Fo Transgenics for Studies of Transcriptional Control in vivo Tissue and Developmental—Specific Regulation of the Human and Rat Growth Hormone/Prolactin/Placental Lactogen Gene Family

2001 ◽  
pp. 79-103
Author(s):  
Peter A. Cattini ◽  
Mary Lynn Duckworth
Keyword(s):  
Growth Hormone ◽  
Gene Family ◽  
Transcriptional Control ◽  
Placental Lactogen ◽  
Rat Growth ◽  
Specific Regulation

scholarly journals Growth hormone protects against radiotherapy-induced cell death

2002 ◽  
pp. 535-541 ◽  
Author(s):  
O Madrid ◽  
S Varea ◽  
I Sanchez-Perez ◽  
L Gomez-Garcia ◽  
E De Miguel ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Cell Death ◽  
Hormone Receptor ◽  
Growth Hormone Receptor ◽  
Molecular Mechanisms ◽  
Dna Double Strand Breaks ◽  
Cell Viability Assay ◽  
Viability Assay ◽  
Rat Growth

BACKGROUND: In vivo treatment with growth hormone reduces radiation-associated mortality. The molecular mechanisms underlying this effect are unknown. It has been described that increased sensitivity to ionising radiation can be due to defects in machinery involved in detection and/or repair of DNA double-strand breaks. OBJECTIVE: To study the mechanisms involved in growth hormone action on the increased survival in irradiated cells. MATERIALS AND METHODS: CHO-4 cells stably expressing the growth hormone receptor were used. A cell viability assay was carried out to analyse the increase in survival induced by growth hormone in irradiated cells. To investigate whether the DNA repair mechanism could be implicated in this effect we performed DNA reactivation assays using pHIV-LUC and pCMV-betagal plasmids as control. Identical studies were also conducted using the radiomimetic drug, bleomycin. RESULTS: Growth hormone protects CHO-4 cells from bleomycin- and radiation-induced cell death. In pHIV-LUC transfected cells, a time-dependent decrease in luciferase activity was observed after irradiation in the absence of growth hormone. However, cells pretreated with this hormone maintained reporter activity. When cells were transfected with irradiated pHIV-LUC plasmid, only the hormone-treated cells recovered the transcriptional activity. CONCLUSIONS: Growth hormone exerts a radioprotective effect in CHO-4 cells stably transfected with the complementary DNA for the rat growth hormone receptor. The radioprotection is triggered directly by the hormone and it is also observed with bleomycin. The increased survival in response to radiation and bleomycin treatment induced by growth hormone correlates with an enhanced ability of the cells to repair damaged DNA.

The Human Placental Lactogen and Growth Hormone Multi-Gene Family

1988 ◽  
pp. 33-57
Author(s):  
Hugo A. Barrera-Saldanña ◽  
Ramiro Ramírez-Solís ◽  
William H. Walker ◽  
Susan L. Fitzpatrick ◽  
Diana Reséndez-Pérez ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Gene Family ◽  
Placental Lactogen ◽  
Human Placental Lactogen

scholarly journals RpoS-Dependent Transcriptional Control ofsprE: Regulatory Feedback Loop

2001 ◽  
Vol 183 (20) ◽  
pp. 5974-5981 ◽  
Author(s):  
Natividad Ruiz ◽  
Celeste N. Peterson ◽  
Thomas J. Silhavy
Keyword(s):  
Escherichia Coli ◽  
Stationary Phase ◽  
Intergenic Region ◽  
Feedback Loop ◽  
Transcriptional Control ◽  
Response Regulator ◽  
Phase Response ◽  
Specific Regulation ◽  
Regulatory Feedback Loop

ABSTRACT The stationary-phase response exhibited by Escherichia coli upon nutrient starvation is mainly induced by a decrease of the ClpXP-dependent degradation of the alternate primary ς factor RpoS. Although it is known that the specific regulation of this proteolysis is exercised by the orphan response regulator SprE, it remains unclear how SprE's activity is regulated in vivo. Previous studies have demonstrated that the cellular content of SprE itself is paradoxically increased in stationary-phase cells in an RpoS-dependent fashion. We show here that this RpoS-dependent upregulation of SprE levels is due to increased transcription. Furthermore, we demonstrate that sprE is part of the two-generssA-sprE operon, but it can also be transcribed from an additional RpoS-dependent promoter located in therssA-sprE intergenic region. In addition, by using an in-frame deletion in rssA we found that RssA does not regulate either SprE or RpoS under the conditions tested.

