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PubMedDate not supplied

Electron microscopic and immunoelectron microscopic demonstration of pancreatic polypeptide cells in glucagonoma: colocalization of pancreatic peptide and glucagon in single secretory granules.

We describe a case of pancreatic tumor in a 65-year-old woman with typical glucagonoma syndrome. Plasma glucagon (GL) and pancreatic polypeptide (PP) were markedly elevated up to 1404 and 1200 pg/ml, respectively. Histologic examination of the metastatic tumors in liver and lymph nodes showed endocrine-type tumors composed of GL-positive cells some of which coexpressed PP immunoreactivity. Electron microscopy revealed the tumor cells with single-type secretory granules similar to normal A cell granules. Double immunogold staining demonstrated both GL and PP immunoreactivities in the same secretory granules. Biologic and diagnostic significance of coexpression of PP and GL in a single secretory granules of pancreatic endocrine tumors is discussed briefly.

Adenoma, Islet Cell↗
PubMed1989

Colocalization of fibroblast growth factor binding sites with extracellular matrix components in normal and keratoconus corneas.

Basic and acidic fibroblast growth factor (bFGF, aFGF) binding sites were determined in frozen sections of normal and keratoconus corneas. After incubation with I-125 radiolabelled growth factors, corneal binding sites were revealed by autoradiography. The growth factors were localized mainly to Descemet's membrane and to the epithelial basement membrane. FGF binding sites were generally similar in normal and keratoconus corneas. The binding specificity was demonstrated by competitive inhibition experiments with an excess of unlabelled growth factors. The binding sites were sensitive to pretreatment of the corneal sections with heparitinase. We have attributed FGF's basement membrane affinity to one of its constituents, proteoheparan sulfate. Proteoheparan sulfate, laminin, collagen type IV, and fibronectin were all revealed by immunofluorescent techniques. While keratoconus cornea stroma had less laminin but more fibronectin than normal corneas the main difference lied in type IV collagen which was overexpressed in keratoconus epithelium.

Adult↗
PubMed1998

An ultrastructural study of the colocalization of biglycan and decorin with AA amyloid fibrils in human renal glomeruli.

An investigation was undertaken on paraformaldehyde-fixed, Lowicryl resin-embedded renal biopsies from patients with AA amyloidosis to study the association of two small chondroitin sulphate/dermatan sulphate proteoglycans, decorin and biglycan, with amyloid fibrils using an ultrastructural immunogold technique. Biglycan was present in glomerular endothelial cells in both normal kidney and in amyloidosis, but little biglycan or decorin was present in the normal mesangial matrix. By contrast, conspicuous amounts of both biglycan and decorin were seen to be associated with amyloid fibrils in the glomerular matrix in cases of renal AA amyloidosis. The results further emphasise the close association between amyloid and extracellular matrix components which are now considered to be an integral part of the amyloid fibrils.

Amyloidosis↗
PubMed2002

Identification of a candidate regulatory region in the human CD8 gene complex by colocalization of DNase I hypersensitive sites and matrix attachment regions which bind SATB1 and GATA-3.

To locate elements regulating the human CD8 gene complex, we mapped nuclear matrix attachment regions (MARs) and DNase I hypersensitive (HS) sites over a 100-kb region that included the CD8B gene, the intergenic region, and the CD8A gene. MARs facilitate long-range chromatin remodeling required for enhancer activity and have been found closely linked to several lymphoid enhancers. Within the human CD8 gene complex, we identified six DNase HS clusters, four strong MARs, and several weaker MARs. Three of the strong MARs were closely linked to two tissue-specific DNase HS clusters (III and IV) at the 3' end of the CD8B gene. To further establish the importance of this region, we obtained 19 kb of sequence and screened for potential binding sites for the MAR-binding protein, SATB1, and for GATA-3, both of which are critical for T cell development. By gel shift analysis we identified two strong SATB1 binding sites, located 4.5 kb apart, in strong MARs. We also detected strong GATA-3 binding to an oligonucleotide containing two GATA-3 motifs located at an HS site in cluster IV. This clustering of DNase HS sites and MARs capable of binding SATB1 and GATA-3 at the 3' end of the CD8B gene suggests that this region is an epigenetic regulator of CD8 expression.

Base Sequence↗
PubMed2005

Colocalization of expansion of the splenic marginal zone population with abnormal B cell activation and autoantibody production in B6 mice with an introgressed New Zealand Black chromosome 13 interval.

