Epithelial sodium channel and the mineralocorticoid receptor in cultured rat M�ller glial cells

Golestaneh, Nady; Kozak, Y. de; Klein, Christophe; Mirshahi, Massoud

doi:10.1002/1098-1136(200102)33:2<160::aid-glia1015>3.0.co;2-4

Cited by 19 publications

(22 citation statements)

References 32 publications

(36 reference statements)

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“…A most notable finding in this study is that the terminal Schwann cells associated with the periodontal Ruffini endings exhibited an intense immunoreaction for ENaCβ, confirmed by double staining and a nerve injury experiment. In contrast to numerous reports on its neuronal localization, glial expression of the DEG/ENaC family also has been limited to retinal Müller cells (6,16) and astrocytes and glioma (4). As far as we know, this is the first report on the localization of ENaCβ in the specialized Schwann cells associated with the mechanoreceptors.…”

Section: Discussioncontrasting

confidence: 57%

“…Previous immunohistochemical studies have shown an expression of ENaCs in the sensory neurons of the rat dorsal root and trigeminal ganglia which innervate cutaneous mechanoreceptors including Meissner's corpuscles and Merkel cells (12) and lanceolate endings in vibrasal follicle-sinus complex (13). However, glial expression of the DEG/ENaC family is limited to retinal Müller cells (6,16) and astrocytes and glioma (4). The periodontal ligament, a dense connective tissue between the alveolar bone and teeth, contains two types of sensory receptors: free and specialized nerve terminals (26).…”

Section: Immunohistochemistry For Enacβmentioning

confidence: 99%

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Immunohistochemical detection of ENaCβ in the terminal Schwann cells associated with the periodontal Ruffini endings of the rat incisor

et al. 2009

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Epithelial sodium channels (ENaCs) are a subfamily of ion channels within the degenerin/ENaC (DEG/ENaC) superfamily. Previous studies have shown the immunolocalization of ENaC in the neural elements of the cutaneous mechanoreceptors as well as dorsal root and trigeminal ganglion neurons, indicating the involvement of this molecule in mechanotransduction. The present study examined the expression of ENaCβ, a major component of ENaC protein, in the mechanoreceptive Ruffini endings in the periodontal ligament of the rat incisors by immunohistochemistry. The expression of ENaCβ in the trigeminal ganglion-which innervates the periodontal Ruffini endings-was also investigated at the mRNA and protein levels. Furthermore, double staining and a nerve injury experiment were applied to clarify its detailed localization in the periodontal Ruffini endings. ENaCβ immunoreaction in the trigeminal ganglion was recognizable in the comparatively large neurons which have been considered to mediate mechanotransduction. Immunohistochemistry for ENaCβ demonstrated dendritic ramifications of the Ruffini endings as well as the rounded cells in the periodontal ligament. Double staining with ENaCβ and either PGP9.5 or S-100 protein showed immunoreaction for ENaCβ in both the axonal and glial elements in the periodontal ligament. Some ENaCβ positive cells with rounded profiles were reactive to non-specific cholinesterase activity. Furthermore, a transection of the inferior alveolar nerve failed to eliminate the rounded cells with ENaCβ reaction, indicating that they were the terminal Schwann cells associated with the periodontal Ruffini endings. These findings suggest that ENaCβ is a key mechanotransducing channel in the periodontal Ruffini endings. Probably, the terminal Schwann cells together with the axon terminals regulate mechanotransduction in the periodontal endings.Epithelial sodium channels (ENaCs) are members of the degenerin/ENaC (DEG/ENaC) family of voltage-insensitive, amiloride-blockable cation channels (21, 25). They are generally composed of four subunits: ENaCα, β, γ and δ. These ENaC subunits have a conserved topology consisting of two membrane-spanning domains with intracellular N-and C-termini and a large glycosylated extracellular region. Of these channels, a heterotetramer containing two ENaCα, one ENaCβ and one ENaCγ shows high sensitivity to amiloride and its analogues (21,25). However, the function of ENaCδ remains unknown though this subunit can also form a functional ion channel. Many studies have shown a wide distribution of ENaCs in various tissues where their expression at the apical membrane mediates unidirectional absorption of Na + (9, 15). These ENaCs can also be regarded as key mechanotransducing channels came from the findings that the mutation

