scholarly journals Clusterin production in the obstructed rabbit kidney: correlations with loss of renal function.

1992 ◽  
Vol 3 (5) ◽  
pp. 1163-1171
Author(s):  
P N Schlegel ◽  
G J Matthews ◽  
Z Cichon ◽  
W K Aulitzky ◽  
C Y Cheng ◽  
...  
Keyword(s):  
Gene Expression ◽  
Renal Function ◽  
Ureteral Obstruction ◽  
Rabbit Kidney ◽  
Sodium Reabsorption ◽  
Mrna Levels ◽  
Mrna Accumulation ◽  
Contralateral Kidney ◽  
Collecting Ducts ◽  
Clusterin Protein

Clusterin, a protein associated with cell death, has been suggested as a marker of renal injury. Correlation of clusterin gene expression with changes in renal function and quantitative measurement of clusterin protein levels after ureteral obstruction have not been previously reported. With unilateral ureteral obstruction in rabbits as the experimental model, the time course of alterations in renal function, clusterin mRNA accumulation, and concentrations of clusterin protein in serum, urine, and renal tissue were investigated. RBF, GFR, and renal concentrating ability (percent sodium reabsorption and urine osmolarity) all decreased (P < 0.05) in the obstructed kidney from control values within 1 day of ureteral obstruction. Clusterin mRNA levels started to rise in the ipsilateral kidney within 12 h of ureteral obstruction and increased up to 10-fold above control levels after 3 days of obstruction. Hybridization histochemistry showed that clusterin mRNA was initially detectable in collecting ducts and distal tubules within 12 h of ureteral obstruction. After 7 days of obstruction, increased accumulation of clusterin mRNA was also detectable in proximal tubular epithelial cells. Clusterin gene expression remained elevated in collecting ducts after 60 days of obstruction. Clusterin expression in the contralateral kidney was increased twofold over control values after 12 h of obstruction. No increase in clusterin mRNA accumulation was detectable after 24 h in the contralateral kidney. Total clusterin protein in the obstructed kidney increased from 0.59 +/- 0.66 (mean +/- 1 SD) to 2.5 +/- 1.3 micrograms after 7 days of ureteral obstruction (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Gene expression after resumption of development of Artemia franciscana cryptobiotic embryos

1994 ◽  
Vol 72 (3-4) ◽  
pp. 78-83 ◽  
Author(s):  
Ricardo Escalante ◽  
Alberto García-Sáez ◽  
Maria-Asunción Ortega ◽  
Leandro Sastre
Keyword(s):  
Gene Expression ◽  
Time Course ◽  
Developmental Stages ◽  
Artemia Franciscana ◽  
Mrna Levels ◽  
Muscle Actin ◽  
Mrna Accumulation ◽  
Α Subunit ◽  
Steady State Levels ◽  
Cyst Development

The steady-state levels of six different mRNAs have been studied during Artemia franciscana development. Some of these mRNAs are present in the cryptobiotic cyst, like those coding for cytoplasmic actins, sarcoplasmic/endoplasmic reticulum Ca2+-ATPase, and the Na+,K+-ATPase α-subunit isoform coded by the clone pArATNa136. The expression of these mRNAs is markedly induced during cyst development. A small increase in mRNA levels can be observed for some genes at very early stages of development (2 h). The main increase is observed between 4 and 16 h of development for all these genes, although the time course of mRNA accumulation is different for each one of the genes studied. Some other genes, like those coding for muscle actin (actin 3) or the Na+,K+-ATPase α-subunit isoform coded by the cDNA clone α2850, are not expressed in the cyst before resumption of development and their expression is induced after 10 or 6 h of development, respectively. These data on the kinetic of mRNA accumulation provide the information required to determine transcriptionally active developmental stages, necessary to study in more detail the mechanisms of transcriptional regulation during activation of cryptobiotic cysts and resumption of embryonic development.Key words: Artemia, gene expression, actin, Na,K-ATPase, Ca2+-ATPase.