Polyclonal B cell activation is a prominent feature of the lupus-prone New Zealand Black (NZB) mouse strain. We have previously demonstrated linkage between a region on NZB chromosome 13 and increased costimulatory molecule expression on B cells. In this study we have produced C57BL/6 congenic mice with an introgressed homozygous NZB interval extending from approximately 24 to 73 cM on chromosome 13 (denoted B6.NZBc13). We show that B6.NZBc13 female mice not only have enhanced B cell activation but also share many other B cell phenotypic characteristics with NZB mice, including expansion of marginal zone and CD5+ B cell populations, increased numbers of IgM ELISPOTs, and increased serum levels of total IgM and IgM autoantibodies. In addition these mice have increased T cell activation, increased numbers of germinal centers, mild glomerulonephritis, and produce high-titer IgM and IgG anti-chromatin Abs. Male B6.NZBc13 mice have a less pronounced cellular phenotype, lacking expansion of the marginal zone B cell population and IgG anti-chromatin Ab production, indicating the presence of gender dimorphism for this locus. Thus, we have identified a genetic locus that recapitulates with fidelity the B cell phenotypic abnormalities in NZB mice, and we demonstrate that this locus is sufficient to induce an autoimmune phenotype. The data provide further support to the contention that immune abnormalities leading to altered B cell activation and selection contribute to the development of autoimmunity in NZB mice.

Animals↗
PubMed2005

Sera from patients with type 2 diabetes and neuropathy induce autophagy and colocalization with mitochondria in SY5Y cells.

The etiology of diabetic neuropathy is multifactorial and not fully elucidated, although oxidative stress and mitochondrial dysfunction are major factors. We reported previously that complement-inactivated sera from type 2 diabetic patients with neuropathy induce apoptosis in cultured neuronal cells, possibly through an autoimmune immunoglobulin-mediated pathway. Recent evidence supports an emerging role for autophagy in a variety of diseases. Here we report that exposure of human neuroblastoma SH-SY5Y cells to sera from type 2 diabetic patients with neuropathy is associated with increased levels of autophagosomes that is likely mediated by increased titers of IgM or IgG autoimmune immunoglobulins. The increased presence of macroautophagic vesicles was monitored using a specific immunohistochemical marker for autophagosomes, anti-LC3-II immunoreactivity, as well as the immunohistochemical signal for beclin-1, and was associated with increased co-localization with mitochondria in the cells exposed to diabetic neuropathic sera. We also report that dorsal root ganglia removed from streptozotocin-induced diabetic rats exhibit increased levels of autophagosomes and co-localization with mitochondria in neuronal soma, concurrent with enhanced binding of IgG and IgM autoimmune immunoglobulins. To our knowledge, this is the first evidence that the presence of autophagosomes is increased by a serum factor, likely autoantibody(ies) in a pathological condition. Stimulation of autophagy by an autoantibody-mediated pathway can provide a critical link between the immune system and the loss of function and eventual demise of neuronal tissue in type 2 diabetes.

Animals↗
PubMed1999

[The colocalization of neurotransmitters in the presynaptic boutons of inhibitory synapses in the lamprey spinal cord].

Using the electron microscopy immunocytochemistry, the GABA and glycine immunoreactivity was studied in presynaptic axon terminals of the spinal cord central gray in the lamprey Lampetra fluviatilis. All immunopositive presynaptic terminals contacting motoneurones or non-identified post-synaptic profiles were divided into only GABA- (44%), only glycine-immunopositive terminals (26%), and both GABA- and glycine-containing terminals (30%). The glycine-immunopositive axon terminals contained flattened synaptic vesicles. Large dense core vesicles were co-localised with conventional synaptic vesicles in 74% of GABA-containing presynaptic terminals.

Animals↗
PubMed2000

Selective enhancement of beta-adrenergic receptor signaling by overexpression of adenylyl cyclase type 6: colocalization of receptor and adenylyl cyclase in caveolae of cardiac myocytes.

