Silver nanoparticles increase connexin43‐mediated gap junctional intercellular communication in HaCaT cells through activation of reactive oxygen species and mitogen‐activated protein kinase signal pathway

Qin, Yu; Han, Limin; Yang, Di; Wei, Haidong; Liu, Yue; Xu, Jianfeng; Autrup, Herman; Deng, Furong; Guo, Xiaojing

doi:10.1002/jat.3563

Cited by 16 publications

(9 citation statements)

References 53 publications

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“…These results suggested that Cx26, rather than Cx43, might be involved in the GJIC inhibition of BPA in HaCaT cells. We also found that the GJIC inhibition of BPA could be partly rescued by ICI Previous studies have shown that HaCaT cells can express phosphorylated Cx43, but the phosphorylated forms were not evident in western blots (Qin et al, 2017;Tacheau, Laboureau, Mauviel, & Verrecchia, 2008). Similar results were also obtained in this study.…”

Section: Figuresupporting

confidence: 91%

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Effects of bisphenol A on gap junctions in HaCaT cells as mediated by the estrogen receptor pathway

Zhang

Liu

et al. 2018

J of Applied Toxicology

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Bisphenol A (BPA) is widely used as the raw material for the production of plastics and paper products. People can be exposed to BPA through dermal contact, particularly for cashiers in contact with thermal paper every day. BPA is a known endocrine disruptor that has been shown to be carcinogenic. Many tumors show weak gap junctional intercellular communication (GJIC) function. The aim of this study was to investigate the effects and possible mechanisms of BPA's action on GJIC of human HaCaT skin cells. The results showed that BPA increased cell proliferation rates, prolonged GJIC photobleaching fluorescence recovery times and reduced overall fluorescence recovery rates at 0.01, 0.1 and 1 μm. BPA downregulated connexin (Cx)26 mRNA level at 0.1 μm. Estrogen receptor (ER) antagonist ICI 182 780 at 5 nm partially blocked the above effects of BPA indicating involvement of the ER pathway with BPA exposure. However, BPA did not influence Cx43 mRNA and protein levels. Our immunofluorescence data showed that Cx26 was expressed in the cytoplasm and plasma membrane, and was involved in the formation of gap junctions between adjacent cells, while Cx43 was expressed only in the cytoplasm. Therefore, our data indicate that Cx26 gap junctions may be involved in the GJIC inhibition caused by BPA. In conclusion, our results indicate that BPA can promote human skin cell proliferation, inhibit skin cell GJIC function but not formation and downregulate Cx26 mRNA levels partially through the ER pathway. We hypothesize that BPA can exhibit carcinogenicity by inhibiting GJIC.

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Section: Figuresupporting

confidence: 91%

“…Previous studies have shown that HaCaT cells can express phosphorylated Cx43, but the phosphorylated forms were not evident in western blots (Qin et al, ; Tacheau, Laboureau, Mauviel, & Verrecchia, ). Similar results were also obtained in this study.…”

Section: Discussionmentioning

confidence: 92%

Effects of bisphenol A on gap junctions in HaCaT cells as mediated by the estrogen receptor pathway

Zhang

Liu

et al. 2018

J of Applied Toxicology

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“…Further, the potential molecular mechanisms in EPA-induced Cx43 expression were determined in B16F10 cells. Recently, a different MAPK kinase expression might involve the particles-induced regulation of Cx43 expression 18. In this study, the phosphorylation of JNK and p38 were increased after EPA treatment, but the phosphorylation of ERK was not observed (Fig.…”

Section: Resultsmentioning

confidence: 52%

Eicosapentaenoic acids enhance chemosensitivity through connexin 43 upregulation in murine melanoma models

Yang¹,

Kuo²,

Wu³

et al. 2019

Int. J. Med. Sci.

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Chemotherapy is now in common use for the treatment of tumors; however, with tumor growth retardation comes the severe side effects that occur after a chemotherapy cycle. Eicosapentaenoic acids (EPA) used in combination with chemotherapy has an additive effects and provides a rationale for using EPA in tandem with chemotherapy. To improve the efficacy and safety of this combination therapy, a further understanding that EPA modulates with the tumor microenvironment is necessary. Connexin 43 (Cx43) is involved in enhancing chemosensitivity that was suppressed in a tumor microenvironment. We aim to investigate the role of EPA in chemosensitivity in murine melanoma by inducing Cx43 expression. The dose-dependent upregulation of Cx43 expression and gap junction intercellular communication were observed in B16F10 cells after EPA treatment. Furthermore, EPA significantly increased the expression levels of mitogen-activated protein kinases (MAPK) signaling pathways. The EPA-induced Cx43 expression was reduced after MAPK inhibitors. Knockdown Cx43 in B16F10 cells reduced the therapeutic effects of combination therapy (EPA plus 5-Fluorouracil). Our results demonstrate that the treatment of EPA is a tumor induced Cx43 gap junction communication and enhances the combination of EPA and chemotherapeutic effects.

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“…The same phenomenon has also been observed in Fig 5(A) shows that the anti-oxidative activity of AP may help in protecting the skin from UVA-induced ROS over-expression, which acts as a free radical scavenger. A previous reports clearly showed that the main reasons that influence AgNP-induced Cx43 upregulation include: changes in reactive oxygen content and activation of extracellular signal-regulated kinase and c-Jun N-terminal kinas [ 60 ]. Interestingly, we found that the AP protection mechanism is different from silver nanoparticles.…”

Section: Discussionmentioning

confidence: 99%

Photoprotective effect of Astragalus membranaceus polysaccharide on UVA-induced damage in HaCaT cells

Wang

Bai

et al. 2020

PLoS ONE

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Background The skin provides a predominant barrier against chemical, physical and microbial incursion. The intemperate exposure to ultraviolet A (UVA) radiation can cause excessive cellular oxidative stress, leading to skin damage, proteins damage and mitochondrial dysfunction. There is sufficient evidences supporting the proposal that mitochondria is highly implicated in skin photo-damage. Methods In the present study, a polysaccharide isolated from Astragalus membranaceus was further purified to be an α-glucan, which was further investigated its beneficial influence on UVAinduced photo-damage in HaCaT cells. Results Our results showed that the purified Astragalus membranaceus polysaccharide (AP) can protect HaCaT cells from UVA-induced photo-damage through reducing UVA-induced intracellular ROS production and mitochondrial membrane potential, thereby altering ATP content. It was found that the UVA induced damage in HaCaT cells could be effectively restored by co-treatment with AP. Conclusions AP exhibited promising potential for advanced application as multifunctional skin care products and drugs.

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Silver nanoparticles increase connexin43‐mediated gap junctional intercellular communication in HaCaT cells through activation of reactive oxygen species and mitogen‐activated protein kinase signal pathway

Cited by 16 publications

References 53 publications

Effects of bisphenol A on gap junctions in HaCaT cells as mediated by the estrogen receptor pathway

Effects of bisphenol A on gap junctions in HaCaT cells as mediated by the estrogen receptor pathway

Eicosapentaenoic acids enhance chemosensitivity through connexin 43 upregulation in murine melanoma models

Photoprotective effect of Astragalus membranaceus polysaccharide on UVA-induced damage in HaCaT cells

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