Mechanism Of Induction Of Prolactin Synthesis In GH Cells
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Endocrine Pharmacology Summary - JU Medicine
GH -Stimulates lipolysis, elevates blood glucose -Enhances production of IGF-1 Prolactin -To develop lactation after birth -Inhibits release of GnRH (Increases during stress) -Inhibited by dopamine -Release is stimulated by oxytocin -Synthesis is enhanced by Estradiol -No therapeutic use, serum levels are measured to diagnose
The endocrine system
- other two hormones exert their influence on non-endocrine targets - GH, prolactin. a. growth hormone (GH) -protein. - stimulates virtually all cells of body to increase in size and divide, but main targets are bones (stimulation of epiphyseal plate growth) and skeletal muscle (stimulate increase in muscle mass).
The antiangiogenic factor 16K hPRL induces endothelial cell
The 16-kDa N-terminal fragment of human prolactin (16K hPRL) is a potent antiangiogenic factor that has been shown to prevent tumor growth in a xenograph mouse model. In this paper we first demonstrate that 16K hPRL inhibits serum-induced DNA synthesis in adult bovine aortic endothelial (ABAE) cells.
Mechanism of Induction of Prolactin Synthesis in GH Cells
n synthesis in GH cells zation). BRENNESSEL*)harmacology, Harvard Medical School, Boston, Massachusetts 02115 cells by TRH. However, PRL synthesis can be induced by treat-. ment of FiBGH12C1 cells with BrdUrd (7). Production of PRL by FiBGH12C1 cells after treatment with BrdUrd has been as-sociated with incorporation of the drug into DNA in
Hypothalamic/Pituitary Hormones Rana Estrogens Progesterone I
o The effects of GH are primarily mediated by insulin-like growth factor 1 (IGF-1), released from liver in response to GH. B. Disorders of Hypothalamic-Pituitary-Growth Hormone Axis Features of Growth Hormone Deficiency 1. In Children, results in short stature and adiposity, hypoglycemia. This is most commonly due to a deficiency of GHRH. 2.
The regulatory mechanism by which interleukin-6 stimulates GH
Since IL-6 and its receptors are presented in pituitary cells, and it can also stimulate GH secretion, whether or not and by which mechanisms IL-6 regulates GH synthesis still remains unclear. To address this question, in the present study, we examined the effect of IL-6 on human GH (hGH)-gene expression in GH3 rat pituitary tumor cells using
Over-Expression of GH/GHR in Breast Cancer and Oncosuppressor
GH and prolactin on physiological pathway and tumour induction. GH is a peptide hormone, synthesized, accumulated and secreted by the adenohypophysis. The numerous functions carried out by GH include regulation of body grow th, cell proliferation and differentiation and regulation of the
STRESS HORMONE SECRETION AND GUT SIGNAL TRANSDUCER (STAT
proinflammatory cytokine IL-6 production is increased in the gut, through a mechanism yet to be discovered. The increases of PRL, GC, and IL-6 synthesis are then integrated at the STAT5 phosphorylation levels in gut cells, and the resulting effect contributes to the loss of tissue integrity observed in gut after burn injury. In
Glucocorticoids and the preparation for life after birth: are
Collagen and elastin synthesis p-Adrenoreceptor induction Lung liquid re-absorption Structural maturation of alveoli Glycogen deposition Gluconeogenic enzyme induction IGF-gene expression ,%Adrenoreceptor induction Prolactin-receptor induction GH-receptor induction CBG synthesis Angiotensinogen-gene down-regulation
Thyroid glucocorticoid mRNA culturedGH1
GH1 cells that had been incubated with L-[3H]leucine (50,gCi/ml) for 2.5 hr (3). RESULTS Basedona 24-hr incubation, wepreviously reported (12) that, in the absence of thyroid hormone, cortisol inducednoincrease in growth hormone synthesis but in the presence of thyroid hormone, it increased the growth hormone synthesis rate an additional 2- to5
Nerve growth factor affects Ca2+ currents via the p75
In clonal pituitary GH 3 cells, spontaneous action potentials drive the opening of Ca v1(L-type) channels, leading to Ca2+ transients that are coupled to prolactin gene transcription. Nerve growth factor (NGF) has been shown to stimulate prolactin synthesis by GH 3 cells, but the underlying mechanisms are unknown. Here we studied whether NGF
Stimulation of GRP78 gene transcription by phorbol ester and
in GH3 Pituitary Cells THE ACCOMMODATION OF PROTEIN SYNTHESIS TO CHRONIC DEPRIVATION OF INTRACELLULAR SEQUESTERED CALCIUM* (Received for publication, May 9, 1991) Christopher R. Prostko, Margaret A. BrostromS, Eileen M. Galuska-Malara, and Charles 0. Brostrom From the Department of Pharmacobm.
