Plasma membrane Ca2+-ATPase regulates Ca2+ signaling and the proliferation of airway smooth muscle cells

Chen, Yifei; Cao, Jie; Zhong, Jin-nan; Chen, Xia; Cheng, Ming Zhao; Yang, Jiong; Gao, Yuwei

doi:10.1016/j.ejphar.2014.05.055

Cited by 27 publications

(25 citation statements)

References 37 publications

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“…Ca 21 -ATPase is an important Ca 21 binding protein and has considerable capacity in regulating intracellular Ca 21 homeostasis by exporting excessive Ca 21 into extracellular spaces. 50 Ca 21 /Mg 21 -ATPase, which is involved in intracellular Ca 21 concentrations, can be activated by millimolar concentrations of Ca 21 or Mg 21 . 51 CAMK II is a multifunctional serine/threonine protein kinase, and its activity is dependent on intracellular Ca 21 .…”

Section: Discussionmentioning

confidence: 99%

Toxic effects of TiO₂ nanoparticles in primary cultured rat sertoli cells are mediated via a dysregulated Ca²⁺/PKC/p38 MAPK/NF‐κB cascade

Hong

et al. 2017

J Biomedical Materials Res

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Although numerous studies have demonstrated that titanium dioxide nanoparticles (TiO NPs) can be accumulated in various animal organs and can cause toxicity, there is currently only limited data regarding reproductive toxicity especially on the toxic mechanisms of TiO NPs in Sertoli cells. In order to investigate the mechanism of reproductive toxicity, primary cultured rat Sertoli cells were exposed to 5, 15, or 30 μg/mL TiO NPs for 24 h, and TiO NPs internalization, expression of PKC (p-PKC) and p38 MAPK (p-p38 MAPK) as well as calcium homeostasis were examined. Our findings demonstrated that TiO NPs crossed the membrane into the cytoplasm or nucleus, and significantly suppressed cell viability of primary cultured rat Sertoli cells in a concentration-dependent manner. Furthermore, immunological dysfunction caused by TiO NPs was involved in the increased expression of NF-κB, TNF-α, and IL-1β, and decreased IκB expression. TiO NPs significantly decreased Ca -ATPase and Ca /Mg -ATPase activity and enhanced intracellular Ca levels, and up-regulated the expression of p-PKC and p-p38 MAPK in a dose-dependent manner in primary cultured rat Sertoli cells. Taken together, these findings indicate that TiO NPs may induce immunological dysfunction of primary cultured rat Sertoli cells by stimulating the Ca /PKC/p38 MAPK cascade, which triggers NF-κB activation and ultimately induces the expression of inflammatory cytokines in primary cultured rat Sertoli cells. © 2017 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 105A: 1374-1382, 2017.

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Section: Discussionmentioning

confidence: 99%

Toxic effects of TiO₂ nanoparticles in primary cultured rat sertoli cells are mediated via a dysregulated Ca²⁺/PKC/p38 MAPK/NF‐κB cascade

Hong

et al. 2017

J Biomedical Materials Res

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“…Shortly afterwards, the expression of this pump in canine ASM was reported ( 107 ). More recently, in rat bronchial myocytes, the presence of PMCA1 and PMCA4 was confirmed, and the participation of these two isoforms in Ca 2+ homeostasis was demonstrated ( 108 ).…”

Section: Ca 2+ -Atpases In Asmmentioning

confidence: 90%

“…By measuring [Ca 2+ ] i in the absence of extracellular Ca 2+ , the addition of thapsigargin, a SERCA blocker, to rat bronchial nmyocytes produced a transient Ca 2+ peak that returned to its basal value. At this point, lanthanum, a PMCA blocker, induced a sustained [Ca 2+ ] i increment that promoted apoptosis ( 108 ), demonstrating the central functional role of the two pumps in Ca 2+ handling in ASM. In this regard, it has been proposed that there is a functional coupling between PMCA and SERCA to maintain Ca 2+ homeostasis ( 49 ).…”

