Expression of glucocorticoid receptor mRNA and protein in the olfactory mucosa: Physiologic and pathophysiologic implications

Robinson, A. H. N.; Kern, Robert C.; Foster, James D.; Fong, Karen; Pitovski, Dimitri Z.

doi:10.1097/00005537-199808000-00026

Cited by 50 publications

(48 citation statements)

References 21 publications

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“…In our sections of OE from mice, supporting cells and ORNs were positive for GR expression. These findings regarding the distribution of GRs in OE were consistent with those reported by Nishimura et al and Robinson et al [6,7]. In our section of OE, GR-positive cells were observed 2 weeks postnatal for the first time.…”

Section: Discussionsupporting

confidence: 93%

Glucocorticoids enhance regeneration of murine olfactory epithelium

Takanosawa¹,

Nishino²,

Ohta³

et al. 2009

Acta Oto-Laryngologica

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Section: Discussionsupporting

confidence: 93%

Glucocorticoids enhance regeneration of murine olfactory epithelium

Takanosawa¹,

Nishino²,

Ohta³

et al. 2009

Acta Oto-Laryngologica

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“…9). This technique closely correlates with the presence of functional nuclear steroid hormone receptor protein (Castagnetta & Caruba 1995, Bodine et al 1997, Malayer & Woods 1998, Robinson et al 1998, such as the MR in the anterior pituitary (Reul et al 1990, Rosenfeld et al 1990, Turner 1990, Rothuizen et al 1993, Schobitz et al 1994, Smith et al 1994, McCormick et al 1998.…”

Section: Discussionmentioning

confidence: 96%

Glucocorticoid and mineralocorticoid regulation of angiotensin II type 1 receptor binding and inositol triphosphate formation in WB cells

Shelat¹,

Flanagan-Cato²,

Sj³

1999

Journal of Endocrinology

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Mineralocorticoids, glucocorticoids, and angiotensin II (AngII) act cooperatively to maintain body fluid homeostasis. Mineralocorticoids, such as aldosterone and deoxycorticosterone-acetate (DOCA), function synergistically with AngII in the brain to increase salt appetite and blood pressure. In addition, glucocorticoids increase AngII-induced drinking and pressor responses and may also facilitate the actions of aldosterone on salt appetite. The AngII Type 1 (AT1) receptor mediates many of the physiological and behavioral actions of AngII. This receptor is coupled to the G-protein Gq, which mediates AngII-induced inositol triphosphate (IP3) formation. The WB cell line, a liver epithelial cell line that expresses the AT1 receptor, was used to examine the cellular basis of glucocorticoid and mineralocorticoid regulation of AT1 function. In this study corticosterone and dexamethasone treatments increased the number of AT1 receptors by activating the glucocorticoid receptor (GR). This increase in AT1 binding resulted in enhanced AngII-stimulated IP3 formation. However, only supraphysiological doses of aldosterone or DOCA increased AT1 binding, and this effect also was mediated by GR activation. Furthermore, despite evidence that mineralocorticoids and glucocorticoids function together to increase AngII-stimulated actions in vivo, aldosterone and dexamethasone did not act synergistically to affect AT1 binding, Gq expression, or IP3 formation. These results indicate that GR activation, and the subsequent increases in AT1 binding and in AngII-stimulated IP3 formation, may represent a cellular mechanism underlying the synergy between adrenal steroids and AngII.

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“…Mediators released by lymphocytes and macrophages are known to trigger hypersecretion in respiratory and Bowman's glands [22]. Olfactory mucus, produced by Bowman's glands, is a highly specialized substance vastly different from nasal respiratory mucus, serving a function analogous to cochlear endolymph [23,24]. Hypersecretion would likely alter the ion concentrations of olfactory mucus, affecting the microenvironment of olfactory neurons and possibly the transduction process [25].…”

Section: Pathology In Chronic Rhinosinusitis With Olfactory Dysfunctionmentioning

confidence: 99%

“…Moreover, the presence of these inflammatory cells in the olfactory mucosa provides a direct mechanism for the action of corticosteroids on anosmia. Type II corticosteroid receptors are found in these inflammatory cells and activation with a systemic glucocorticoid would rapidly suppress the local cytokine response [23,25]. In addition to secretory effects, these same cytokines and mediators may be toxic to neurons [12,26].…”

Section: Pathology In Chronic Rhinosinusitis With Olfactory Dysfunctionmentioning

confidence: 99%

Chronic Rhinosinusitis and Olfactory Dysfunction

Raviv

Kern²

2006

Taste and Smell

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Chronic rhinosinusitis encompasses a group of disorders characterized by inflammation of the mucosa of the nose and paranasal sinuses of at least 12 weeks' duration. In addition to nasal obstruction and discharge, chronic sinusitis is a common cause of olfactory dysfunction. However, smell loss is often overlooked in the clinical setting of sinusitis, with attention instead focused on the respiratory complaints of nasal obstruction, hypersecretion, and facial pressure and pain. Olfactory dysfunction can result in problems including safety concern, hygiene matters, appetite disorders, and changes in emotional and sexual behavior. Although smell loss related to sinonasal disease is probably the most treatable form of olfactory dysfunction, most studies show that improved olfactory sensation in this setting is usually transient and incomplete.

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Expression of glucocorticoid receptor mRNA and protein in the olfactory mucosa: Physiologic and pathophysiologic implications

Cited by 50 publications

References 21 publications

Glucocorticoids enhance regeneration of murine olfactory epithelium

Glucocorticoids enhance regeneration of murine olfactory epithelium

Glucocorticoid and mineralocorticoid regulation of angiotensin II type 1 receptor binding and inositol triphosphate formation in WB cells

Chronic Rhinosinusitis and Olfactory Dysfunction

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