We investigated the effect of adenovirally mediated overexpression of adenylyl cyclase type 6 (AC6), a major form of AC expressed in mammalian heart, on G protein-coupled receptor regulation of cAMP production in neonatal rat ventricular myocytes. Following gene transfer of AC6, isoproterenol- and forskolin-stimulated increases in cAMP were markedly enhanced, whereas basal levels of cAMP and responses to several other agonists that stimulate cAMP formation, e. g., prostaglandin E(2) (PGE(2)), H(2) agonist, glucagon, and A(2) agonist were not increased. Studies to test whether the selective enhancement in beta-adrenergic receptor (AR) response might result from inhibition of AC6 by Galpha(i) and Gbetagamma indicated that pertussis toxin-sensitive inhibition by the muscarinic cholinergic agonist carbachol was unaltered in myocytes overexpressing AC6. Pertussis toxin treatment failed to reveal an enhancement by AC6 overexpression of basal or PGE(2)-stimulated cAMP. Immunoblot analysis of membrane fractions indicated that beta(1)-AR and AC6 are expressed in fractions enriched in caveolin-3 and morphologic caveolae. The data suggest that loss of G(i)-mediated inhibition is not the mechanism for enhancement of beta-AR-stimulated cAMP formation and that key components of beta-AR-mediated activation of AC exist in caveolae of cardiac myocytes, providing a means by which beta-AR response is selectively enhanced by increasing AC6 expression.

Adenylyl Cyclases↗
PubMed2000

Partial colocalization of NADPH-diaphorase and acetylcholinesterase positivity in spinal cord neurons.

The freely diffusible radical, nitric oxide (NO), has been assumed to act as a retrograde signaling molecule that modulates transmitter release. Acetylcholine (ACh) is known to function as a typical neurotransmitter. In the present work we have examined the presence of both transmitters (NO and ACh) and their possible relations in the rabbit spinal cord. In our experiments we have used histochemical methods for the visualization of acetylcholinesterase (AChE) and NADPH diaphorase (NADPH-d) which label neurons that express nitric oxide synthase (NOS). Both histochemical methods were performed separately or together on the same sections of the thoracic spinal cord. NADPH-d positive dark blue stained neurons were seen mostly in superficial and deep layers of the dorsal horn, preganglionic autonomic neurons and pericentral area. The presence of AChE positive amber yellow neurons was confirmed mostly in motoneurons located in the ventral horns and in neurons of the pericentral and intermediate zone. Besides the above mentioned neurons, also double-labeled neurons were found which contained both the yellow and dark blue histochemical product. Their presence was confirmed in the intermediate zone and in the pericentral area. Thus, the co-existence of NADPH-d and AChE occurred in the location of interneurons. Our observations suggest that NO may play a role in the control of cholinergic neuronal activity and that NO can be involved in the modulation of synaptic transmission.

Acetylcholine↗
PubMed2001

Colocalization of tyrosine hydroxylase and GAD65 mRNA in mesostriatal neurons.

Although dopamine has been considered as the only neurotransmitter in the nigrostriatal pathway, studies carried out in the last two decades have suggested the existence of a nondopaminergic nigrostriatal projection, and more recently, gamma-aminobutyric acid (GABA) has been identified as its neurotransmitter. In this study, we used the combination of immunocytochemistry for tyrosine hydroxylase (TH; a marker of dopaminergic neurons), in situ hybridization (ISH) for two different isoforms of glutamic acid decarboxylase (GAD65 and GAD67, the rate-limiting enzyme in GABA synthesis) and retrograde tracing techniques to investigate the possible existence of nigrostriatal neurons containing both neurotransmitters (dopamine and GABA) in the rat. Our results revealed that approximately 10% of mesostriatal dopaminergic neurons, most of them lying in the medial region of the substantia nigra pars compacta (SNC) and neighbouring A10 region, contain GAD65 mRNA. These findings reveal a third nigrostriatal pathway formed by dopaminergic/GABAergic neurons. Contrasting with the idea that in the basal ganglia, dopamine and GABA are released from different cell populations, the results suggest a more complex dopamine/GABA interaction than previously assumed, probably including cotransmission.

Animals↗
PubMed2001

Colocalization of mu-opioid receptors and activated G-proteins in rat cingulate cortex.

