scholarly journals Effect of melatonin from slow-release implants on aquaporins (AQP1 and AQP4) in the ovine choroid plexus

2017 ◽  
Vol 63 (No. 1) ◽  
pp. 32-42 ◽  
Author(s):  
A. Szczepkowska ◽  
M.T. Skowroński ◽  
M. Kowalewska ◽  
S. Milewski ◽  
J. Skipor
Keyword(s):  
Mrna Expression ◽  
Choroid Plexus ◽  
Turnover Rate ◽  
Slow Release ◽  
Apical Membrane ◽  
Immunohistochemical Analysis ◽  
Exon 2 ◽  
Seasonally Breeding ◽  
Short Days ◽  
Csf Production

Aquaporins (AQPs) play important role in the cerebrospinal fluid (CSF) secretion and AQP1 and AQP4 are localized in the choroid plexus (CP), which is the main place of CSF production. In ewes, seasonally breeding animals, the turnover rate (TOR) of CSF is photoperiodically modulated and melatonin, a biochemical signal about changing photoperiod, is used to advance the onset of the breeding season by mimicking the stimulatory effect of short days (SD). This study evaluates the effect of melatonin implantation during long days (LD) on AQPs expression in the ovine CP. Studies were performed on ovariectomized, estradiol implanted ewes treated with placebo (n = 6) or with melatonin (n = 6) during LD. Ewes were sacrificed 40 days after melatonin/placebo implantation and CPs from the lateral/third brain ventricles were collected for Real-time and Western blot analyses. Additionally, for immunohistochemical analysis, CP samples were collected from ewes (n = 3) sacrificed during LD. We demonstrated an apical membrane localization of AQP1 and a diffused distribution of AQP4 in the epithelial cells of CP. The mRNA expression of AQP1 was 20 times higher than the expression of all AQP4 isoforms, and among them AQP4 isoforms containing exon 2 constituted approximately 38%. The melatonin implantation significantly (P < 0.05) increased the mRNA expression of AQP1 and AQP4 and the protein level of AQP4 isoforms (33 and 28 kDa). For AQP1 we observed a significant (P < 0.05) decrease of glycosylated (33 kDa) and a significant (P < 0.05) increase of unglycosylated (23 kDa) predominant protein form. Therefore it can be suggested that at least AQP1, which is involved in CSF production and has been demonstrated to be modulated by melatonin implantation, is linked with the photoperiodic modulation of the CSF production in ewes.

Surgical removal of bilateral papillomas of the choroid plexus of the lateral ventricles with resolution of hydrocephalus

1979 ◽  
Vol 50 (5) ◽  
pp. 677-681 ◽  
Author(s):  
Steven K. Gudeman ◽  
Humbert G. Sullivan ◽  
Michael J. Rosner ◽  
Donald P. Becker
Keyword(s):  
Cerebrospinal Fluid ◽  
Choroid Plexus ◽  
Large Volume ◽  
Surgical Removal ◽  
Tumor Removal ◽  
Content Type ◽  
Lateral Ventricles ◽  
Csf Diversion ◽  
Csf Production ◽  
Fine Print

✓ The authors report a patient with bilateral papillomas of the choroid plexus of the lateral ventricles with documentation of cerebrospinal fluid (CSF) hypersecretion causing hydrocephalus. Special attention is given to the large volume of CSF produced by these tumors (removal of one tumor reduced CSF outflow by one-half) and to the fact that CSF diversion was not required after both tumors were removed. Since tumor removal alone was sufficient to stop the progression of hydrocephalus, we feel that this case supports the concept that elevated CSF production by itself is sufficient to cause hydrocephalus in patients with papillomas of the choroid plexus.

scholarly journals Matrix GLA protein modulates branching morphogenesis in fetal rat lung

2004 ◽  
Vol 286 (6) ◽  
pp. L1179-L1187 ◽  
Author(s):  
Kirk A. Gilbert ◽  
Stephen R. Rannels
Keyword(s):  
Mrna Expression ◽  
Time Course ◽  
Immunohistochemical Analysis ◽  
Fetal Lung ◽  
Branching Morphogenesis ◽  
Matrix Gla Protein ◽  
Antibody Treatment ◽  
Developmentally Regulated