ON THE MECHANISM OF 5-BROMODEOXYURIDINE INDUCTION OF PROLACTIN
induces prolactin synthesis in a clonal strain of rat pituitary tumor cells (GH,2C~), and in a substrain of GH~2C~ cells isolated by exposure of these cells to 30 /xg/ml BrdUrd. Prolactin synthesis in the BrdUrd resistant (BrdUr&) cells can be detected after 8-10 d of treatment with the drug (30 /~g/ ml).
Misfolded growth hormone causes fragmentation of the Golgi
growth hormone would alter trafficking of a plasma membrane protein, we cotransfected the cells with the thyrotropin-releasing hormone (TRH) receptor and either wild-type or ∆32-71 growth hormone. Cells expressing ∆32-71 growth hormone, unlike those expressing wild-type growth hormone, failed to show normal TRH receptor localization or binding.
Hepatic steroid hydroxylating enzymes are controlled by the
The GH receptor (GH-R) is a member of a receptor superfa-mily. Other members include receptors for prolactin, erythropoietin, and interleukin 2,4,6, and 7 (37). In addition to a plasma membrane receptor, a circulating GH-binding protein (GH-BP) with slightly lower affinity for GH, and en-coded by a shorter but highly homologous mRNA, has been
Calcium and Calmodulin Regulation of Prolactin Gene Expression
circumstances stimulate prolactin gene transcription with a resultant increase in mRNA levels. White et al. (1981) de- prived clonal GH, cells of extracellular calcium and then added calcium chlo- ride to the culture fluid, which resulted in over fivefold stimulation of prolactin mRNA levels.
1, Biagio Colori 2, Roberta Scanferlato
Increased protein synthesis by ribosomes GH is the main mediator of the postnatal growth of somatic cells (Le Roith et al. 2001), and its effects on cell growth and differentiation are mediated through Fig. 1. Growth hormone interacts with many genes (oncogenes and oncosuppressors) that are part of growth different mechanism. At the
The mechanism of reproduction and hormonal function in
lobe contains the corticotrophs (ACTH cells), the mammotrophs (prolactin cells, PRL cells), the somatotrophs (growth hormone cells, GH cells), the thyrotrophs (THS cells) and the gonadotrophs (LH/FSH cells). Many pioneering studies on the pituitary of fish were conducted by Madeleine Firstly two gonadotroph cell type
Control of follicular growth and development
Fig. 2. Receptor sites that are present on granulosa or theca cells. I = insulin, GFI = growth hormone, EGF = epidermal growth factor, IGF = insulin-like growth factor, IL, = 132-adren-ergic hormones. GABA = gamma amino butyric acid, PRL = prolactin. PG = prostaglandin, LIDL/LDL = high and low density lipoproteins, LI-I = luteinizing hormone.
Evidence for a role of calmodulin in the regulation of
GH, cells are a clonal line of rat pituitary tumor cells which make and secrete PRL and growth hormone (1). Numerous studies have shown that cytosolic Ca2+ plays a central role in the regulation of PRL secretion in these cells (cf. Refs. 2-8). Moreover, the Ca2+-binding protein, calmodulin, has been
Proc. Nati. Acad.Sci. USA74(1977) 125l-Prolactin 100r 801-D 60.SCu O 40 E E 201 NRS anti-Prolactin Unlabeled 0 prolactin, ng/tube 7 500500 L610 1000 C30 NMS anti-GH FIG. 1.
Triiodothyronine Stimulates Specifically Growth Hormone mRNA
rat pituitary tumor (GH3) cells directed, in a dose-related man-ner, the synthesis of proteins that were precipitated by antisera specific to rat growth hormone (somatotropin) and rat prolactin. A marked decrease in growth hormone secretion and growth hormone mRNA activity was observed when cells were grown in a medium deficient in thyroid hormone.
Role of the growth hormone IGF-1 axis in cancer
Keywords: autocrine GH breast cancer colon cancer epidemiology GH receptor growth hormone insulin-like growth factor-1 nuclear GH receptor prolactin prostate cancer signal transducer and activator of transcription-5 Role of the growth hormone IGF-1 axis in cancer Expert Rev. Endocrinol.
Late complications of childhood acute lymphoblastic leukaemia
Growth hormone GH was isolated from the bovine pituitary gland in 1944, and from the human pituitary in 1956. GH is secreted in an intermittent pulsatile pattern from the pituitary and is under the control of two interacting hypothalamic factors one stimulatory, growth hormone releasing hormone (GHRH) and the other inhibitory,
NICU Congenital Hypopit
(GH); GHIH has the opposite effect. GH maintains healthy body composition (muscle/fat mass) and growth Oxytocin: role in orgasm, the ability to trust, body temperature, sleep cycles, and the release of breast milk. Prolactin-releasing hormone (PRH) or prolactin-inhibiting hormone (PIH) (also known as
A Human Prolactin Antagonist, hPRL-G129R, Inhibits Breast
Gly 120 of hGH (19) plays a critical role in the action of GH in stimulating growth enhancement. The mechanism of these GH antagonists was further studied by other groups (22, 23). It is generally accepted that GH transduces its signal via a sequential receptor binding mechanism to form a one hormone-two recep-tor complex (22, 23).
