Activation of epithelial sodium channel in human middle ear epithelial cells by dexamethasone

Son, Eun Ju; Kim, Sung Hunh; Park, Hun Yi; Kim, Su Jin; Yoon, Joo Heon; Chung, Hyun Pil; Choi, Jae Young

doi:10.1016/j.ejphar.2008.11.012

Cited by 16 publications

(19 citation statements)

References 35 publications

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“…It was reported that dexamethasone stimulated ENaC activity and ENaC-dependent fluid absorption in the epithelial cells of the human middle ear [13]. Also, Choi et al showed that interleukin-1beta suppressed ENaC-b subunit expression and ENaCdependent fluid absorption in human middle ear epithelial cells [14].…”

Section: Discussionmentioning

confidence: 97%

Expression of ENaC in LPS-induced inflammation of middle ear mucosa

Song

Kwon

Cho

et al. 2012

Acta Oto-Laryngologica

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The level of ENaC-α expression decreased 0.50-fold and 0.55-fold at 6 and 12 h, respectively (p < 0.05), but it normalized at 24 h. It increased 3.64-fold at 72 h and 3.24-fold at 120 h (p < 0.05). At 6 and 12 h after the LPS injection into the middle ear cavity, inflammation was induced and ENaC-α immunoreactivity decreased. At 24 h, ENaC-α immunoreactivity was normalized, then at 72 and 120 h after the injection it was increased.

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Section: Discussionmentioning

confidence: 97%

Expression of ENaC in LPS-induced inflammation of middle ear mucosa

Song

Kwon

Cho

et al. 2012

Acta Oto-Laryngologica

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“…There are many reports that Dex affects expression of ion channels in various cells (Nakajima et al 2008;BenMohamed et al 2009;McTavish et al 2009;Son et al 2009;Wei et al 2009), but there are no reports concerning Dex and ion channels in PDL fibroblasts. Dex may cause physiologic reactions on PDL fibroblasts through the modulation of ion channels expression.…”

mentioning

confidence: 95%

Dexamethasone-induced up-regulation of two-pore domain K+ channel genes, TASK-1 and TWIK-2, in cultured human periodontal ligament fibroblasts

Yamamoto

Ohara

Nishikawa

et al. 2011

In Vitro Cell.Dev.Biol.-Animal

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Two-pore domain K(+) channels are widely expressed in many types of cells, and have various important functions, especially maintaining the resting membrane potential. In the previous report, we have confirmed the presence of several kinds of two-pore domain K(+) channels in the periodontal ligament (PDL) fibroblasts. It is well known that dexamethasone (Dex) regulates the functions of various kinds of ion channels. In this work, we investigate if Dex affects the gene expressions of the two-pore domain K(+) channels in the PDL fibroblasts. We also examined the effects of other steroid hormones on the K(+) channels gene expression. The mRNA levels of two-pore domain K(+) channels in human PDL fibroblasts were examined in the presence or absence of Dex by RT-PCR. The effects of other steroid hormones (aldosterone, estrogen, 1α,25-dihydroxyvitamin D(3) [1,25-(OH)(2)D(3)], and retinoic acid) were also examined. Dex significantly induced the expression of TASK-1 and TWIK-2 in mRNA levels in both a dose- and a time-dependent manner. The stimulatory effects of Dex were completely abolished by a glucocorticoid receptor antagonist. 1,25-(OH)(2)D(3) also increased the TASK-1 mRNA levels but had no effect on TWIK-2 expression. Dex, one of the potent glucocorticoid, probably have a protective role against external stimuli by maintaining the membrane potential of PDL fibroblasts through the up-regulation of TASK-1 and TWIK-2 K(+) channels.

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“…MUC5AC and MUC5B are mucins genes, and they reflect the mucins production and OM induction [16]. ENaC-α , ENaC-β , and ENaC-γ are genes encoding epithelial sodium channels and they reflect the mucociliary transport in the middle ear mucosa [17]. AQP-4 is gene of aquaporin in middle ear mucosa and it reflects the homeostasis of the middle ear cavity [18].…”

Section: Methodsmentioning

confidence: 99%

Effect of Lead on Human Middle Ear Epithelial Cells

Kim

Shin

et al. 2018

BioMed Research International

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Lead is a ubiquitous metal in the environment, but no studies have examined lead toxicity on the middle ear. Here, we investigated lead toxicity and its mechanism in human middle ear epithelial cells (HMEECs). Moreover, we investigated the protective effects of amniotic membrane extract (AME) and chorionic membrane extract (CME) against lead toxicity in HMEECs. Cell viability was analyzed using the cell counting kit, and reactive oxygen species (ROS) activity was measured using a cellular ROS detection kit. After lead(II) acetate trihydrate treatment, mRNA levels of various genes were assessed by semiquantitative real-time polymerase chain reaction. Following treatment with AME or CME after lead exposure, the changes in cell viability, ROS activity, and gene expression were analyzed. Exposure to >100 g/mL of lead(II) acetate trihydrate caused a significant decrease in cell viability and increased ROS production in HMEECs. Lead exposure significantly increased the mRNA expression of genes encoding inflammatory cytokines and mucins. Administration of AME or CME restored cell viability, reduced ROS activity, and ameliorated mRNA levels. Our findings suggest that environmental lead exposure is related to the development of otitis media, and AME and CME may have antioxidative and anti-inflammatory effects against lead toxicity.

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Activation of epithelial sodium channel in human middle ear epithelial cells by dexamethasone

Cited by 16 publications

References 35 publications

Expression of ENaC in LPS-induced inflammation of middle ear mucosa

Expression of ENaC in LPS-induced inflammation of middle ear mucosa

Dexamethasone-induced up-regulation of two-pore domain K+ channel genes, TASK-1 and TWIK-2, in cultured human periodontal ligament fibroblasts

Effect of Lead on Human Middle Ear Epithelial Cells

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