The regulation of matrix γ-carboxyglutamic acid protein (MGP) expression during the process of lung branching morphogenesis and development was investigated. MGP mRNA expression was determined over an embryonic and postnatal time course and shown to be developmentally regulated. Immunohistochemical analysis revealed increased staining for MGP in peripheral mesenchyme surrounding distal epithelial tubules. Fetal lung explants were used as an in vitro growth model to examine expression and regulation of MGP during branching morphogenesis. MGP mRNA expression over the culture interval mimicked the in vivo time course. Explants cultured in the presence of antibodies against MGP showed gross dilation and reduced terminal lung bud counts, accompanied by changes in MGP, sonic hedgehog, and patched mRNA expression. Similarly, antifibronectin antibody treatment resulted in explant dilation and reduced MGP expression, providing evidence for an interaction with MGP and fibronectin. Conversely, intraluminal microinjection of anti-MGP antibodies had no effect either on explant growth or MGP expression, supporting the hypothesis that MGP exerts its effects through the mesenchyme. Taken together, the results suggest that MGP plays a role in lung growth and development, likely via temporally and spatially specific interactions with other branching morphogenesis-related proteins to influence growth processes.

scholarly journals Personalized approach to assessing mRNA expression of histidine-rich glycoprotein and immunohistochemical markers in diseases of the breast

2019 ◽  
Vol 484 (5) ◽  
pp. 624-628 ◽  
Author(s):  
A. I. Autenshlyus ◽  
A. V. Golovanova ◽  
A. A. Studenikina ◽  
I. I. Brusentsov ◽  
A. V. Proskura ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Epithelial Mesenchymal Transition ◽  
Immunohistochemical Analysis ◽  
Breast Diseases ◽  
Biopsy Material ◽  
Mesenchymal Transition ◽  
Benign Breast Diseases ◽  
Immunohistochemical Markers ◽  
Atypical Cells ◽  
Personalized Approach

Biopsy material of patients with malignant and benign breast diseases was examined. HRG mRNA expression was detected in 70% of cases in biopsy material obtained from patients with nonspecific invasive carcinoma and in 66.7% of cases in biopsy material of patients with benign breast diseases. Immunohistochemical analysis revealed expression of collagen II, the beta-1 integrin, and E-cadherin – markers of epithelial–mesenchymal transition. The use of RT-qPCR combined with immunohistochemical study made it possible to identify atypical cells, which can be regarded as precancerous changes, in individual patients.

scholarly journals The evolutionary and integrative roles of transthyretin in thyroid hormone homeostasis

2002 ◽  
Vol 175 (1) ◽  
pp. 61-73 ◽  
Author(s):  
G Schreiber
Keyword(s):  
Thyroid Hormone ◽  
Choroid Plexus ◽  
Molecular Mechanism ◽  
Amino Acid Sequences ◽  
Open Reading Frames ◽  
Darwinian Evolution ◽  
Hormone Binding ◽  
Exon 2 ◽  
Hormone Homeostasis ◽  
Made In

In larger mammals, thyroid hormone-binding plasma proteins are albumin, transthyretin (TTR) and thyroxine (T4)-binding globulin. They differ characteristically in affinities and release rates for T4 and triiodothyronine (T3). Together, they form a 'buffering' system counteracting thyroid hormone permeation from aqueous to lipid phases. Evolution led to important differences in the expression pattern of these three proteins in tissues. In adult liver, TTR is only made in eutherians and herbivorous marsupials. During development, it is also made in tadpole and fish liver. More intense TTR synthesis than in liver is found in the choroid plexus of reptilians, birds and mammals, but none in the choroid plexus of amphibians and fish, i.e. species without a neocortex. All brain-made TTR is secreted into the cerebrospinal fluid, where it becomes the major thyroid hormone-binding protein. During ontogeny, the maximum TTR synthesis in the choroid plexus precedes that of the growth rate of the brain and occurs during the period of maximum neuroblast replication. TTR is only one component in a network of factors determining thyroid hormone distribution. This explains why, under laboratory conditions, TTR-knockout mice show no major abnormalities. The ratio of TTR affinity for T4 over affinity for T3 is higher in eutherians than in reptiles and birds. This favors T4 transport from blood to brain providing more substrate for conversion of the biologically less active T4 into the biologically more active T3 by the tissue-specific brain deiodinases. The change in affinity of TTR during evolution involves a shortening and an increase in the hydrophilicity of the N-terminal regions of the TTR subunits. The molecular mechanism for this change is a stepwise shift of the splice site at the intron 1/exon 2 border of the TTR gene. The shift probably results from a sequence of single base mutations. Thus, TTR evolution provides an example for a molecular mechanism of positive Darwinian evolution. The amino acid sequences of fish and amphibian TTRs are very similar to those in mammals, suggesting that substantial TTR evolution occurred before the vertebrate stage. Open reading frames for TTR-like sequences already exist in Caenorhabditis elegans, yeast and Escherichia coli genomes.