Tubulin gene expression in the Chlamydomonas reinhardtii cell cycle: elimination of environmentally induced artifacts and the measurement of tubulin mRNA levels

1988 ◽  
Vol 89 (3) ◽  
pp. 397-403
Author(s):  
D.S. Nicholl ◽  
J.A. Schloss ◽  
P.C. John
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Cell Division ◽  
Chlamydomonas Reinhardtii ◽  
Environmental Conditions ◽  
Mrna Levels ◽  
Tubulin Gene ◽  
Mrna Accumulation ◽  
Tubulin Mrna ◽  
Flagellar Proteins

To investigate the involvement of tubulin gene expression in controlling cell division events in Chlamydomonas reinhardtii we have measured tubulin mRNA levels during the cell cycle under different environmental conditions. In C. reinhardtii cells grown under the synchronizing conditions of 14 h of light followed by 10 h of darkness, mRNAs for tubulin and associated flagellar proteins were found to accumulate periodically with a peak just prior to cell division. This was not seen when previously synchronized cells were transferred to constant environmental conditions in a turbidostat, suggesting that dramatic changes in tubulin mRNA levels are not required for successful completion of the cell cycle. A hypothesis to explain the patterns of tubulin mRNA accumulation found under different environmental conditions is presented.

scholarly journals Epidermal growth factor and phorbol myristate acetate increase expression of the mRNA for cytosolic phospholipase A2 in glomerular mesangial cells

1993 ◽  
Vol 295 (3) ◽  
pp. 763-766 ◽  
Author(s):  
A P Maxwell ◽  
H J Goldberg ◽  
A H N Tay ◽  
Z G Li ◽  
G S Arbus ◽  
...  
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Phospholipase A2 ◽  
Mesangial Cells ◽  
Mrna Levels ◽  
Glomerular Mesangial Cells ◽  
Pla2 Activity ◽  
Mrna Accumulation ◽  
Epidermal Growth

We have previously shown that phospholipase A2 (PLA2) activity is rapidly activated by epidermal growth factor (EGF) and phorbol 12-myristate 13-acetate (PMA) in renal mesangial cells and other cell systems in a manner that suggests a covalent modification of the PLA2 enzyme(s). This PLA2 activity is cytosolic (cPLA2) and is distinct from secretory forms of PLA2, which are also stimulated in mesangial cells in response to cytokines and other agonists. However, longer-term regulation of cPLA2 in renal cells may also occur at the level of gene expression. Cultured rat mesangial cells were used as a model system to test the effects of EGF and PMA on the regulation of cPLA2 gene expression. EGF and PMA both produced sustained increases in cPLA2 mRNA levels, with a parallel increase in enzyme activity over time. Inhibition of protein synthesis by cycloheximide increased basal cPLA2 mRNA accumulation in serum-starved mesangial cells, and the combination of EGF and cycloheximide resulted in super-induction of cPLA2 gene expression compared with EGF alone. Actinomycin D treatment entirely abrogated the effect of EGF on cPLA2 mRNA accumulation. These findings suggest that regulation of cPLA2 is achieved by factors controlling gene transcription and possibly mRNA stability, in addition to previously characterized posttranslational modifications.

Differential regulation of Na-K-ATPase isoform gene expression by T3 during rat brain development

1991 ◽  
Vol 261 (1) ◽  
pp. C124-C131 ◽  
Author(s):  
I. Corthesy-Theulaz ◽  
A. M. Merillat ◽  
P. Honegger ◽  
B. C. Rossier
Keyword(s):  
Gene Expression ◽  
Brain Development ◽  
Culture System ◽  
Mrna Level ◽  
Mrna Abundance ◽  
Mrna Levels ◽  
Basal Transcription ◽  
Mrna Accumulation ◽  
Atpase Gene ◽  
Beta 2

A fetal rat telencephalon organotypic cell culture system was found to reproduce the developmental pattern of Na-K-adenosinetriphosphatase (ATPase) gene expression observed in vivo [Am. J. Physiol. 258 (Cell Physiol. 27): C1062-C1069, 1990]. We have used this culture system to study the effects of triiodothyronine (T3; 0.003-30 nM) on mRNA abundance and basal transcription rates of Na-K-ATPase isoforms. Steady-state mRNA levels were low at culture day 6 (corresponding to the day of birth) but distinct for each isoform alpha 3 much greater than beta 1 = beta 2 greater than alpha 2 greater than alpha 1. At culture day 6, T3 did not modify mRNA abundance of any isoform. At culture day 12 (corresponding to day 7 postnatal), T3 increased the mRNA level of alpha 2 (4- to 7-fold), beta 2 (4- to 5-fold), alpha 1 (3- to 6-fold), and beta 1 (1.5-fold), whereas alpha 3 mRNA levels remained unchanged. Interestingly, the basal transcription rate for each isoform differed strikingly (alpha 2 greater than alpha 1 much greater than beta 1 = beta 2 greater than alpha 3) but remained stable throughout 12 days of culture and was not regulated by T3. Thus we observed an inverse relationship between rate of transcription and rate of mRNA accumulation for each alpha-isoform, suggesting that alpha 1- and alpha 2-mRNA are turning over rapidly whereas alpha 3-mRNA is turning over slowly. Our data indicate that one of the mechanisms by which T3 selectively controls Na-K-ATPase gene expression during brain development in vitro occurs at the posttranscriptional level.

