The decline in ACTH receptor mRNA expression in the baboon fetal adrenal gland in late gestation is not related to programmed cell death.

1996 ◽  
Vol 3 (2) ◽  
pp. 123A
Author(s):  
E ALBRECHT
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Adrenal Gland ◽  
Mrna Expression ◽  
Late Gestation ◽  
Receptor Mrna ◽  
Acth Receptor

Prolactin and the expression of suppressor of cytokine signaling-3 in the sheep adrenal gland before birth

2006 ◽  
Vol 291 (5) ◽  
pp. R1399-R1405 ◽  
Author(s):  
S. Gentili ◽  
J. S. Schwartz ◽  
M. J. Waters ◽  
I. C. McMillen
Keyword(s):  
Adrenal Gland ◽  
Mrna Expression ◽  
Tissue Growth ◽  
Late Gestation ◽  
Cytokine Signaling ◽  
Suppressor Of Cytokine Signaling ◽  
Subsequent Increase ◽  
Fetal Sheep

The fetal pituitary-adrenal axis plays a key role in the fetal response to intrauterine stress and in the timing of parturition. The fetal sheep adrenal gland is relatively refractory to stimulation in midgestation (90–120 days) before the prepartum activation, which occurs around 135 days gestation (term = 147 ± 3 days). The mechanisms underlying the switch from adrenal quiescence to activation are unclear. Therefore, we have investigated the expression of suppressor of cytokine signaling-3 (SOCS-3), a putative inhibitor of tissue growth in the fetal sheep adrenal between 50 and 145 days gestation and in the adrenal of the growth-restricted fetal sheep in late gestation. SOCS-3 is activated by a range of cytokines, including prolactin (PRL), and we have, therefore, determined whether PRL administered in vivo or in vitro stimulates SOCS-3 mRNA expression in the fetal adrenal in late gestation. There was a decrease ( P < 0.005) in SOCS-3 expression in the fetal adrenal between 54 and 133 days and between 141 and 144 days gestation. Infusion of the dopaminergic agonist, bromocriptine, which suppressed fetal PRL concentrations but did not decrease adrenal SOCS-3 mRNA expression. PRL administration, however, significantly increased adrenal SOCS-3 mRNA expression ( P < 0.05). Similarly, there was an increase ( P < 0.05) in SOCS-3 mRNA expression in adrenocortical cells in vitro after exposure to PRL (50 ng/ml). Placental and fetal growth restriction had no effect on SOCS-3 expression in the adrenal during late gestation. In summary, the decrease in the expression of the inhibitor SOCS-3 after 133 days gestation may be permissive for a subsequent increase in fetal adrenal growth before birth. We conclude that factors other than PRL act to maintain adrenal SOCS-3 mRNA expression before 133 days gestation but that acute elevations of PRL can act to upregulate adrenal SOCS-3 expression in the sheep fetus during late gestation.

Higher Expression of Whole Blood MicroRNA-21 in Patients with Ankylosing Spondylitis Associated with Programmed Cell Death 4 mRNA Expression and Collagen Cross-linked C-telopeptide Concentration

2014 ◽  
Vol 41 (6) ◽  
pp. 1104-1111 ◽  
Author(s):  
Chun-Huang Huang ◽  
James Cheng-Chung Wei ◽  
Wei-Chiao Chang ◽  
Shang-Yan Chiou ◽  
Chia-Hsuan Chou ◽  
...  
Keyword(s):  
Cell Death ◽  
Ankylosing Spondylitis ◽  
Programmed Cell Death ◽  
Mrna Expression ◽  
Whole Blood ◽  
Bone Erosion ◽  
Healthy Controls ◽  
Antiinflammatory Drugs ◽  
Programmed Cell Death 4 ◽  
Positive Correlations