scholarly journals Prognostic Significance of Stromal Periostin Expression in Non-Small Cell Lung Cancer

2020 ◽  
Vol 21 (19) ◽  
pp. 7025
Author(s):  
Katarzyna Ratajczak-Wielgomas ◽  
Alicja Kmiecik ◽  
Jedrzej Grzegrzołka ◽  
Aleksandra Piotrowska ◽  
Agnieszka Gomulkiewicz ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Prognostic Factor ◽  
Small Cell Lung Cancer ◽  
Mrna Expression ◽  
Cancer Cells ◽  
Cell Lung Cancer ◽  
Prognostic Significance ◽  
Immunohistochemical Analysis ◽  
Small Cell ◽  
Small Cell Lung

Background: The microenvironment of solid tumours is significant in cancer development and progression. The aim of this study was to determine periostin (POSTN) expression by cancer-associated fibroblasts (CAFs) in non-small-cell lung cancer (NSCLC), as well as to assess associations with clinicopathological factors and prognosis. Materials and Methods: Immunohistochemical analysis of POSTN expression was performed on NSCLC (N = 700) and non-malignant lung tissue (NMLT) (N = 110) using tissue microarrays. Laser capture microdissection (LCM) for isolation of stromal and cancer cells of NSCLC was employed, and subsequently, POSTN mRNA expression was detected by real-time PCR. Immunofluorescence reaction and colocalisation analysis were performed by confocal microscopy. Results: Expression of POSTN in CAFs was significantly higher in NSCLC and in the adenocarcinoma (AC) and squamous cell carcinoma (SCC) subtypes compared to NMLT. POSTN expression in CAFs increased with clinical cancer stage, grades (G) of malignancy, and lymph node involvement in NSCLC. Higher POSTN expression in CAFs was an independent prognostic factor for overall survival (OS). LCM confirmed significantly higher POSTN mRNA expression in the stromal cells (CAFs) compared to the lung cancer cells. Conclusions: POSTN produced by CAFs might be crucial for NSCLC progression and can be an independent negative prognostic factor in NSCLC.

Expression and localization of epithelial sodium channel in mammalian urinary bladder

1998 ◽  
Vol 274 (1) ◽  
pp. F91-F96 ◽  
Author(s):  
Peter R. Smith ◽  
Scott A. Mackler ◽  
Philip C. Weiser ◽  
David R. Brooker ◽  
Yoon J. Ahn ◽  
...  
Keyword(s):  
In Situ Hybridization ◽  
Urinary Bladder ◽  
Mrna Expression ◽  
Northern Blot ◽  
Apical Membrane ◽  
Bladder Epithelium ◽  
Rat Urinary Bladder ◽  
Luminal Membrane ◽  
Electrophysiological Studies

