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他帕昔琼阻断电磁场诱导的 HEK293 细胞内钙离子增加。

Thapsigargin blocks electromagnetic field-elicited intracellular Ca increase in HEK 293 cells.

机构信息

Leverhulme Quantum Biology Doctoral Training Centre, University of Surrey, Guildford, Surrey, UK.

School of Veterinary Medicine, Faculty of Health and Medical Sciences, University of Surrey, Guildford, Surrey, UK.

出版信息

Physiol Rep. 2022 May;10(9):e15189. doi: 10.14814/phy2.15189.

DOI:10.14814/phy2.15189
PMID:35510320
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9069166/
Abstract

Biological effects of electromagnetic fields (EMFs) have previously been identified for cellular proliferation and changes in expression and conduction of diverse types of ion channels. The major effect elicited by EMFs seems to be directed toward Ca homeostasis. This is particularly remarkable since Ca acts as a central modulator in various signaling pathways, including, but not limited to, cell differentiation and survival. Despite this, the mechanisms underlying this modulation have yet to be unraveled. Here, we assessed the effect of EMFs on intracellular [Ca ], by exposing HEK 293 cells to both radio-frequency electromagnetic fields (RF-EMFs) and static magnetic fields (SMFs). We detected a constant and significant increase in [Ca ] subsequent to exposure to both types of fields. Strikingly, the increase was nulled by administration of 10 μM Thapsigargin, a blocker of sarco/endoplasmic reticulum Ca -ATPases (SERCAs), indicating the involvement of the endoplasmic reticulum (ER) in EMF-related modulation of Ca homeostasis.

摘要

电磁场(EMFs)的生物学效应先前已被确定为细胞增殖以及多种类型的离子通道表达和传导的变化。电磁场引起的主要效应似乎是针对钙稳态的。这尤其值得注意,因为钙在各种信号通路中充当中央调节剂,包括但不限于细胞分化和存活。尽管如此,这种调节的机制尚未被揭示。在这里,我们通过将 HEK 293 细胞暴露于射频电磁场(RF-EMFs)和静磁场(SMFs)来评估电磁场对细胞内[Ca ]的影响。我们检测到暴露于这两种场后[Ca ]持续且显著增加。引人注目的是,施用 10 μM 毒胡萝卜素(一种肌浆/内质网 Ca -ATP 酶(SERCA)的阻断剂)可使增加无效,表明内质网(ER)参与了电磁场相关的钙稳态调节。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c1a2/9069166/458279e5f931/PHY2-10-e15189-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c1a2/9069166/b9907e9eefcb/PHY2-10-e15189-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c1a2/9069166/041a3e441a6f/PHY2-10-e15189-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c1a2/9069166/7a056586cc1a/PHY2-10-e15189-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c1a2/9069166/ad30535f3bdf/PHY2-10-e15189-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c1a2/9069166/458279e5f931/PHY2-10-e15189-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c1a2/9069166/b9907e9eefcb/PHY2-10-e15189-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c1a2/9069166/041a3e441a6f/PHY2-10-e15189-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c1a2/9069166/7a056586cc1a/PHY2-10-e15189-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c1a2/9069166/ad30535f3bdf/PHY2-10-e15189-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c1a2/9069166/458279e5f931/PHY2-10-e15189-g003.jpg

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