Objective.Bone loss is a recognized feature of ankylosing spondylitis (AS). The binding of microRNA-21 (miR-21) to programmed cell death 4 (PDCD4) could inhibit the expression of PDCD4 and further induce the activation of osteoclasts. In the present study, we compared the difference in miR-21 expression between patients with AS and healthy controls, and evaluated the relationships of miR-21, PDCD4 mRNA, and bone erosion in patients with AS. The influences of nonsteroidal antiinflammatory drugs (NSAID) and disease-modifying antirheumatic drugs (DMARD) on the expressions of miR-21 and PDCD4 mRNA in patients with AS were also assessed.Methods.Whole blood miR-21 and PDCD4 mRNA expression were evaluated by quantitative real-time PCR among 122 patients with AS and 122 healthy controls. The serum level of collagen cross-linked C-telopeptide (CTX) was measured using ELISA.Results.When compared to controls, patients with AS had significantly higher levels of miR-21, PDCD4 mRNA, and CTX. MiR-21 expression was negatively correlated with PDCD4 mRNA expression in patients with AS who were taking neither NSAID nor DMARD. Interestingly, significantly positive correlations between miR-21 expression with PDCD4 mRNA expression (r = 0.33, p = 0.01) and CTX level (r = 0.44, p < 0.01) were observed in patients with AS who were taking sulfasalazine. Positive correlations of miR-21 and CTX level were also observed in AS patients with disease duration < 7.0 years (r = 0.36, p = 0.004) and active disease (r = 0.42, p = 0.001).Conclusion.The expression of miR-21 might have a role in the development of AS.

scholarly journals Increased lung preproET-1 and decreased ETB-receptor gene expression in fetal pulmonary hypertension

1998 ◽  
Vol 274 (4) ◽  
pp. L535-L541 ◽  
Author(s):  
D. Dunbar Ivy ◽  
Timothy D. Le Cras ◽  
Marilee P. Horan ◽  
Steven H. Abman
Keyword(s):  
Gene Expression ◽  
Pulmonary Hypertension ◽  
Smooth Muscle ◽  
Steady State ◽  
Mrna Expression ◽  
Receptor Gene ◽  
Ductus Arteriosus ◽  
Receptor Expression ◽  
Late Gestation ◽  
Receptor Mrna

Endothelin (ET)-1, a potent vasoconstrictor and smooth muscle mitogen, is produced from its precursor, preproET-1, by endothelin-converting enzyme (ECE)-1 activity. ET-1 may bind to two receptors, ETAand ETB, that mediate vasoconstriction and vasodilation in the ovine fetal lung, respectively. ET-1 contributes to high pulmonary vascular resistance in experimental perinatal pulmonary hypertension induced by ligation of the ductus arteriosus in the fetal lamb. Physiological studies in this model have demonstrated enhanced ETA- and diminished ETB-receptor activities and a threefold increase in lung immunoreactive ET-1 protein content. We hypothesized that increased ET production and an imbalance in receptor expression would favor vasoconstriction and smooth muscle cell hypertrophy in pulmonary hypertension and may be partially due to alterations in gene expression. To test this hypothesis, we studied lung mRNA expression of preproET-1, ECE-1, and the ETAand ETBreceptors in normal and hypertensive fetal lambs. Total RNA was isolated from whole lung tissue in normal late-gestation fetuses (135 ± 3 days; 147 days = term) and from animals with pulmonary hypertension after ductus arteriosus ligation for 8 days (134 ± 4 days). Ductus arteriosus ligation increased right ventricular hypertrophy [control 0.56 ± 0.02 vs. hypertension 0.85 ± 0.05; right ventricle/(left ventricle + septum); P < 0.05]. Northern blot analysis was performed using cDNA probes and was normalized to the signal for 18S rRNA. We found a 71 ± 24% increase in steady-state preproET-1 mRNA ( P < 0.05) and a 62 ± 5% decrease in ETBmRNA ( P < 0.05) expression in ductus arteriosus ligation. ECE-1 and ETA-receptor mRNA expression did not change. We conclude that chronic intrauterine pulmonary hypertension after ductus arteriosus ligation increases steady-state preproET-1 mRNA and decreases ETB-receptor mRNA without changing ECE-1 mRNA or ETA-receptor mRNA expression. These findings suggest that increased ET-1 production and decreased ETB-receptor expression may contribute to increased vasoconstrictor tone in this experimental model of neonatal pulmonary hypertension.

scholarly journals Methods to measure calcitonin receptor activity, up-regulated in cell stress, apoptosis and autophagy

F1000Research ◽  
2021 ◽  
Vol 10 ◽  
pp. 1019
Author(s):  
Peter Wookey ◽  
Pragya Gupta ◽  
Lucas Bittencourt ◽  
Shane Cheung ◽  
David Hare ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Cell Stress ◽  
Data Sets ◽  
Apoptotic Cells ◽  
Calcitonin Receptor ◽  
Receptor Mrna ◽  
Receptor Isoforms ◽  
High Fluorescence Intensity ◽  
High Fluorescence

