Protective role of AQP3 in UVA-induced NHSFs apoptosis via Bcl2 up-regulation

Xie, Hongfu; Liu, Fangfen; Lei-shan, Liu; Jian, Dan; Luo, Ying; Yi, Yuxin; Chen, Xiang; Li, Ji

doi:10.1007/s00403-013-1324-y

Cited by 25 publications

(26 citation statements)

References 43 publications

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“…As UVA irradiation increases, oxidative stress levels and apoptosis increase, which further decreases AQP3 expression. In contrast, in AQP3-overexpressing primary normal human skin fibroblasts that have been exposed to severe UVA irradiation, apoptosis and oxidative stress were strongly decreased (Xie et al 2013). Recently resveratrol, a natural polyphenol was found to downregulate AQP3 expression in human keratinocytes (Wu et al 2014).…”

Section: Discussionmentioning

confidence: 94%

“…EPA attenuates UVB-induced cell death and downregulation of cell proliferation Recent report has indicated that overexpression of AQP3 protected against high-dose UVA-induced oxidative stress and apoptosis in human skin fibroblasts (Xie et al 2013). Therefore, we have investigated the protective effects of EPA against UVB-induced cytotoxicity.…”

Section: Epa Induces Erk Activation In Cultured Human Keratinocytesmentioning

confidence: 98%

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EPA attenuates ultraviolet radiation-induced downregulation of aquaporin-3 in human keratinocytes

Jeon

Kang

Lee³

et al. 2014

Arch. Pharm. Res.

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Eicosapentaenoic acid (EPA) is an omega-3 polyunsaturated fatty acid (ω-3 PUFA) that protects against photodamage and photocarcinogenesis in mammals. Aquaporin-3 (AQP3) is a water/glycerol transport protein that is found in basal layer keratinocytes. In this study, we have investigated the protective effect of EPA against ultraviolet B (UVB)-induced AQP3 downregulation in human keratinocytes. EPA treatment was found to increase AQP3 gene and protein expression in human epidermal keratinocytes (HaCaT). Using a specific inhibitor, we observed that the effect of EPA on AQP3 expression was mediated by extracellular signal-regulated kinase (ERK) activation. UVB radiation induced AQP3 downregulation in HaCaT cells, and it was found that EPA treatment attenuated UVB-induced AQP3 reduction and the associated cell death. UVB-induced downregulation of AQP3 was blocked by EPA and p38 inhibitor SB203580. Collectively, the present results show that EPA increased AQP3 expression and that this led to a reduction UVB-induced photodamage.

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Section: Discussionmentioning

confidence: 94%

Section: Epa Induces Erk Activation In Cultured Human Keratinocytesmentioning

confidence: 98%

EPA attenuates ultraviolet radiation-induced downregulation of aquaporin-3 in human keratinocytes

Jeon

Kang

Lee³

et al. 2014

Arch. Pharm. Res.

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“…We previously demonstrated that upregulation of AQP3 expression contributes to the proliferative activity of GC cells 3. AQP3 expression has also been implicated in the regulation of cell apoptosis 35,36. But the association between AQP3 expression and cell apoptosis in GC has not been elucidated in detail.…”

Section: Discussionmentioning

confidence: 99%

“…Xie et al35 demonstrated that AQP3 contributes to the inhibition of cell apoptosis in normal human skin fibroblasts by upregulating the expression level of Bcl-2, an anti-apoptosis protein. Hou et al17 also reported that AQP3 knockdown clearly induces cell apoptosis in non-small cell lung cancer but failed to clarify the detailed pathogenic mechanism.…”

Section: Discussionmentioning

confidence: 99%

Silencing of AQP3 induces apoptosis of gastric cancer cells via downregulation of glycerol intake and downstream inhibition of lipogenesis and autophagy