Regulation of immunity in rats by lactogenic and growth hormones

1983 ◽  
Vol 102 (3) ◽  
pp. 351-357 ◽  
Author(s):  
Eva Nagy ◽  
Istvan Berczi ◽  
Henry G. Friesen
Keyword(s):  
Growth Hormone ◽  
Contact Dermatitis ◽  
Blood Cells ◽  
Antibody Formation ◽  
Human Growth ◽  
Growth Hormones ◽  
Placental Lactogen ◽  
Bovine Growth Hormone ◽  
Human Placental Lactogen ◽  
Rat Growth

Abstract. Antibody formation to sheep red blood cells and the development of contact dermatitis in response to dinitrochlorobenzene are impaired in hypophysectomized (Hypo-X) rats. Rat prolactin, rat growth hormone, bovine prolactin, bovine growth hormone, human placental lactogen and human growth hormone all restored the immunological competence of Hypo-X animals. The possible mechanism of action of these hormones on immune reactions is discussed.

Placental Lactogen/Growth Hormone Gene Family

1993 ◽  
pp. 171-180
Author(s):  
Henry G. Friesen ◽  
May C. Robertson ◽  
Mary Lynn Duckworth ◽  
Ingo Schroedter ◽  
Ni Quan ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Gene Family ◽  
Placental Lactogen ◽  
Growth Hormone Gene

Effects of in Vivo Administration of Antiserum to Rat Growth Hormone on Body Growth and Insulin Responsiveness in Adipose Tissue

Endocrinology ◽  
1983 ◽  
Vol 112 (5) ◽  
pp. 1559-1566 ◽  
Author(s):  
INGRID GAUSE ◽  
STAFFAN EDEN ◽  
JOHN-OLOV JANSSON ◽  
OLLE ISAKSSON
Keyword(s):  
Growth Hormone ◽  
Adipose Tissue ◽  
Body Growth ◽  
Rat Growth ◽  
Insulin Responsiveness ◽  
In Vivo Administration

A direct growth effect of growth hormone in rat hindlimb shown by arterial infusion

1986 ◽  
Vol 250 (3) ◽  
pp. E231-E235 ◽  
Author(s):  
N. L. Schlechter ◽  
S. M. Russell ◽  
S. Greenberg ◽  
E. M. Spencer ◽  
C. S. Nicoll
Keyword(s):  
Growth Hormone ◽  
Direct Action ◽  
Intermittent Infusion ◽  
Systemic Effect ◽  
Growth Effect ◽  
Constant Infusion ◽  
Growth Effects ◽  
Rat Growth ◽  
The Right

We have developed a method for infusing substances into one hindlimb of the rat via the arterial supply. A catheter attached to an osmotic minipump is inserted into the right superior vesical artery and advanced to the junction of the right common iliac artery. This arrangement permits either constant or pulsatile infusion for 7 days. We employed this method to study the direct action of rat growth hormone (rGH) on the proximal tibial epiphysial plate in hypophysectomized rats. Infusion of neither the solvent nor ovine prolactin (2 micrograms X rat-1 X day -1) affected epiphysial plate width compared with control (uninfused) legs. The rGH infused at 0.4 and 2.0 micrograms X rat-1 X day-1 produced dose-related local growth effects that were of similar magnitude with either constant or pulsatile (eight 1-h pulses/day) infusion. However, the higher dose of rGH also resulted in a systemic effect (i.e., epiphysial plate growth in the uninfused limb), and the pulsatile mode produced a greater systemic effect than that produced by constant infusion. Our results indicate that GH can act directly on cartilage in vivo to maintain growth and that its effectiveness is not enhanced by pulsatile delivery. In contrast, the indirect (i.e., systemic) growth effects of the hormone may be enhanced by intermittent infusion. Our infusion system is well suited for studying the direct effect of substances on hindlimb tissues in conscious, unrestrained rats over extended periods.

Processing of the Primary Transcript for the Rat Growth Hormone Gene In Vivo

DNA ◽  
1988 ◽  
Vol 7 (8) ◽  
pp. 537-544 ◽  
Author(s):  
DAVID G. GARDNER ◽  
GUY CATHALA ◽  
NANCY Y.-C. LAN ◽  
YVONNE DAVID-INOUYE ◽  
JOHN D. BAXTER
Keyword(s):  
Growth Hormone ◽  
Growth Hormone Gene ◽  
Primary Transcript ◽  
Rat Growth
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