Anterior cingulate cortex (ACC) has a role in pain processing, however, little is known about opioid system organization and actions. This rodent study defines opioid architecture in the perigenual and midcingulate divisions of ACC, relates mu-opioid receptor binding and G-protein activation, and localizes such binding to afferent axons with knife-cut lesions and specifically to noradrenergic terminals with immunotoxin lesions (anti-dopamine beta-hydroxylase-saporin; anti-DBH-saporin). [(3)H]Tyr-D-AlaGly-MePhe-Gly-ol (DAMGO) binding was highest in perigenual areas 32 and 24 with a peak in layer I. Midcingulate area 24' and posterior cingulate area 29 had overall lower binding in each layer. In contrast, DAMGO-stimulated [(35)S]guanosine-5'-O-(gamma-thio)-triphosphate (GTPgammaS) binding in area 24' was similar to that in area 24, whereas area 29 had low and homogeneous binding. Undercut lesions reduced [(3)H]DAMGO binding in all layers with the greatest loss in layer I (-65%), whereas DAMGO-stimulated [(35)S]GTPgammaS binding losses occurred in only layers I-III. Anti-DBH-saporin reduced [(3)H]DAMGO binding in layer I of area 24; DAMGO-stimulated [(35)S]GTPgammaS binding was unchanged in areas 24' and 29. Correlation analysis of receptor and G-protein activation before and after undercut lesions suggested there were a greater number of DAMGO receptor sites for each G-protein on axons, than on somata and proximal dendrites. Finally, perigenual and midcingulate cortices have different opioid architectures due to a higher proportion of mu-opioid receptors expressed by afferent axons in areas 24 and 32.

Analgesics, Opioid↗
PubMed2002

A search for colocalization of mglula receptors with CRF or NPY in the rat brain amygdala.

Excitatory neurotransmitter glutamate, as well as corticoliberin (CRF) and neuropeptide Y (NPY) play an important role in fear and anxiety. Among the brain structures engaged in these effects the important one is amygdala. In the present study, a single and double immunohistochemical staining techniques were used in order to visualize CRF, NPY and metabotropic glutamate receptors (mGluR1a) in rat amygdala. MGluR1a belongs to class of postsynaptic excitatory receptors and has a preferable somatic localization. CRF and NPY were localized using rabbit polyclonal antibodies, and mGluR1a using a mouse monoclonal one. Then, ABC-peroxidase and DAB or benzidine were used. Upon single immunostaining, NPY and CRF were found in some nerve cell bodies and fibres in the amygdala. The immunoreactivity of mGluR1 a was observed in some nerve cells, processes and fibres, especially on the border between the central and the basolateral nuclei and ventrally to that region. Double staining revealed mGluR1 a-IR on some CRF- and NPY-immunoreactive nerve cell bodies and processes. The obtained results indicate that mGlu1a receptors may control at least some NPY and CRF neurons in the amygdala.

Amygdala↗
PubMed2002

The human LSm1-7 proteins colocalize with the mRNA-degrading enzymes Dcp1/2 and Xrnl in distinct cytoplasmic foci.

Sm and Sm-like (LSm) proteins form heptameric complexes that are involved in various steps of RNA metabolism. In yeast, the Lsm1-7 complex functions in mRNA degradation and is associated with several enzymes of this pathway, while the complex LSm2-8, the composition of which largely overlaps with that of LSm1-7, has a role in pre-mRNA splicing. A human gene encoding an LSm1 homolog has been identified, but its role in mRNA degradation has yet to be elucidated. We performed subcellular localization studies and found hLSm1 predominantly in the cytoplasm. However, it is not distributed evenly; rather, it is highly enriched in small, discrete foci. The endogenous hLSm4 is similarly localized, as are the overexpressed proteins hLSm1-7, but not hLSm8. The foci also contain two key factors in mRNA degradation, namely the decapping enzyme hDcp1/2 and the exonuclease hXrn1. Moreover, coexpression of wild-type and mutant LSm proteins, as well as fluorescence resonance energy transfer (FRET) studies, indicate that the mammalian proteins hLSm1-7 form a complex similar to the one found in yeast, and that complex formation is required for enrichment of the proteins in the cytoplasmic foci. Therefore, the foci contain a partially or fully assembled machinery for the degradation of mRNA.

Cytoplasm↗
PubMed1992

Colocalization of basal and luminal cell-type cytokeratins in human prostate cancer.