The mammalian urinary bladder exhibits transepithelial Na+ absorption that contributes to Na+ gradients established by the kidney. Electrophysiological studies have demonstrated that electrogenic Na+ absorption across the urinary bladder is mediated in part by amiloride-sensitive Na+ channels situated within the apical membrane of the bladder epithelium. We have used a combination of in situ hybridization, Northern blot analysis, and immunocytochemistry to examine whether the recently cloned epithelial Na+ channel (ENaC) is expressed in the rat urinary bladder. In situ hybridization and Northern blot analyses indicate that α-, β-, and γ-rat ENaC (rENaC) are expressed in rat urinary bladder epithelial cells. Quantitation of the levels of α-, β-, and γ-rENaC mRNA expression in rat urinary bladder, relative to β-actin mRNA expression, indicates that, although comparable levels of α- and β-rENaC subunits are expressed in the urinary bladder of rats maintained on standard chow, the level of γ-rENaC mRNA expression is 5- to 10-fold lower than α- or β-rENaC mRNA. Immunocytochemistry, using an antibody directed against α-rENaC, revealed that ENaCs are predominantly localized to the luminal membrane of the bladder epithelium. Together, these data demonstrate that ENaC is expressed in the mammalian urinary bladder and suggest that amiloride-sensitive Na+ transport across the apical membrane of the mammalian urinary bladder epithelium is mediated primarily by ENaC.

Ossified choroid plexus papilloma of the fourth ventricle: elucidation of the mechanism of osteogenesis in benign brain tumors

2013 ◽  
Vol 12 (1) ◽  
pp. 13-20 ◽  
Author(s):  
Sunil Manjila ◽  
Erin Miller ◽  
Amad Awadallah ◽  
Shunichi Murakami ◽  
Mark L. Cohen ◽  
...  
Keyword(s):  
Brain Tumors ◽  
Bone Formation ◽  
Choroid Plexus ◽  
Fourth Ventricle ◽  
Choroid Plexus Papilloma ◽  
Immunohistochemical Analysis ◽  
Pluripotent Cell ◽  
Bone Trabeculae ◽  
Plexus Papilloma ◽  
Mature Bone

True ossification within benign brain tumors is rare, and the molecular mechanism for this process is poorly understood. The authors report a case of ossified choroid plexus papilloma (CPP) and analyze it to help elucidate the underlying molecular basis of osteogenesis in benign brain tumors. A 21-year-old man presented with headache and depression that progressed over years. Computed tomography, MRI, and angiography demonstrated a large heavily calcified fourth ventricular tumor with a vascular blush and no hydrocephalus. The tumor was resected and was found to be an ossified CPP. Immunohistochemical staining for VEGF, Sox2, BMP-2, osterix, osteopontin, and osteocalcin was performed in an attempt to elucidate the mechanism of bone formation. The tumor was extensively ossified with mature bone trabeculae. Immunostaining for VEGF was positive. Additional staining showed the presence of osteocalcin in this ossified tumor but not in samples of nonossified CPPs collected from other patients. Staining for osterix and osteopontin was equivocally positive in the ossified CPP but also in the nonossified CPPs examined. The presence of osteocalcin in the ossified CPP demonstrates that there is true bone formation rather than simple calcification. Its appearance within cells around the trabeculae suggests the presence of osteoblasts. The presence of osterix suggests that a pluripotent cell, or one that is already partially differentiated, may be differentiated into an osteoblast through this pathway. This represents the first systematic immunohistochemical analysis of osteogenesis within choroid plexus tumors.

scholarly journals BMI1,ALDH1A1, andCD133Transcripts Connect Epithelial-Mesenchymal Transition to Cancer Stem Cells in Lung Carcinoma

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Ana Koren ◽  
Matija Rijavec ◽  
Izidor Kern ◽  
Eva Sodja ◽  
Peter Korosec ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Mrna Expression ◽  
Whole Blood ◽  
Epithelial Mesenchymal Transition ◽  
Immunohistochemical Analysis ◽  
Underlying Mechanism ◽  
Primary Tumors ◽  
Mesenchymal Transition ◽  
Cellular Models ◽  
Nsclc Patients

