Heat stress and hydrocortisone are independent stimulators of triiodothyronine-induced growth hormone production in cultured rat somatotrophic tumour cells

1991 ◽  
Vol 124 (4) ◽  
pp. 417-424 ◽  
Author(s):  
Lawrence E. Shapiro ◽  
Claire P. Katz ◽  
Susan H. S. Wasserman ◽  
Charles R. DeFesi ◽  
Martin I. Surks

Abstract. We have reported that, in cultured GC cells, the stress of incubation at 41°C enhances thyroid hormone stimulation of growth hormone (GH) in a manner similar to the effects observed in a model of nonthyroidal disease in rats. Since glucocorticoids are potentially involved in stress responses both in vivo and in cell culture, we studied the role of glucocorticoid in the enhancement of (which are rat somatotrophic tumor cells) triiodothyronine (T3)-induced GH synthesis due to heat stress. Hydrocortisone addition increased T3-induced GH synthesis and GH mRNA content in cultured GC cells at both 37°C and 41°C. Depletion of glucocorticoid endogenous to serum supplement of the tissue culture medium did not prevent the enhancement of T3-induced GH synthesis that occurred during incubation at 41°C. The levels and affinity of glucocorticoid cytosolic receptors were not enhanced during incubation at 41°C. Lastly, no change in the sedimentation coefficient of the cytosolic glucocorticoid receptor or in its translocation into the nucleus occurred during incubation at 41°C. Thus, the enhancement of T3-induced GH production in GC cells by heat stress appeared independent of the effect of glucocorticoids and not mediated through glucocorticoid receptors.

2021 ◽  
Author(s):  
Yuanyuan Wang ◽  
S.M. Impa ◽  
Ramanjulu Sunkar ◽  
S.V. Krishna Jagadish
Keyword(s):  

1980 ◽  
Vol 95 (3) ◽  
pp. 319-327 ◽  
Author(s):  
Oddvar Naess ◽  
Egil Haug ◽  
Kaare Gautvik

Abstract. The effect of corticosterone and dexamethasone on the production of growth hormone and prolactin was studied in rat pituitary tumour cells (GH3-cells) in culture. Corticosterone and dexamethasone caused a dose-dependent stimulation of growth hormone synthesis, and the highest concentration (10−6 mol/l) increased growth hormone levels to 250% of controls. This concentration, however, decreased prolactin synthesis to 25% of the control values. The cytosol fractions from monolayer cultures as well as from tumours of GH3-cells were found to possess receptor molecules for glucocorticoid hormones, having a sedimentation constant close to 8 S in a salt-free buffer and 4 S in the presence of 0.5 mol/l KCL. Isoelectric point of the receptor was 5.8. Scatchard analysis showed one single class of binding sites with high affinity (Kd 2.1 ± 0.4 (sd × 10−9 mol/l). Studies on the steroid specificity revealed that dexamethasone had the highest affinity for the receptor. Corticosterone, cortisol and progesterone had also high affinity, whereas testosterone and oestradiol-17β had no significant affinity for the receptors. After in vivo administration of [3H]dexamethasone to GH3 tumour-bearing rats, radioactivity could be extracted from purified nuclei bound to 4 S macromolecules. The presence of receptors for glucocorticosteroid hormones in the GH3-cells, suggests that these hormones may alter growth hormone and prolactin production at the anterior pituitary level.


1992 ◽  
Vol 127 (5) ◽  
pp. 416-419 ◽  
Author(s):  
Koji Nakagawa ◽  
Tatsuya Ishizuka ◽  
Chikara Shimizu ◽  
Yoshito Ito ◽  
Ichiji Wakabayashi

There is increasing evidence to suggest that supraphysiological doses of glucocorticoids suppress growth hormone secretion in vivo by augmenting somatostatin release from the hypothalamus; previously, we reported an increase in hypothalamic somatostatin content in dexamethasone-treated rats. To further examine whether the production of somatostatin really is augmented, hypothalamic somatostatin mRNA levels were determined by the Northern blot technique in female rats receiving 330 μg of dexamethasone daily for three days. In two series of experiments, hypothalamic somatostatin mRNA levels in dexamethasone-treated rats were significantly (p<0.05) increased to 133±19 (mean±sd)% and 153±38% of the controls. In the dexamethasone-treated rats, plasma growth hormone levels were markedly suppressed compared with those of the controls. These results further support the hypothesis that pharmacological doses of glucocorticoids increase the production and release of somatostatin from the hypothalamus and thus inhibit growth hormone secretion, overriding the direct stimulatory effect of glucocorticoids on growth hormone production at the pituitary level.


