS-immunoreactive (nNOS-IR) activity with some also containing VIP-IR; only a few neurons also contained GAL-IR. Ileal and colonic VIP-IR nerves often appeared to be interneurons innervating nNOS nerves. Many antral neurons contained VIP-IR with nearly all also containing GAL-IR. A few also contained nNOS-IR. The predominance of nNOS-IR neurons relative to VIP-IR and GAL-IR neurons in the ileal and colonic, but not the antral, myenteric plexus is consistent with NO being the primary inhibitory mediator in the intestine but not in the antrum.

Animals↗

PubMed2000

Colocalization of neurotransmitter receptors on astrocytes in explant cultures of rat CNS.

In recent years evidence has accumulated that astrocytes express functional receptors for a variety of neurotransmitters/neuromodulators. By means of electrophysiological and combined autoradiographic and immunohistochemical methods we have demonstrated the colocalization of cholinergic, adrenergic and peptidergic receptors on astrocytes in explant cultures from various regions of rat central nervous system. A great number of biochemical and electrophysiological studies from other laboratories have shown that most of the neurotransmitters exert their effects on second messenger systems and on Ca2+-activated K+-channels. Furthermore, certain neurotransmitters are involved in the regulation of energy metabolism by stimulating enzymatic breakdown of glycogen in astrocytes. It was suggested that there is a cross-talk between the various neurotransmitter receptors on the glial membrane and that these receptors act in a synergistic or antagonistic way. The coexistence of cholinergic and peptidergic receptors on astrocytes is of great interest since both neurotransmitter systems are involved in cognitive functions and are impaired in patients with Alzheimer's dementia. The question is therefore raised whether not only neurones but also astrocytes might be involved in neurodegenerative disorders such as Alzheimer's disease.

Animals↗

PubMed1998

Colocalization of the cyclin B homologue p56 and beta-tubulin during the cell cycle in a unicellular eucaryote dinoflagellate.

We provide evidence for an unusual behavior of the cyclin B homologue, p56, in the dinoflagellate Crypthecodinium cohnii. p56, of which we previously demonstrated the presence in this original eukaryotic protist, is present all along the cell cycle progression, and is exclusively cytoplasmic as revealed after immunofluorescence labeling with anti-p56 Ab and counterstaining with Dapi. It was never found in the nucleus as is the case in higher eukaryotic cells. During mitosis, p56 was essentially associated with the mitotic apparatus: centrosomes and mitotic spindle, as shown after double immunofluorescence labeling with anti p56 and anti beta-tubulin Ab. Using high pressure freeze fixation, we clearly detected in transmission electron microscopy (TEM) the localization of p56 cyclin B homologue and beta-tubulin: single immunogold labeling demonstrated that p56 is localized along the whole cell cortex, along the cleavage furrow of anaphase to cytokinesis cells and into cytoplasmic channels passing throughout the mitotic nucleus where is located the mitotic spindle. Double immunogold labeling realized with anti-p56 and anti-beta-tubulin antibodies confirm that p56 antigens colocalize with beta-tubulin in many sites. The significance of the exclusively cytoplasmic localization of the cyclin B homologue is discussed.

Animals↗