Insulin-like growth factor-II in human fetal adrenals: regulation by ACTH, protein kinase C and growth factors

1993 ◽  
Vol 137 (3) ◽  
pp. 533-542 ◽  
Author(s):  
V. Ilvesmäki ◽  
W. F. Blum ◽  
R. Voutilainen
Keyword(s):  
Gene Expression ◽  
Protein Kinase C ◽  
Growth Factors ◽  
Growth Factor ◽  
Culture Medium ◽  
Mrna Levels ◽  
Mrna Accumulation ◽  
Polypeptide Growth Factors ◽  
Kinase C ◽  
Factor Ii

ABSTRACT Insulin-like growth factor-II (IGF-II) may be one of the most important local growth factors in human fetal adrenals (HFAs), where its mRNA levels are upregulated by ACTH. We have investigated whether protein kinase C (PKC)-dependent mechanisms and various polypeptide growth factors participate in the regulation of IGF-II gene expression in cultured HFA cells, and whether HFA cells secrete IGF-II peptide into the culture medium. ACTH enhanced IGF-II mRNA accumulation dose- and time-dependently, maximally four- to sixfold, and this increase was inhibited dose-dependently (0·01-100 μg/l) by 12-O-tetradecanoyl phorbol-13-acetate (TPA), a PKC activator. TPA decreased basal IGF-II mRNA levels by approximately 55%. Staurosporine, a PKC inhibitor, abolished the inhibitory effects of TPA and induced accumulation of IGF-II mRNA. Dibutyryl cyclic AMP, cholera toxin and forskolin increased IGF-II mRNA accumulation as much as ACTH, and TPA inhibited these stimulations in a similar way. ACTH increased the IGF-II peptide concentration in most experiments, but this increase was modest in comparison with IGF-II mRNA changes. TPA, although it decreased IGF-II mRNA levels, tended to increase IGF-II peptide in the medium. Additions of GH, IGF-I and IGF-II to the cell culture medium also increased IGF-II mRNA accumulation. Transforming growth factor-β1 inhibited IGF-II mRNA accumulation to the same extent as TPA. Epidermal growth factor and basic fibroblast growth factor did not change IGF-II mRNA levels. Our results confirm previous reports that ACTH is an important regulator of IGF-II in human fetal adrenals, and show that IGF-II gene expression is under multifactorial control, which includes the PKC system and polypeptide growth factors. Journal of Endocrinology (1993) 137, 533–542

V2 vasopressin receptor deficiency causes changes in expression and function of renal and hypothalamic components involved in electrolyte and water homeostasis

2008 ◽  
Vol 295 (4) ◽  
pp. F1177-F1190 ◽  
Author(s):  
Nicole Schliebe ◽  
Rainer Strotmann ◽  
Kathy Busse ◽  
Doreen Mitschke ◽  
Heike Biebermann ◽  
...  
Keyword(s):  
Gene Expression ◽  
Collecting Duct ◽  
Clinical Signs ◽  
Sodium Reabsorption ◽  
Vasopressin Receptor ◽  
Mrna Levels ◽  
Carbonic Anhydrases ◽  
Altered Expression ◽  
Study Gene Expression ◽  
V2 Vasopressin Receptor

Polyuria, hypernatremia, and hypovolemia are the major clinical signs of inherited nephrogenic diabetes insipidus (NDI). Hypernatremia is commonly considered a secondary sign caused by the net loss of water due to insufficient insertion of aquaporin-2 water channels into the apical membrane of the collecting duct cells. In the present study, we employed transcriptome-wide expression analysis to study gene expression in V2 vasopressin receptor (Avpr2)-deficient mice, an animal model for X-linked NDI. Gene expression changes in NDI mice indicate increased proximal tubular sodium reabsorption. Expression of several key genes including Na+-K+-ATPase and carbonic anhydrases was increased at the mRNA levels and accompanied by enhanced enzyme activities. In addition, altered expression was also observed for components of the eicosanoid and thyroid hormone pathways, including cyclooxygenases and deiodinases, in both kidney and hypothalamus. These effects are likely to contribute to the clinical NDI phenotype. Finally, our data highlight the involvement of the renin-angiotensin-aldosterone system in NDI pathophysiology and provide clues to explain the effectiveness of diuretics and indomethacin in the treatment of NDI.

scholarly journals AT1 receptor-mediated enhancement of collecting duct renin in angiotensin II-dependent hypertensive rats

