The effects of interleukin-1 and prostaglandin E 2 on accumulation of collagen and steady-state levels of proα1(I) collagen messenger RNA in experimental granulation tissue in rats

1997 ◽  
Vol 289 (4) ◽  
pp. 219-223 ◽  
Author(s):  
Kari Rapala ◽  
Jyrki Heino ◽  
Juha Peltonen ◽  
M. Laato
Keyword(s):  
Steady State ◽  
Granulation Tissue ◽  
Messenger Rna ◽  
Interleukin 1 ◽  
Prostaglandin E ◽  
Steady State Levels

Expression of the Caeruloplasmin Gene in the Adult and Neonatal Rat Liver

1989 ◽  
Vol 77 (3) ◽  
pp. 259-263 ◽  
Author(s):  
L. Barrow ◽  
M. S. Tanner ◽  
D. R. Critchley
Keyword(s):  
Steady State ◽  
Rat Liver ◽  
Messenger Rna ◽  
Wilson’S Disease ◽  
Wilson's Disease ◽  
Serum Copper ◽  
Neonatal Rat ◽  
Neonatal Rats ◽  
Significant Difference ◽  
Steady State Levels

1. It has been suggested that low levels of serum caeruloplasmin in Wilson's disease result from the failure to switch from a fetal to an adult mode of caeruloplasmin gene expression. To investigate postnatal expression of the caeruloplasmin gene, steady-state levels of caeruloplasmin messenger RNA in adult and neonatal rat liver were measured. 2. Copper parameters observed in neonatal rats were similar to those seen in Wilson's disease: hepatic copper concentration was significantly elevated (neonatal 164 ± 35 μg/g, adults 50 ± 8 μg/g, P < .001) and serum copper and caeruloplasmin levels were low (neonatal 0.5 ± 0.1 μg/ml, adults 1.3 ± 0.2 μg/ml, P < .001; neonatal 0.20 ± 0.04 arbitrary units, adults 0.69 ± 0.16 arbitrary units, P < .001), respectively. 3. Caeruloplasmin messenger RNA levels were analysed by Northern and dot blotting using a 12P-labelled caeruloplasmin complementary DNA probe. A caeruloplasmin messenger RNA of approximately 4.4 kilobases was detected in both adult and neonatal rat liver, with no significant difference observed in steady-state levels. 4. A step subsequent to caeruloplasmin gene transcription must therefore be impaired in neonatal rats.

scholarly journals Regulation of Pituitary Corticotropin-Releasing Hormone-Binding Protein Messenger Ribonucleic Acid Levels by Restraint Stress and Adrenalectomy**This work is supported by National Institutes of Health Grant DK-42730 (to A.F.S) and by a Young Investigator Award (to A.F.S.) from the National Alliance for Research on Schizophrenia and Depression.

Endocrinology ◽  
1998 ◽  
Vol 139 (11) ◽  
pp. 4435-4441 ◽  
Author(s):  
Shanna J. McClennen ◽  
Daniel N. Cortright ◽  
Audrey F. Seasholtz
Keyword(s):  
Steady State ◽  
Stress Response ◽  
Messenger Rna ◽  
Restraint Stress ◽  
Adrenal Axis ◽  
Acute Restraint Stress ◽  
Steady State Levels ◽  
Hypothalamus Pituitary Adrenal Axis ◽  
Pituitary Adrenal Axis ◽  
Acth Release

Abstract CRH is the primary hypothalamic regulator of the stress response in higher organisms, where it acts as the key mediator of ACTH release in the hypothalamus-pituitary-adrenal axis. The 37-kDa CRH-binding protein (CRH-BP) is known to bind CRH and antagonize CRH-induced ACTH release in vitro. The expression of this protein in anterior pituitary corticotrophs suggests a role for CRH-BP in modulation of the stress response. To investigate the in vivo role of rat CRH-BP, the regulation of pituitary CRH-BP gene expression by acute restraint stress and/or adrenalectomy was examined using ribonuclease protection assays. After restraint stress, steady-state levels of CRH-BP transcripts increase two to three times over basal level and remain significantly higher than basal levels for 120 min after the start of restraint. Adrenalectomy decreases CRH-BP messenger RNA steady-state levels to 8% of control levels. These results demonstrate that pituitary CRH-BP messenger RNA levels are increased in response to acute restraint stress and that glucocorticoids play a significant role in this positive regulation. These data also suggest that increased CRH-BP levels, in response to stress, may modulate the endocrine stress response by providing an additional feedback mechanism to maintain homeostasis of the hypothalamus-pituitary-adrenal axis.

