Insulin upregulates the expression of epithelial sodium channel in vitro and in a mouse model of acute lung injury: Role of mTORC2/SGK1 pathway

He, Jing; Qi, Di; Wang, Daoxin; Deng, Wang; Yuan, Yue; Feng, Liqun; Zhu, Tao; Zhao, Yan; Zhang, Chunrong

doi:10.1016/j.yexcr.2014.09.024

Cited by 20 publications

(19 citation statements)

References 58 publications

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“…Previous experimental studies showed that ENaC and Na-K-ATPase proteins are decreased in acute lung injury/ARDS cell culture and animal models [6, 13, 21, 22]. Furthermore, alveolar fluid clearance is impaired in ARDS patients [9].…”

Section: Discussionmentioning

confidence: 99%

The Expression of Water and Ion Channels in Diffuse Alveolar Damage Is Not Dependent on DAD Etiology

et al. 2016

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IntroductionAquaporins and ion channels are membrane proteins that facilitate the rapid movement of water and solutes across biological membranes. Experimental and in vitro studies reported that the function of these channels and pulmonary edema resolution are impaired in acute lung injury (ALI). Although current evidence indicates that alveolar fluid clearance is impaired in patients with ALI/diffuse alveolar damage (DAD), few human studies have addressed the alterations in pulmonary channels in this clinical condition. Additionally, it is not known whether the primary cause of DAD is a relevant variable for the channel dysfunction.MethodsAutopsied lungs of 43 patients with acute respiratory failure (ARF) due to DAD of three different etiologies, non-pulmonary sepsis, H1N1 viral infection and leptospirosis, were compared to 18 normal lungs. We quantified the expression of aquaporin (AQP) 1, AQP3, AQP5, epithelial Na+ channel (ENaC) and sodium potassium ATPase (Na-K-ATPase) in the alveolar septum using immunohistochemistry and image analysis.ResultsThe DAD group presented with increased expression of AQP3, AQP5 and Na-K-ATPase and decreased expression of ENaC compared to controls. However, there was no difference in protein expression within the DAD groups of different etiologies.ConclusionWater and ion channels are altered in patients with ARF due to DAD. The cause of DAD does not seem to influence the level of impairment of these channels.

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Section: Discussionmentioning

confidence: 99%

The Expression of Water and Ion Channels in Diffuse Alveolar Damage Is Not Dependent on DAD Etiology

et al. 2016

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“…Of interest, a recent study conducted on human endometriotic tissues showed that prostaglandin E2 induced SGK1 expression significantly (24). Moreover, SGK1 ‐as an upstream kinase of ENaC‐regulates Na + signaling in different cells by altering the expression of this Na + channel (41, 42), which enhances ENaC open probability (43), attenuates its degradation, and promotes its trafficking (44). Therefore, SGK1 is speculated to be involved in this maternal‐embryo cascade.…”

Section: Involvement Of Sgk1 In Implantationmentioning

confidence: 99%

Involvement of serum glucocorticoid‐regulated kinase 1 in reproductive success

Lou

Mao

et al. 2016

FASEB j.

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Reproductive processes, in particular events that concern pregnancy, are fine-tuned to produce offspring. Reproductive success is of prime importance for the survival of every species. The highly conserved and ubiquitously expressed serum glucocorticoid-regulated kinase 1 (SGK1) was first implicated in infertility as a regulator of a Na channel. In this review, we emphasize the prominent role of SGK1 during early pregnancy: 1) balancing uterine luminal fluid secretion and reabsorption to aid blastocyst adhesion and to import nutrients and energy; 2) transducing signals from the blastocyst to the receptive endometrium; 3) inducing multiple genes that are involved in uterine receptivity and trophoblast invasion; 4) regulating cell differentiation and antioxidant defenses at the fetomaternal interface; and 5) contributing to the proliferation and survival of decidual stromal cells. Accordingly, SGK1 coordinates many cellular processes that are crucial to reproductive activities. Aberrant expression or function of SGK1 results in implantation failure and early pregnancy loss. Further investigation of the molecular mechanisms of the function of SGK1 might provide novel diagnostic tools and interventions for reproductive complications.-Lou, Y., Hu, M., Mao, L., Zheng, Y., Jin, F. Involvement of serum glucocorticoid-regulated kinase 1 in reproductive success.

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“…Upon stimulations of hormonal and non-hormonal signals, SGK1 regulates Na + transport in various cells by altering ENaC expression [93,94], enhancing this channel’s activity and open probability ( P o ) [95], facilitating ENaC channel trafficking, and attenuating its degradation and recycling [96]. …”

Section: Serum and Glucocorticoid Regulated Kinase 1 (Sgk1)-dependmentioning

confidence: 99%

“…Furthermore, in the lipopolysaccharide (LPS)-induced acute lung injury (ALI), activation of SGK1 promotes both the total gene expression and the surface abundance of ENaC, leading to a protective effect in the case of LPS-induced ALI [74,82,94]. Therefore, SGK1 is essential to the induction and maintenance of controlled Na + absorption in the respiratory system, and is involved in the hormonal management of respiratory distress and pulmonary edema, which are clinical manifestations of abnormal pulmonary Na + absorption [91].…”

Section: Physiological Role Of Sgk1 In Na+ Transportmentioning

confidence: 99%

“…SGK1 is co-expressed with ENaC in the human ocular ciliary epithelium and basal cells of corneal endothelium [74,82,94]. The activation of ENaC, NKCC2 and Na + /K + -ATPase induced by SGK1 could contribute to sodium transport in the human ocular ciliary epithelium and corneal endothelium, and further account for corneal transparency [22,23].…”

Section: Physiological Role Of Sgk1 In Na+ Transportmentioning

confidence: 99%

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Serum and Glucocorticoid Regulated Kinase 1 in Sodium Homeostasis

Lou

Zhang

Luo

et al. 2016

IJMS

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The ubiquitously expressed serum and glucocorticoid regulated kinase 1 (SGK1) is tightly regulated by osmotic and hormonal signals, including glucocorticoids and mineralocorticoids. Recently, SGK1 has been implicated as a signal hub for the regulation of sodium transport. SGK1 modulates the activities of multiple ion channels and carriers, such as epithelial sodium channel (ENaC), voltage-gated sodium channel (Nav1.5), sodium hydrogen exchangers 1 and 3 (NHE1 and NHE3), sodium-chloride symporter (NCC), and sodium-potassium-chloride cotransporter 2 (NKCC2); as well as the sodium-potassium adenosine triphosphatase (Na+/K+-ATPase) and type A natriuretic peptide receptor (NPR-A). Accordingly, SGK1 is implicated in the physiology and pathophysiology of Na+ homeostasis. Here, we focus particularly on recent findings of SGK1’s involvement in Na+ transport in renal sodium reabsorption, hormone-stimulated salt appetite and fluid balance and discuss the abnormal SGK1-mediated Na+ reabsorption in hypertension, heart disease, edema with diabetes, and embryo implantation failure.

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Insulin upregulates the expression of epithelial sodium channel in vitro and in a mouse model of acute lung injury: Role of mTORC2/SGK1 pathway

Cited by 20 publications

References 58 publications

The Expression of Water and Ion Channels in Diffuse Alveolar Damage Is Not Dependent on DAD Etiology

The Expression of Water and Ion Channels in Diffuse Alveolar Damage Is Not Dependent on DAD Etiology

Involvement of serum glucocorticoid‐regulated kinase 1 in reproductive success

Serum and Glucocorticoid Regulated Kinase 1 in Sodium Homeostasis

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