2005 ◽  
Vol 289 (3) ◽  
pp. F632-F637 ◽  
Author(s):  
Minolfa C. Prieto-Carrasquero ◽  
Hiroyuki Kobori ◽  
Yuri Ozawa ◽  
Astrid Gutiérrez ◽  
Dale Seth ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Collecting Duct ◽  
Receptor Activation ◽  
Sodium Reabsorption ◽  
Mrna Levels ◽  
Ang Ii ◽  
Distal Nephron ◽  
Hypertensive Rats ◽  
Kidney Medulla ◽  
Collecting Ducts

Angiotensin II (ANG II)-infused rats exhibit increases in distal nephron renin expressed in principal cells of connecting tubules and collecting ducts. This study was performed to determine whether the augmentation of distal nephron renin involves ANG II type 1 (AT1) receptor activation. Male Sprague-Dawley rats (200–220 g) were divided into three groups: 1) sham operated ( n = 8); 2) ANG II infused (80 ng/min, 13 days, n = 8); and 3) ANG II infused plus AT1 receptor blocker (ARB), olmesartan (5 mg/days, n = 8). ANG II infusion increased systolic blood pressure (BP; 178 ± 4 vs. 122 ± 1 mmHg; P < 0.001) and suppressed plasma renin activity (PRA; 0.08 ± 0.1 vs. 5.3 ± 0.8 ng ANG I·ml−1·h−1). ARB treatment prevented the increase in BP (113 ± 6 mmHg) and led to increases in PRA (15.8 ± 1.5 ng ANG I·ml−1·h−1). Renin protein levels measured in the kidney medulla, to avoid contribution from juxtaglomerular appartus cells, were higher in ANG II-infused rats [1.64 ± 0.3 vs. 1.00 ± 0.1 densitometric units (DU) compared with sham-operated rats; P < 0.05], and ARB treatment prevented this increase (1.01 ± 0.1). Similarly, renin immunoreactivity increased in medullary collecting ducts of ANG II-infused compared with sham-operated rats (2.5 ± 0.3 vs. 1.0 ± 0.2 DU; P < 0.001), which was also prevented by ARB (1.01 ± 0.06). Renin qRTPCR in ANG II-infused rats showed higher mRNA levels in the kidney medulla compared with sham-operated rats (5.5 ± 2.3 vs. 0.04 ± 0.02 ratio to GAPDH mRNA levels; P < 0.001); however, renin transcript levels were normalized in the ARB-treated rats. These data demonstrate that the augmentation of distal nephron renin in ANG II-infused hypertensive rats is AT1 receptor mediated. The augmented distal tubular renin may contribute to increased intratubular ANG II levels and distal nephron sodium reabsorption in ANG II-dependent hypertension.

Glucocorticoids increase insulin-like growth factor-II mRNA accumulation in cultured human phaeochromocytoma cells

1994 ◽  
Vol 142 (1) ◽  
pp. 29-35 ◽  
Author(s):  
J Liu ◽  
A I Kahri ◽  
P Heikkilä ◽  
W F Blum ◽  
R Voutilainen
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Protein Kinase ◽  
Primary Cultures ◽  
Cdna Probe ◽  
Mrna Levels ◽  
Insulin Like Growth Factor ◽  
Mrna Accumulation ◽  
Cytoplasmic Rna ◽  
Factor Ii

Abstract Human phaeochromocytomas abundantly express insulin-like growth factor-II (IGF-II), but its regulation and biological role in these neoplasms is not known at present. To clarify the regulation of IGF-II gene expression in phaeochromocytomas, we studied the effects of glucocorticoids, nerve growth factor (NGF), and protein kinase A and C regulators in primary cultures of human phaeochromocytoma cells. Cytoplasmic RNA was extracted and analysed by Northern and dot blotting with a 32P-labelled cDNA probe for IGF-II. Dexamethasone treatment (500 ng/ml) for 3 and 7 days resulted in a 260% and 515% increase in the accumulation of IGF-II mRNA respectively. The stimulatory effect of dexamethasone was time-and dose-dependent. The increases in the 6·0 and 2·2 kb species of IGF-II mRNAs were the most apparent. Cortisol (1 μg/ml) increased the amount of IGF-II mRNA by threefold compared with the control. NGF (200 ng/ml), dibutyryl cyclic AMP (1 mm) and 12-O-tetradecanoyl phorbol-13-acetate (a protein kinase C activator; 100 ng/ml) had no significant effect on IGF-II mRNA levels. These data suggest that IGF-II gene expression in human phaeochromocytomas may be regulated by microenvironmental glucocorticoids. Journal of Endocrinology (1994) 142, 29–35