scholarly journals Down-regulation of actin genes precedes microfilament network disruption and actin cleavage during p53-mediated apoptosis

1997 ◽  
Vol 110 (4) ◽  
pp. 489-495 ◽  
Author(s):  
I. Guenal ◽  
Y. Risler ◽  
B. Mignotte
Keyword(s):  
Steady State ◽  
Interleukin 1 ◽  
Simian Virus 40 ◽  
State Level ◽  
Simian Virus ◽  
T Antigen ◽  
Mrna Levels ◽  
Down Regulation ◽  
Actin Genes ◽  
Steady State Levels

Inactivation of Simian Virus 40 large T antigen, in cells immortalized with conditional mutants, leads to activation of p53 and apoptosis. We used the mRNA differential display method to identify genes differentially expressed during this process. We found that steady-state levels of mRNA for cytoplasmic actins decreased early during apoptosis. We also showed that, although the steady-state level of the corresponding proteins is not profoundly affected, they are substrates for an interleukin 1-beta converting enzyme (ICE)-like protease activated during the process. However, only a very small fraction of actin is proteolysed during the early stages of apoptosis. The microfilament network is affected and non polymerized actin accumulates in apoptotic bodies after the decrease of mRNA levels, but before a significant amount of actin is cleaved. This suggests that down-regulation of actin genes may be involved in microfilament rearrangements during p53-mediated apoptosis.

scholarly journals Levels of messenger RNA encoding ovarian receptors for FSH and LH in cattle during superovulation with equine chorionic gonadotrophin versus FSH

1998 ◽  
Vol 156 (2) ◽  
pp. 373-378 ◽  
Author(s):  
K Soumano ◽  
JG Lussier ◽  
CA Price
Keyword(s):  
Steady State ◽  
Messenger Rna ◽  
Chorionic Gonadotrophin ◽  
Corpora Lutea ◽  
Mrna Levels ◽  
Slot Blot ◽  
Lh Receptor ◽  
Prostaglandin F2 Alpha ◽  
Steady State Levels ◽  
Slot Blot Analysis

This study tested the hypothesis that luteal LH receptor (LHr) and follicular LHr and FSH receptor (FSHr) steady-state mRNA levels are greater during superovulation with equine chorionic gonadotrophin (eCG) compared with that with FSH. Heifers were stimulated with eCG (n = 10) or FSH (n = 10), and ovaries were recovered the day before and at 12 and 24 h after luteolysis was induced with prostaglandin F2 alpha (PGF2 alpha). Total RNA was purified from individual follicles and corpora lutea. Steady-state levels of LHr and FSHr mRNA were assessed by slot blot analysis employing homologous cDNA probes. There were no differences in luteal LHr between FSH- and eCG-stimulated animals before luteolysis, and hybridization signals were detected in only one of six animals by 12 h after injection of PGF2 alpha. After PGF2 alpha injection, steady-state levels of follicular LHr were 4-fold lower (P < 0.05) and follicular FSHr mRNA levels were 2.4-fold lower (P < 0.05) in eCG- compared with FSH-treated cattle. In eCG-treated animals, induction of luteolysis led to a significant increase in follicular LHr mRNA levels (P < 0.01) and a significant decrease in follicular FSHr mRNA levels (P < 0.01). There was no such effect of luteolysis in FSH-treated animals. We conclude that superovulation with eCG, compared with FSH, results in lower follicular levels of LHr and FSHr mRNA but does not affect luteal LHr mRNA levels.

Differences in the steady-state levels of c-fos, c-jun and c-myc messenger RNA during mitogen-induced liver growth and compensatory regeneration

Hepatology ◽  
1993 ◽  
Vol 17 (6) ◽  
pp. 1109-1116 ◽  
Author(s):  
Pierpaolo Coni ◽  
Gabriella Simbula ◽  
Alessandra Carcereri de Prati ◽  
Marta Menegazzi ◽  
Hisanori Suzuki ◽  
...  
Keyword(s):  
Steady State ◽  
Messenger Rna ◽  
Liver Growth ◽  
Steady State Levels ◽  
Compensatory Regeneration
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