2020 ◽  
Vol 18 (3) ◽  
pp. 168-178
Author(s):  
Devender Sharma ◽  
Jai Prakash Jaiswal ◽  
Navin Chander Gahtyari ◽  
Anjana Chauhan ◽  
Rashmi Chhabra ◽  
...  

AbstractGenetic improvement along with widened crop base necessitates for the detailed understanding of the genetic diversity and population structure in wheat. The present investigation reports the discovery of a total of 182 alleles by assaying 52 simple sequence repeats (SSRs) on 40 genotypes of bread wheat. Unweighted neighbour-joining method grouped these genotypes into two main clusters. Highly heat tolerant and intermediate tolerant cultivars were grouped in the same cluster, whereas remaining genotypes, particularly sensitive ones, were assigned different cluster. Similarly, the entire population was structured into two sub-populations (K = 2), closely corresponding with the other distance-based clustering patterns. The marker-trait association was discovered for four important physiological parameters, viz. canopy temperature depression, membrane thermostability index (MSI), normalized difference vegetation index and heat susceptibility index, indicating for heat stress (HS) tolerance in wheat. Both general and mixed linear models of association studies during 2017 and 2018, revealed the association of SSR markers, wmc222 (17.60%, PV) and gwm34 (20.70%, PV) with the mean phenotypic value of MSI. Likewise, SSR markers barc183, gwm75, gwm11 and cfd7 revealed a unique relationship with four selected physiological traits. Candidate genes discovered using in silico tools had nine SSR markers within the genic regions reported to play a role in heat and drought stress responses in plants. The information generated about these genic regions may be explored further in expression studies in-vivo to impart HS tolerance in bread wheat.


Microbiology ◽  
2011 ◽  
Vol 157 (6) ◽  
pp. 1816-1822 ◽  
Author(s):  
Samuele Peppoloni ◽  
Brunella Posteraro ◽  
Bruna Colombari ◽  
Lidia Manca ◽  
Axel Hartke ◽  
...  

Enterococcus faecalis is a significant human pathogen worldwide and is responsible for severe nosocomial and community-acquired infections. Although enterococcal meningitis is rare, mortality is considerable, reaching 21 %. Nevertheless, the pathogenetic mechanisms of this infection remain poorly understood, even though the ability of E. faecalis to avoid or survive phagocytic attack in vivo may be very important during the infection process. We previously showed that the manganese-cofactored superoxide dismutase (MnSOD) SodA of E. faecalis was implicated in oxidative stress responses and, interestingly, in the survival within mouse peritoneal macrophages using an in vivo–in vitro infection model. In the present study, we investigated the role of MnSOD in the interaction of E. faecalis with microglia, the brain-resident macrophages. By using an in vitro infection model, murine microglial cells were challenged in parallel with the wild-type strain JH2-2 and its isogenic sodA deletion mutant. While both strains were phagocytosed by microglia efficiently and to a similar extent, the ΔsodA mutant was found to be significantly more susceptible to microglial killing than JH2-2, as assessed by the antimicrobial protection assay. In addition, a significantly higher percentage of acidic ΔsodA-containing phagosomes was found and these also underwent enhanced maturation as determined by the expression of endolysosomal markers. In conclusion, these results show that the MnSOD of E. faecalis contributes to survival of the bacterium in microglial cells by influencing their antimicrobial activity, and this could even be important for intracellular killing in neutrophils and thus for E. faecalis pathogenesis.


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