Induction of Cisplatin Resistance by Hormones in Breast Cancer
Growth hormone: GH is a 23 kDa pituitary hormone with a similar structure to, and some overlapping functions with, PRL. Likewise, GH is also expressed in many extrapituitary sites . In addition to acting via its cognate receptor (GHR), a class 1 cytokine receptor, human GH (hGH) binds to and activates the hPRLR.
β-Cells at the crossroads: choosing between insulin granule
doi: 10.1111/j.1463-1326.2009.01107.x β-Cells at the crossroads: choosing between insulin granule production and proliferation Yanmei Liu,1,3 Hassan Mziaut,1 Anna Ivanova1,3 and Michele Solimena1,2,3
PHARMACOLOGY/THERAPEUTICS II BLOCK III HANDOUTS 2015 16
3. Hypothalamic-Pituitary-Growth Hormone Axis A. Physiological Actions of Growth Hormone (GH) In childhood GH promotes linear growth, growth of long bones, cartilage, muscle, : organ systems; it is a major determinant of adolescent growth spurt. In adulthood major effects are : metabolicIt increases protein synthesis and bone
Serum prolactin levels in women with rheumatoid arthritis
mechanism is not known, it is proposed that prolactin is secreted by synovial cells and lymphocytes which do have dopamine receptors. Also remission of arthritis with anti-prolactin drugs suggests the role of prolactin in rheumatoid arthritis. In conclusion, elevated serum prolactin levels in the cases of rheumatoid arthritis may
Does pituitary stalk compression cause hyperprolactinemia?
fore have a role in the induction and maintenance of the stalk pressure effect. Growth factors may also play an impor- tant part in prolactin secretion. Epidermal growth factor (EGF) increases prolactin gene expression, reduces growth hormone (GH) synthesis in GH 3 and GH4 cells, and is
Drugs Acting on The Endocrine System - Weebly
synthesis of adrenal steroid Used to diagnose and differentiate primary and secondary adrenal insufficiency TSH (thyroid-stimulating hormone/ Thyrotropin synthesis of thyroid hormones TRH (thyrotropin-releasing hormone) GH (growth hormone) growth and development of tissue Stimulates protein, carbohydrate, and lipid metabolism
Somatostatin-Dopamine Chimeric Molecules in Neuroendocrine
Feb 01, 2021 therapy for well-differentiated NENs . Due to the robust effect on prolactin (PRL) and growth hormone (GH) secretion inhibition, also dopamine agonists (DAs) were intensively studied in NENs [7,8]. Moreover, the relevant role of both somatostatin and dopamine systems is currently exploited for the diagnosis (68Ga-DOTATATE and 18F-DOPA PET)
Cell Cycle Features: Pituitary adenoma growth
growth.10,11 Intriguingly, although IL-6 stimulates DNA synthesis and cell number in the GH3 pituitary cell line, similar concentrations of IL-6 actually inhibit growth of normal rat pituitary cells.12 In several tumor types (ACTH, PRL-, GH-secreting and non-functioning adenomas), IL-6
Regulated Expression of the Prolactin Gene in Rat Pituitary
fusion of PRL+ cells with a nuclear monolayer of the PRL-, BrdUrdr GH cell strain. PRL production is a characteristic of 928-9b cells, but the level of PRL production (2-4 Ftg/mg protein/24 h) is much lowerthan that of thePRL+ strain, GH4C, (15-25 ,ug/mg protein/24 h). Levels of cytoplasmictranslatable mRNAPRL and cytoplasmicPRL
Growth hormone gene A regulation: a paradigm for cell-type
GH-expressing cells -,e first detected on embryonic day 16 while a stable population of prolactin-expressing cells is detected only 10 12 days after birth. Ablation experiments indicate that 80-90% of prolactip-expressmg cells are derived from GH-expressing cells by direct descent; however, a small
Induction of erythroid proliferation and diﬀerentiation by a
(EPO) is still lacking. Prolactin-like protein E (PLP-E) was recently found to stimulate expression of the adult beta major globin gene in mouse erythroleukemia cells. Here we demonstrate that PLP-E transiently expressed in COS-7 cells stimulates proliferation and erythroid diﬀeren-tiation of murine and human erythroid progenitor cell lines.