Epithelial-mesenchymal transition (EMT) is the underlying mechanism of tumor invasion and metastasis. Evidences from lung cancer cellular models show EMT can trigger conversion to a cancer stem cell (CSC) phenotype. In this study, we assessed mRNA expression levels of EMT-inducing transcription factors (BMI1,TWIST1), CSC (CD133,ALDH1A1), and epithelial (EpCAM) markers in primary tumor and whole blood samples obtained from 57 patients with operable non-small-cell lung cancer (NSCLC) as well as in circulating tumor cells (CTCs) of 13 patients with metastatic disease; then possible associations between marker expressions were evaluated. In primary tumors as well as in whole blood, correlations betweenBMI1andALDH1A1and betweenBMI1andCD133mRNA expressions were identified. No correlations betweenTWIST1and CSC markers were observed.BMI1mRNA expression in tumors positively correlated withBMI1mRNA expression in blood. The immunohistochemical analysis confirmed coexpression of BMI1 and CSC markers in tumors. Gene expression profiling in CTCs revealed upregulated expression of EMT/CSC markers in CTCs. Our results suggest CSCs are present in both, tumor tissue and blood of NSCLC patients, whereas Bmi1 may play an important role in initiation and maintenance of CSCs and might be involved in the blood-borne dissemination of NSCLC.

Prostaglandins that increase renin production in response to ACE inhibition are not derived from cyclooxygenase-1

2002 ◽  
Vol 283 (3) ◽  
pp. R638-R646 ◽  
Author(s):  
Hui-Fang Cheng ◽  
Sue-Wan Wang ◽  
Ming-Zhi Zhang ◽  
James A. McKanna ◽  
Richard Breyer ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Enzyme Inhibitor ◽  
Plasma Renin ◽  
Immunohistochemical Analysis ◽  
Renin Activity ◽  
Prostaglandin E ◽  
Receptor Subtype ◽  
Renin Mrna ◽  
Cox 2 ◽  
Cox 1

It is well known that nonselective, nonsteroidal anti-inflammatory drugs inhibit renal renin production. Our previous studies indicated that angiotensin-converting enzyme inhibitor (ACEI)-mediated renin increases were absent in rats treated with a cyclooxygenase (COX)-2-selective inhibitor and in COX-2 −/− mice. The current study examined further whether COX-1 is also involved in mediating ACEI-induced renin production. Because renin increases are mediated by cAMP, we also examined whether increased renin is mediated by the prostaglandin E2 receptor EP2 subtype, which is coupled to Gs and increases cAMP. Therefore, we investigated if genetic deletion of COX-1 or EP2 prevents increased ACEI-induced renin expression. Age- and gender-matched wild-type (+/+) and homozygous null mice (−/−) were administered captopril for 7 days, and plasma and renal renin levels and renal renin mRNA expression were measured. There were no significant differences in the basal level of renal renin activity from plasma or renal tissue in COX-1 +/+ and −/− mice. Captopril administration increased renin equally [plasma renin activity (PRA): +/+ 9.3 ± 2.2 vs. 50.1 ± 10.9; −/− 13.7 ± 1.5 vs. 43.9 ± 6.6 ng ANG I · ml−1 · h−1; renal renin concentration: +/+ 11.8 ± 1.7 vs. 35.3 ± 3.9; −/− 13.0 ± 3.0 vs. 27.8 ± 2.7 ng ANG I · mg protein−1 · h−1; n = 6; P < 0.05 with or without captopril]. ACEI also increased renin mRNA expression (+/+ 2.4 ± 0.2; −/− 2.1 ± 0.2 fold control; n = 6–10; P < 0.05). Captopril led to similar increases in EP2 −/− compared with +/+. The COX-2 inhibitor SC-58236 blocked ACEI-induced elevation in renal renin concentration in EP2 null mice (+/+ 24.7 ± 1.7 vs. 9.8 ± 0.4; −/− 21.1 ± 3.2 vs. 9.3 ± 0.4 ng ANG I · mg protein−1 · h−1; n = 5) as well as in COX-1 −/− mice (SC-58236-treated PRA: +/+ 7.3 ± 0.6; −/− 8.0 ± 0.9 ng ANG I · ml−1 · h−1; renal renin: +/+ 9.1 ± 0.9; −/− 9.6 ± 0.5 ng ANG I · mg protein−1 · h−1; n = 6–7; P < 0.05 compared with no treatment). Immunohistochemical analysis of renin expression confirmed the above results. This study provides definitive evidence that metabolites of COX-2 rather than COX-1 mediate ACEI-induced renin increases. The persistent response in EP2 nulls suggests involvement of prostaglandin E2 receptor subtype 4 and/or prostacyclin receptor (IP).

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