1 alpha,25-(OH)2 vitamin D3 enhances expression of the genes encoding Ca(2+)-binding proteins MRP-8 and MRP-14

1992 ◽  
Vol 262 (1) ◽  
pp. C235-C242 ◽  
Author(s):  
A. Sellmayer ◽  
S. M. Krane ◽  
A. J. Ouellette ◽  
J. V. Bonventre
Keyword(s):  
Gene Expression ◽  
Cell Differentiation ◽  
Calcium Binding ◽  
Binding Proteins ◽  
Myeloid Cell ◽  
Relative Increase ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Mrna Accumulation ◽  
Dihydroxyvitamin D3

Two closely related Ca(2+)-binding proteins, migration inhibitory factor-related protein (MRP)-8 and MRP-14, are synthesized under specific conditions of myeloid cell differentiation. Because 1 alpha,25-dihydroxyvitamin D3 [1,25-(OH)2D3] induces myeloid cell differentiation and expression of other S-100 class calcium-binding proteins, we examined the effects of 1,25-(OH)2D3 on MRP mRNA levels in human U-937 histiocytic lymphoma cells. 1,25-(OH)2D3 increased MRP-8 and MRP-14 mRNA levels in a time- and dose-dependent manner. MRP mRNA levels were maximal at 24 h and remained elevated for at least 96 h after exposure of the cells to 1,25-(OH)2D3. MRP-8 mRNA accumulation required 100- to 1,000-fold higher concentrations of 25-(OH)D3, which binds to the 1,25-(OH)2D3 intracellular receptor with 100- to 1,000-fold lower affinity. Other differentiating agents, dimethyl sulfoxide, retinoic acid, and dexamethasone, also increased levels of MRP-8 and MRP-14 mRNA. Phorbol myristate acetate enhanced MRP-14 mRNA levels to a greater extent than MRP-8 mRNA levels, suggesting differential regulation of MRP gene expression by protein kinase C. The 1,25-(OH)2D3-induced relative increase in MRP mRNA levels was not changed by a 1,000-fold reduction in extracellular [Ca2+]. Thus 1,25-(OH)2D3 is potentially a physiological modulator of MRP gene expression. Expression of the MRP-8 and MRP-14 genes may be important for differentiation of myeloid cells.

scholarly journals Superoxide, H2O2, and iron are required for TNF-α-induced MCP-1 gene expression in endothelial cells: role of Rac1 and NADPH oxidase

2004 ◽  
Vol 286 (3) ◽  
pp. H1001-H1007 ◽  
Author(s):  
Xi-Lin Chen ◽  
Qiang Zhang ◽  
Ruozhi Zhao ◽  
Russell M. Medford
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Nadph Oxidase ◽  
Gene Activation ◽  
Dominant Negative ◽  
Mrna Levels ◽  
Text Generation ◽  
Mrna Accumulation ◽  
Tnf Α ◽  
Diphenylene Iodonium

Reactive oxygen species (ROS) play an important but not yet fully defined role in the expression of inflammatory genes such as monocyte chemoattractant protein (MCP)-1. We used complementary molecular and biochemical approaches to explore the roles of specific ROS and their molecular linkage to inflammatory signaling in endothelial cells. Adenovirus-mediated expression of superoxide dismutase and catalase inhibited TNF-α-induced MCP-1 gene expression, suggesting important roles of superoxide ([Formula: see text]) and H2O2 in MCP-1 gene activation. In addition, the iron chelator 1,2-dimethyl-3-hydroxypyridin-4-one and the hydroxyl radical scavengers dimethylthiourea and dimethyl sulfoxide inhibited TNF-α-induced MCP-1 expression, suggesting important roles of iron and hydroxyl radicals in inflammatory signal activation. In contrast, scavenging of peroxynitrite with 5,10,15,20-tetrakis-(4-sulfonatophenyl)prophyrinato iron (III) chloride had no effect on TNF-α-induced MCP-1 expression. Inhibition of NADPH oxidase, the major oxidase responsible for [Formula: see text] generation, with diphenylene iodonium suppressed TNF-α-induced MCP-1 mRNA accumulation. Rac1 is an upstream signaling molecule for the activation of NADPH oxidase and [Formula: see text] generation. Expression of dominant negative N17Rac1 by adenovirus suppressed TNF-α-induced MCP-1 mRNA levels and MCP-1 protein secretion. Expression of N17Rac1 inhibited TNF-α-induced MCP-1 and NF-κB transcriptional activity. These data suggest that ROS such as superoxide and H2O2 derived from Rac1-activated NADPH oxidase mediate TNF-α-induced MCP-1 expression in endothelial cells.

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