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Section: Discussioncontrasting

confidence: 57%

Section: Immunohistochemistry For Enacβmentioning

confidence: 99%

Immunohistochemical detection of ENaCβ in the terminal Schwann cells associated with the periodontal Ruffini endings of the rat incisor

et al. 2009

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“…Müller cells may be critical in the vascular protective effects of LS because they express RAAS components 8,23 and ENaCα. 24,37,38 Furthermore, in response to HS and LS, Müller cells modulate their levels of ENaCα expression, which in the setting of HS was attenuated by MR and AT1R blockade.…”

Section: Discussionmentioning

confidence: 99%

Retinal Vasculopathy Is Reduced by Dietary Salt Restriction

Deliyanti

Armani

Casely

et al. 2014

ATVB

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Objective— Neovascularization and vaso-obliteration are vision-threatening events that develop by interactions between retinal vascular and glial cells. A high-salt diet is causal in cardiovascular and renal disease, which is linked to modulation of the renin–angiotensin–aldosterone system. However, it is not known whether dietary salt influences retinal vasculopathy and if the renin–angiotensin–aldosterone system is involved. We examined whether a low-salt (LS) diet influenced vascular and glial cell injury and the renin–angiotensin–aldosterone system in ischemic retinopathy. Approach and Results— Pregnant Sprague Dawley rats were fed LS (0.03% NaCl) or normal salt (0.3% NaCl) diets, and ischemic retinopathy was induced in the offspring. An LS diet reduced retinal neovascularization and vaso-obliteration, the mRNA and protein levels of the angiogenic factors, vascular endothelial growth factor, and erythropoietin. Microglia, which influence vascular remodeling in ischemic retinopathy, were reduced by LS as was tumor necrosis factor-α. Macroglial Müller cells maintain the integrity of the blood–retinal barrier, and in ischemic retinopathy, LS reduced their gliosis and also vascular leakage. In retina, LS reduced mineralocorticoid receptor, angiotensin type 1 receptor, and renin mRNA levels, whereas, as expected, plasma levels of aldosterone and renin were increased. The aldosterone/mineralocorticoid receptor–sensitive epithelial sodium channel alpha (ENaCα), which is expressed in Müller cells, was increased in ischemic retinopathy and reduced by LS. In cultured Müller cells, high salt increased ENaCα, which was prevented by mineralocorticoid receptor and angiotensin type 1 receptor blockade. Conversely, LS reduced ENaCα, angiotensin type 1 receptor, and mineralocorticoid receptor expression. Conclusions— An LS diet reduced retinal vasculopathy, by modulating glial cell function and the retinal renin–angiotensin–aldosterone system.

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“…ENaC subunits have been detected in retina and in Muller glia (55,56,148,149,277), and amiloride affects multiple components of the electroretinogram (55). In a mouse model of glaucoma, neuronal retinal expression of ␣ENaC increased, while that of ␤-and ␥ENaC decreased (113).…”

Section: Enac In the Peripheral And Central Nervous Systems And In Sementioning

confidence: 99%

ENaCs and ASICs as therapeutic targets

Qadri

Rooj

Fuller

2012

American Journal of Physiology-Cell Physiology

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The epithelial Na+channel (ENaC) and acid-sensitive ion channel (ASIC) branches of the ENaC/degenerin superfamily of cation channels have drawn increasing attention as potential therapeutic targets in a variety of diseases and conditions. Originally thought to be solely expressed in fluid absorptive epithelia and in neurons, it has become apparent that members of this family exhibit nearly ubiquitous expression. Therapeutic opportunities range from hypertension, due to the role of ENaC in maintaining whole body salt and water homeostasis, to anxiety disorders and pain associated with ASIC activity. As a physiologist intrigued by the fundamental mechanics of salt and water transport, it was natural that Dale Benos, to whom this series of reviews is dedicated, should have been at the forefront of research into the amiloride-sensitive sodium channel. The cloning of ENaC and subsequently the ASIC channels has revealed a far wider role for this channel family than was previously imagined. In this review, we will discuss the known and potential roles of ENaC and ASIC subunits in the wide variety of pathologies in which these channels have been implicated. Some of these, such as the role of ENaC in Liddle's syndrome are well established, others less so; however, all are related in that the fundamental defect is due to inappropriate channel activity.

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Epithelial sodium channel and the mineralocorticoid receptor in cultured rat M�ller glial cells

Cited by 19 publications

References 32 publications

Immunohistochemical detection of ENaCβ in the terminal Schwann cells associated with the periodontal Ruffini endings of the rat incisor

Immunohistochemical detection of ENaCβ in the terminal Schwann cells associated with the periodontal Ruffini endings of the rat incisor

Retinal Vasculopathy Is Reduced by Dietary Salt Restriction

ENaCs and ASICs as therapeutic targets

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