Functional and morphological changes associated with the ageing of primary cultures of embryonic adrenal gland cells derived from the Pekin duck

1992 ◽  
Vol 269 (3) ◽  
pp. 535-545 ◽  
Author(s):  
James Cronshaw ◽  
M. A. Collie ◽  
W. N. Holmes
1992 ◽  
Vol 268 (1) ◽  
pp. 157-165 ◽  
Author(s):  
James Cronshaw ◽  
B. K. Reese ◽  
M. A. Collie ◽  
W. N. Holmes
Keyword(s):  

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Tao Chen

Abstract Recent studies have shown that obesity is a major risk factor for idiopathic hyperaldosteronism (IHA). IHA patients have greater AGV than normal controls. However, it is unclear whether such changes are caused by obesity and whether losing weight could reverse the morphological and functional abnormalities of the adrenal gland. This study was to investigate the association of obesity with adrenal gland volume (AGV) and the effects of weight loss on AGV. This study recruited obese patients (N=25) who underwent sleeve gastrectomy and age- and sex-matched normal-weight (N=25) and overweight healthy volunteers (HV) (N=21). Thin-slice computed tomography was used to evaluate adrenal morphological changes. AGV was measured semiautomatically based on the digital imaging and communications in medicine (DICOM) image. The effects of weight loss on AGV were evaluated in patients for one year or more after sleeve gastrectomy. The results showed that left, right and total AGV were larger in obese patients than those in overweight and normal- weight HVs (6.77±0.36, 5.76±0.31, and 12.53±0.64 cm3 vs. 3.88±0.14, 3.09± 0.13 and 6.97± 0.24 cm3 vs. 3.38±0.23, 2.67±0.15 and 6.04±0.36 cm3). No statistically significant difference was identified between overweight and normal-weight HVs. Sleeve gastrectomy significantly reduced body weight (-27.1±2.5 kg), left AGV (-0.80±0.26 cm3), and right AGV (-0.88±0.20 cm2). However, the adrenal volume in five patients was not reduced, despite significant weight loss postsurgery. In brief, obesity leads to increased AGV, and in some cases, this effect seems to be irreversible. We speculate that obesity causes permanently adrenal morphological changes (increased volume or hyperplasia), and under certain circumstances, it results in excessive aldosterone secretion via altered adipokines (leptin, CTRP1, etc.).


The adrenal gland is an endocrine gland, which in the process of organogenesis is formed from ecto- and mesoderm derivatives. The mechanisms that make cell types of different origins unite, migration routes, and cell interactions are still not fully understood. One of the tools for studying these mechanisms is the primary cell culture obtained from the adrenal gland. The aim of our work was to compare the morphological features of primary cell cultures of model animals belonging to different orders – pigs, rabbits and mice in vitro under various cultivation conditions (growth surface pattern, presence of growth factors), as well as developing methodological approaches for obtaining and maintaining primary cultures of adrenal cell of neonatal animals. Cultivation was performed under standard conditions of temperature and humidity, carbon dioxide concentration, on culture surfaces with normal and reduced adhesiveness in a nutrient medium DMEM enriched with 10% fetal calf serum (FTS) or growth supplements B-27 and FGF. It was established that cell cultures of adrenal neonatal rabbits and piglets that were cultured under conditions of normal adhesion and using FCS had a heterogeneous composition, and were presented as a monolayer consisting of cells of several morphological types, and multicellular spheroids (MS). When cultivated on the surface with reduced adhesive properties in cultures of adrenal glands of piglets and rabbits, a cell monolayer was not formed, but flotation MCs were formed. After transferring MCs of both species to the adhesive culture surface on day 14, cell eviction, their migration from the MCs and formation of a monolayer are observed. Similar stages in the development of primary cell cultures derived from rabbits and piglets suggest the existence of a universal cellular composition in the neonatal adrenal glands of these species and allow applying the same approaches to the primary cultures derived from them. Unlike other studied species, monolayer and MS formation does not occur in cell cultures of mouse neonatal adrenal glands. Cultures consist of single attached and floating cells and small cell aggregates.


2014 ◽  
Vol 16 (73) ◽  
pp. 416 ◽  
Author(s):  
Noura Gannouni ◽  
Abada Mhamdi ◽  
Michèle El May ◽  
KhémaisBen Rhouma ◽  
Olfa Tebourbi

Endocrinology ◽  
2012 ◽  
Vol 153 (2) ◽  
pp. 721-731 ◽  
Author(s):  
Yewei Xing ◽  
William E. Rainey ◽  
John W. Apolzan ◽  
Omar L. Francone ◽  
Ruth B. S. Harris ◽  
...  

Very low-density lipoproteins (VLDL) are a class of large lipoprotein synthesized in the liver. The key function of VLDL, in vivo, is to carry triglyceride from the liver to adipose tissue. As a steroidogenic organ, the adrenal gland mainly uses lipoproteins as sources of cholesterol. Although VLDL receptors have been detected in the human adrenal, the function of VLDL in the adrenal gland remains unknown. Herein, we used primary cultures of human and bovine adrenal cells and the adrenocortical cell line H295R as models to determine the effects of VLDL on adrenal steroidogenesis. Our studies revealed that VLDL significantly increased aldosterone synthesis in all of the models tested. This increase was largely due to VLDL's stimulation of the expression of steroidogenic acute regulatory (StAR) protein and aldosterone synthase (CYP11B2). VLDL increased CYP11B2 mRNA expression in a concentration-dependent manner. Effects of VLDL on CYP11B2 transcript levels were not additive with angiotensin II or potassium but were additive with the cAMP pathway agonists ACTH and forskolin. Nifedipine completely inhibited the effects of VLDL on CYP11B2 mRNA, suggesting that calcium is the main signal transduction pathway used by VLDL in adrenal cells. Indeed, VLDL increased cytosolic free calcium levels. An in vivo study conducted in sucrose-fed rats showed a positive correlation between elevated triglyceride (VLDL) levels in plasma and CYP11B2 expression in the adrenal. In conclusion, we have shown that VLDL can stimulate aldosterone synthesis in adrenocortical cells by increasing StAR and CYP11B2 expression, an event likely mediated by a calcium-initiated signaling cascade.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Hubert Stangl ◽  
Anita Krammetsvogl ◽  
Martin Lesiak ◽  
Christine Wolff ◽  
Rainer H. Straub

Abstract In experimental arthritis, glucocorticoid secretion is inadequate relative to inflammation. We hypothesized that IL-1 is a key factor for inadequate glucocorticoid secretion in arthritic rats. Collagen type II—induced arthritis (CIA) in DA rats was the model to study effects of IL-1 on adrenal function. In the CIA model, an increase of intraadrenal MHCII-positive cells was observed. MHCII-positive cells or bone marrow-derived dendritic cells inhibited glucocorticoid secretion of adrenal gland cells. IL-1, but also IL-18 and the inflammasome were critical in glucocorticoid inhibition. Arthritic compared to control adrenal gland cells produced higher amounts of CXC chemokines from MHCII+ adrenal cells, particularly CINC-2, which is strongly dependent on presence of IL-1. In CIA, macrophages and/or dendritic cells inhibit glucocorticoid secretion via IL-1 in adrenal glands. These findings show that activated macrophages and/or dendritic cells inhibit glucocorticoid secretion in experimental arthritis and that IL-1β is a decisive factor.


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