Rat glomerulosa cells in primary culture and E. coli lipopolysaccharide action

Salamanca, Andrés Bordalí; Garcı́a, R.

doi:10.1016/s0960-0760(03)00134-1

Cited by 8 publications

(4 citation statements)

References 28 publications

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“…Although there is little published data on the adrenal MC2R and how LPS may affect it, there is some suggestion that LPS may directly influence the MC2R-mediated GC response. LPS can suppress the ACTH-induced GC response in fasciculata reticularis and glomerulosa cells 27 28 . Prior exposure to LPS can induce endotoxin tolerance in the adrenal, with the corticosterone response to LPS or ACTH being suppressed in primary fasciculata reticularis cells from rats that had previously been given LPS 29 .…”

Section: Discussionmentioning

confidence: 99%

Overfeeding during a critical postnatal period exacerbates hypothalamic-pituitary-adrenal axis responses to immune challenge: a role for adrenal melanocortin 2 receptors

Cai

Ziko

Barwood

et al. 2016

Sci Rep

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Early life diet can critically program hypothalamic-pituitary-adrenal (HPA) axis function. We have previously shown rats that are overfed as neonates have exacerbated pro-inflammatory responses to immune challenge with lipopolysaccharide (LPS), in part by altering HPA axis responses, but how this occurs is unknown. Here we examined neonatal overfeeding-induced changes in gene expression in each step of the HPA axis. We saw no differences in glucocorticoid or mineralocorticoid receptor expression in key regions responsible for glucocorticoid negative feedback to the brain and no differences in expression of key HPA axis regulatory genes in the paraventricular nucleus of the hypothalamus or pituitary. On the other hand, expression of the adrenal melanocortin 2 receptor (MC2R) is elevated after LPS in control rats, but significantly less so in the neonatally overfed. The in vitro adrenal response to ACTH is also dampened in these rats, while the in vivo response to ACTH does not resolve as efficiently as it does in controls. These data suggest neonatal diet affects the efficiency of the adrenally-mediated response to LPS, potentially influencing how neonatally overfed rats combat bacterial infection.

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Section: Discussionmentioning

confidence: 99%

Overfeeding during a critical postnatal period exacerbates hypothalamic-pituitary-adrenal axis responses to immune challenge: a role for adrenal melanocortin 2 receptors

Cai

Ziko

Barwood

et al. 2016

Sci Rep

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“…A primary adrenal cell isolation protocol was adapted as described previously (Enríquez de Salamanca and García, 2003;Supornsilchai et al, 2005). In brief, mouse adrenal glands were removed, and the attached fat tissue was trimmed off.…”

Section: Methodsmentioning

confidence: 99%

The High-Affinity cAMP-Specific Phosphodiesterase 8B Controls Steroidogenesis in the Mouse Adrenal Gland

Tsai¹,

Shimizu‐Albergine²,

Beavo³

2010

Mol Pharmacol

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The functions of the phosphodiesterase 8B (PDE8) family of phosphodiesterases have been largely unexplored because of the unavailability of selective pharmacological inhibitors. Here, we report a novel function of PDE8B as a major regulator of adrenal steroidogenesis using a genetically ablated PDE8B mouse model as well as cell lines treated with either a new PDE8-selective inhibitor or a short hairpin RNA (shRNA) construct against PDE8B. We demonstrate that PDE8B is highly enriched in mouse adrenal fasciculata cells, and show that PDE8B knockout mice have elevated urinary corticosterone as a result of adrenal hypersensitivity toward adrenocorticotropin. Likewise, ablation of PDE8B mRNA transcripts by an shRNA construct potentiates steroidogenesis in the commonly used Y-1 adrenal cell line. We also observed that the PDE8-selective inhibitor (PF-04957325) potentiates adrenocorticotropin stimulation of steroidogenesis by increasing cAMP-dependent protein kinase activity in both primary isolated adrenocortical cells and Y-1 cells. It is noteworthy that PDE8s have their greatest control under low adrenocorticotropin-stimulated conditions, whereas other higher K m PDE(s) modulate steroidogenesis more effectively when cells are fully stimulated. Finally, both genetic ablation of PDE8B and long-term pharmacological inhibition of PDE8s cause increased expression of steroidogenic enzymes. We conclude that PDE8B is a major regulator of one or more pools of cAMP that promote steroidogenesis via both short-and long-term mechanisms. These findings further suggest PDE8B as a potential therapeutic target for the treatment of several different adrenal diseases.

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“…Contradictory in vitro data exists on whether TLR can directly influence cortisol secretion from adrenocortical cells. Bacterial LPS, a ligand for TLR-4, was found to directly stimulate cortisol release from human adrenocortical cell line NCI-H295R [16] , whereas another study documented that LPS in fact inhibits ACTH-induced corticosterone secretion in rat adrenocortical cells [17] . Nevertheless, TLRs are expressed in mice, rat and human adrenal cortex and adrenocortical cell lines ( fig.…”

Section: The Link Between Tlrs Hpa Axis Function and Malfunctioning mentioning

confidence: 98%

Toll-Like Receptors in Endocrine Disease and Diabetes

Kanczkowski

Ziegler

Zacharowski

et al. 2008

Neuroimmunomodulation

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The body’s ability to keep a steady homeostatic state is crucial to health and life. This involves providing an adequate response to a variety of challenges both physical and mental, such as microbial invasion and emotional distress. Interplay between the neuroendocrine and immune systems is essential in either case. Studies have demonstrated that toll-like receptors, or TLRs, play a regulatory role in both systems, and have been proposed as a possible link between the immune, hormonal and metabolic systems. As part of the innate immune system, these receptors control the identification by the body of microbial invaders and its immediate reaction in immune and inflammatory response. What are referred to as pattern recognition receptors are mostly expressed by cells involved in hematopoietic linkage, but an increasing number of studies have demonstrated their expression in other cell types such as neurons and endocrine cells on the hypothalamic-pituitary-adrenal (HPA) axis, thyrocytes, adipocytes and islets of Langerhans. Together with endocrine and metabolic dysregulation, immune system overreaction is often associated with infection and autoimmunity, clearly indicating TLR involvement at organ level which affects organ function. Several diseases such as autoimmune thyroid and pancreatic diseases, septic dysregulation of the HPA axis, diabetes and the metabolic syndrome have been linked to TLR activation and polymorphism. To gain insight into stress response and adaptation, we need to know more about TLRs and the specific physiological role they play in the endocrine and metabolic system and its processes.

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Rat glomerulosa cells in primary culture and E. coli lipopolysaccharide action

Cited by 8 publications

References 28 publications

Overfeeding during a critical postnatal period exacerbates hypothalamic-pituitary-adrenal axis responses to immune challenge: a role for adrenal melanocortin 2 receptors

Overfeeding during a critical postnatal period exacerbates hypothalamic-pituitary-adrenal axis responses to immune challenge: a role for adrenal melanocortin 2 receptors

The High-Affinity cAMP-Specific Phosphodiesterase 8B Controls Steroidogenesis in the Mouse Adrenal Gland

Toll-Like Receptors in Endocrine Disease and Diabetes

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