Liang

Zhang

et al. 2017

OTT

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Gastric cancer (GC) has a poor prognosis and is a leading cause of cancer-related death. Optimal therapeutic targets have not been identified. AQP3 is capable of transporting glycerol across the cytomembrane. Previous studies have shown that AQP3 is involved in proliferation, invasion and migration by regulating glycerol and lipid metabolism in diverse cancer cell types. However, the potential roles of glycerol and lipid metabolism in AQP3-related cell apoptosis in GC remain unclear. In this study, we observed that AQP3 expression was upregulated in tumor tissues, and positively correlated with tumor size, lymph node metastasis and glycerol concentration in human GC samples. Silencing of AQP3 resulted in decreased glycerol intake and impaired lipid synthesis, which contributed to increased cell apoptosis. Furthermore, inhibition of autophagy induced by AQP3 knockdown promoted cell apoptosis. Administration of either glycerol or rapamycin restored cell viability, and overexpression of AQP3 increased cell viability by upregulating cellular glycerol metabolism and autophagy. Our study demonstrates that the increase in cell apoptosis of AQP3-deficient GC cells is a consequence of reduced glycerol uptake and lipogenesis and is associated with autophagy inhibition induced by AQP3 deficiency.

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“…In addition, altered AQP3 expression and production have also been linked to several skin diseases such as eczema [9, 38], psoriasis, non-melanoma skin cancers [23, 31, 44, 52] and vitiligo [29]. Recently, AQP3 has also been shown to play a protective role in UV-induced apoptosis in fibroblasts [54] and has also been suggested to be a participating factor in skin aging [45]. Thus, AQP3 is a key player in the skin and identifying compounds that modulate its activity could yield new therapeutic actives for drug development and skin care.…”

Section: Introductionmentioning

confidence: 99%

N-Acetylglutaminoyl-S-farnesyl-l-cysteine (SIG-1191): an anti-inflammatory molecule that increases the expression of the aquaglyceroporin, aquaporin-3, in human keratinocytes

et al. 2016

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Isoprenylcysteine (IPC) small molecules were discovered as signal transduction modulating compounds ~25 years ago. More recently, IPC molecules have demonstrated antioxidant and anti-inflammatory properties in a variety of dermal cells as well as antimicrobial activity, representing a novel class of compounds to ameliorate skin conditions and disease. Here, we demonstrate a new IPC compound, N-acetylglutaminoyl-S-farnesyl-l-cysteine (SIG-1191), which inhibits UVB-induced inflammation blocking pro-inflammatory cytokine interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) production. To investigate further the previously reported hydrating potential of IPC compounds, SIG-1191 was tested for its ability to modulate aquaporin expression. Specifically, aquaporin 3 (AQP3) the most abundant aquaporin found in skin has been reported to play a key role in skin hydration, elasticity and barrier repair. Results show here for the first time that SIG-1191 increases AQP3 expression in both cultured normal human epidermal keratinocytes as well as when applied topically in a three-dimensional (3D) reconstructed human skin equivalent. Additionally, SIG-1191 dose dependently increased AQP3 protein levels, as determined by specific antibody staining, in the epidermis of the 3D skin equivalents. To begin to elucidate which signaling pathways SIG-1191 may be modulating to increase AQP3 levels, we used several pharmacological pathway inhibitors and determined that AQP3 expression is mediated by the Mitogen-activated protein kinase/Extracellular signal-regulated kinase kinase (MEK) pathway. Altogether, these data suggest SIG-1191 represents a new IPC derivative with anti-inflammatory activity that may also promote increased skin hydration based on its ability to increase AQP3 levels.

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Protective role of AQP3 in UVA-induced NHSFs apoptosis via Bcl2 up-regulation

Cited by 25 publications

References 43 publications

EPA attenuates ultraviolet radiation-induced downregulation of aquaporin-3 in human keratinocytes

EPA attenuates ultraviolet radiation-induced downregulation of aquaporin-3 in human keratinocytes

Silencing of AQP3 induces apoptosis of gastric cancer cells via downregulation of glycerol intake and downstream inhibition of lipogenesis and autophagy

N-Acetylglutaminoyl-S-farnesyl-l-cysteine (SIG-1191): an anti-inflammatory molecule that increases the expression of the aquaglyceroporin, aquaporin-3, in human keratinocytes

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