In the epithelium of secretory acini of the prostate two different cell types can be discriminated on the basis of localization, morphology, and degree of differentiation, the luminal and basal cells. The possibility of a developmental relationship between basal and luminal cells has been a subject of interest in several studies. According to the stem cell model at least three cell types, i.e., stem, amplifying, and transit cells, can be discriminated in the epithelium of prostate secretory acini. We previously reported that in the process of degeneration and regeneration in normal rat prostate a population of cells could be identified as candidates for the amplifying cells. These cells showed a keratin expression profile intermediate between those of basal and luminal cells. We now show, by using keratin antibodies, that also in normal human prostate at least three subpopulations of cells can be identified, one of them putatively representing amplifying cells as defined in the stem cell model. Furthermore, these antibodies were used to obtain a better insight into the different cell types involved in the etiology and progression of prostatic carcinoma. Both primary and hormone-independent prostatic tumors were investigated. Our results indicated that the candidate stem cell population was absent in prostatic carcinoma. Unlike earlier reports on the unique presence of cells with luminal characteristics in prostatic carcinoma, we identified also a population of cells coexpressing basal and luminal cell-type cytokeratins in primary and hormone-independent prostatic carcinoma. Since amplifying cells are defined in the stem cell model as precursors of transit (luminal) cells in the hierarchical pathway of prostatic epithelium differentiation, we postulate that on the basis of the keratin expression profile this subpopulation is most likely the target for neoplastic transformation.

Antibodies, Monoclonal↗
PubMed2004

[Estrogen receptor alpha and colocalization of Bcl-2 in hippocampus of Alzheimer's disease].

OBJECTIVE: To investigate the possible mechanism by which estrogen regulates apoptosis through the estrogen receptor. METHODS: By means of fluorescence immunocytochemistry, the present study investigated the distribution of Bcl-2 and the colocolization of Bcl-2 and ERalpha immunoreactivity in the hippocampus of 10 Alzheimer's disease (AD) patients and 10 aged controls. RESULTS: Bcl-2 immunoreactivity was widely distributed in neurons, concentrating predominantly on the subfields CA3 and CA4 in the stratum pyramidale of hippocampus both in controls and in AD patients. Bcl-2 staining in the labeled neuron was observed mainly in the cytoplasm and neuritic processes, but a few nuclei were also positive. Bcl-2 labeling was also detected in the astrocytes mainly in AD, but sparsely in controls. Double-labeled fluorescence immunocytochemistry showed that most Bcl-2-immunolabeled neurons also exhibited positive staining for ERalpha. CONCLUSIONS: Estrogen may function as a regulator of apoptosis to modulate the expression of Bcl-2 in neurons and astrocytes in hippocampus of AD through ERalpha.

Alzheimer Disease↗
PubMedDate not supplied

Colocalization of different types of amyloid in the walls of cerebral blood vessels of patients suffering from cerebral amyloid angiopathy and spontaneous intracranial hemorrhage: a report of 5 cases.

Four cases of spontaneous intracranial hemorrhage (ICH) are described in which the diagnosis of a cerebral amyloid angiopathy (CAA) was made in the biopsy specimens. In one further case CAA was detected on autopsy after intracranial hemorrhage (ICH). Amyloidotic degeneration of the vessel walls appeared to be the most likely reason for the ICH which in these cases especially involved superficial neocortical regions. In all cases, co-deposition of A4beta-amyloid and ALlambda-amyloid was found in diseased leptomeningeal and cortical vessels. Besides CAA, all 5 patients suffered from other diseases which had affected the blood vessel walls such as atherosclerosis, diabetes mellitus or arterial hypertension. However, no signs of systemic amyloidosis could be detected in these cases. It is suggested that the observed co-deposition of 2 amyloid subtypes is based on the combination of 2 different diseases, one of which results in a local production of A4beta-amyloid in the tunica media of cerebral blood vessels and another one, e.g. arterial hypertension, which impairs the permeability of the blood vessels by affection of the tunica intima allowing for the pathological penetration of circulating immunoglobulin lambda-light chains into the vessel wall. Subsequently, the preexisting A4beta-amyloid might have induced the polymerization of the lambda-light chains to ALlambda-amyloid in the media of the vessels and could have aggravated the amyloidotic degeneration of the vessel walls.

Adult↗
PubMed2006

Human RAB24, interestingly and predominantly distributed in the nuclei of COS-7 cells, is colocalized with cyclophilin A and GABARAP.

As an atypical member of the Rab family, Rab24 has several attributes distinguishing this protein from the other members. Based on the yeast two-hybrid system, interaction between human RAB24 and two proteins, cyclophilin A (CyP-A) and gamma-aminobutyric acid type A receptor-associated protein (GABARAP), was detected and identified in COS-7 cells. Interestingly, RAB24 is predominantly localized in the nuclei of COS-7 cells, which is different from previous reports using other cell lines. RAB24 (D123I) can trigger the accumulation of intracellular inclusions, with small quantities of intranuclear inclusions in some cells. The GTPase activity of RAB24 and its two mutants was detected.

Adaptor Proteins, Signal Transducing↗