The expression of the calcitonin receptor (CT Receptor) is widespread throughout the life cycle of mammals and in many diseases, and in these contexts the functions of the common isoforms is largely unknown. The relatively recent development of anti-CT Receptor antibodies that bind separate epitopes on the CTa Receptor and CTb Receptor isoforms has advanced our knowledge and understanding of these events. CT Receptor at the protein level is upregulated in programmed cell death including apoptosis (as described in a previous publication) and autophagy, which is discussed in our upcoming, unpublished review. Incomplete data sets are cited in this review on the upregulation of CACLR (encoding CT Receptor) mRNA, in particular the insert-positive isoform (CTb Receptor), in response to cell stress. Cell stress is induced by growth in depleted foetal bovine serum (dFBS) or without FBS, both of which induce degrees of starvation and autophagy, or dFBS plus staurosporine, which induces apoptosis. Details of the methods deployed to generate these data are described here including measurement of the upregulation of CTb Receptor mRNA with qPCR and nanopore long range sequencing. An anti-CT Receptor antibody also known as CalRexinTM, which binds an epitope in the N-terminal domain, was conjugated to either fluorophore 568, which is accumulated into apoptotic cells as previously reported, or pHrodo Red, a pH dependent fluorescent dye, which is accumulated into autophagic and apoptotic cells.  These conjugates are under development to image programmed cell death. The methods for conjugation and high content imaging on the Operetta platform are described. The high fluorescence intensity at low pH of CalRexin:pHrodo Red in both autophagic and apoptotic cells suggests localisation in autophago-lysosomes and lysosomes respectively. Overall, these observations and the methods that underpin them have contributed to our understanding of the widespread expression of CT Receptor isoforms.

scholarly journals Effect of Thermal Stimulation on Gene Expression Related to Skeletal Muscle-derived Cell Density

2021 ◽  
pp. 73-81
Author(s):  
Masayo Nagai ◽  
Hidesuke Kaji
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Cell Death ◽  
Cell Adhesion ◽  
Cell Growth ◽  
Programmed Cell Death ◽  
Mrna Expression ◽  
Thermal Stimulation ◽  
Heat Stimulation ◽  
Stimulation Of

Aims: Our previous study demonstrated favorable changes in plasma protein levels such as adiponectin by fomentation in healthy people. We also reported that the thermal stimulation caused changes of mRNA levels to prevent atherosclerosis in human skeletal muscle-derived cell (SMDC). However, cell number decreased to 74.6% by heat stimulation. In order to clarify this mechanism, we investigated whether the heat stimulation affects the levels of mRNA related to cell density or number of SMDC. Study Design: Experimental study comparing transcriptome between cells cultured at higher temperature and control cells. Place and Duration of Study: From September 2015 to March 2017, Division of Physiology and Metabolism, University of Hyogo. Methodology: SMDC was cultured at 42°C and 37°C and its gene expression was analyzed by using microarray technique. Results: Thermal stimulation of SMDC significantly altered the expression of 10 genes related to apoptosis, 1 gene related to cell division and 1 gene related to cell adhesion. mRNA expression of apoptosis promoting gene, such as THAP2 (THAP domain containing, apoptosis associated protein 2), PDCD6 (programmed cell death 6), BCL2L13 (BCL2-like 13), LOC728613 (programmed cell death 6 pseudogene), CASP4 (caspase 4), and FAS (Fas cell surface death, receptor) was up-regulated. On the other hand, PAWR (PRKC, apoptosis, WT1, regulator) was downregulated, and mRNA expression of anti-apoptotic genes, such as NOL3 (nucleolar protein 3), CIAPIN1 (cytokine-induced apoptosis inhibitor 1) and NAIF1 (nuclear apoptosis inducing factor1), was up-regulated, Gene Ontology analysis showed alterations in the expression of genes that promote apoptosis and cell growth inhibition. Pathway analysis demonstrated the pathways that promote apoptosis, stimulate cell growth and negatively or positively regulate cell adhesion. Conclusion: The present study suggested that thermal stimulation of SMDC might predominantly promote apoptosis from consistent changes in related gene expression by any analysis.

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