Section: Ca 2+ -Atpases In Asmmentioning

confidence: 99%

Maintenance of intracellular Ca2+ basal concentration in airway smooth muscle (Review)

et al. 2018

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In airway smooth muscle, the intracellular basal Ca2+ concentration [b(Ca2+)i] must be tightly regulated by several mechanisms in order to maintain a proper airway patency. The b[Ca2+]i is efficiently regulated by sarcoplasmic reticulum Ca2+-ATPase 2b, plasma membrane Ca2+-ATPase 1 or 4 and by the Na+/Ca2+ exchanger. Membranal Ca2+ channels, including the L-type voltage dependent Ca2+ channel (L-VDCC), T-type voltage dependent Ca2+ channel (T-VDCC) and transient receptor potential canonical 3 (TRPC3), appear to be constitutively active under basal conditions via the action of different signaling pathways, and are responsible for Ca2+ influx to maintain b[Ca2+]i. The two types of voltage-dependent Ca2+ channels (L- and T-type) are modulated by phosphorylation processes mediated by mitogen-activated protein kinase kinase (MEK) and extracellular-signal-regulated kinase 1 and 2 (ERK1/2). The MEK/ERK signaling pathway can be activated by G-protein-coupled receptors through the αq subunit when the endogenous ligand (i.e., acetylcholine, histamine, leukotrienes, etc.) is present under basal conditions. It may also be stimulated when receptor tyrosine kinases are occupied by the appropriate ligand (cytokines, growth factors, etc.). ERK1/2 phosphorylates L-VDCC on Ser496 of the β2 subunit and Ser1928 of the α1 subunit, decreasing or increasing the channel activity, respectively, and enabling it to switch between an open and closed state. T-VDCC is also probably phosphorylated by ERK1/2, although further research is required to identify the phosphorylation sites. TRPC3 is directly activated by diacylglycerol produced by phospholipase C (PLCβ or γ). Constitutive inositol 1,4,5-trisphosphate production induces the release of Ca2+ from the sarcoplasmic reticulum through inositol triphosphate receptor 1. This ion induces Ca2+-induced Ca2+ release through the ryanodine receptor 2 (designated as Ca2+ ‘sparks’). Therefore, several Ca2+ handling mechanisms are finely tuned to regulate basal intracellular Ca2+ concentrations. It is conceivable that alterations in any of these processes may render airway smooth muscle susceptible to develop hyperresponsiveness that is observed in ailments such as asthma.

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“…As shown in Fig. 1 , TG was added in all experiments after 1 min of imaging, followed by a treatment of RES or LaCl 3 , a known PMCA inhibitor [24] , 5 min after TG addition. As a positive control for PMCA inhibition, we treated MDA and PDF cells with 1 mM LaCl 3 ( Fig.…”

Section: Resultsmentioning

confidence: 99%

Resveratrol inhibits plasma membrane Ca 2+ -ATPase inducing an increase in cytoplasmic calcium

Peterson

Oblad

Mecham

et al. 2016

Biochemistry and Biophysics Reports

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Plasma membrane Ca2+-ATPase (PMCA) plays a vital role in maintaining cytosolic calcium concentration ([Ca2+]i). Given that many diseases have modified PMCA expression and activity, PMCA is an important potential target for therapeutic treatment. This study demonstrates that the non-toxic, naturally-occurring polyphenol resveratrol (RES) induces increases in [Ca2+]i via PMCA inhibition in primary dermal fibroblasts and MDA-MB-231 breast cancer cells. Our results also illustrate that RES and the fluorescent intracellular calcium indicator Fura-2, are compatible for simultaneous use, in contrast to previous studies, which indicated that RES modulates the Fura-2 fluorescence independent of calcium concentration. Because RES has been identified as a PMCA inhibitor, further studies may be conducted to develop more specific PMCA inhibitors from RES derivatives for potential therapeutic use.

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Plasma membrane Ca2+-ATPase regulates Ca2+ signaling and the proliferation of airway smooth muscle cells

Cited by 27 publications

References 37 publications

Toxic effects of TiO₂ nanoparticles in primary cultured rat sertoli cells are mediated via a dysregulated Ca²⁺/PKC/p38 MAPK/NF‐κB cascade

Toxic effects of TiO₂ nanoparticles in primary cultured rat sertoli cells are mediated via a dysregulated Ca²⁺/PKC/p38 MAPK/NF‐κB cascade

Maintenance of intracellular Ca2+ basal concentration in airway smooth muscle (Review)

Resveratrol inhibits plasma membrane Ca 2+ -ATPase inducing an increase in cytoplasmic calcium

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Plasma membrane Ca2+-ATPase regulates Ca2+ signaling and the proliferation of airway smooth muscle cells

Cited by 27 publications

References 37 publications

Toxic effects of TiO2 nanoparticles in primary cultured rat sertoli cells are mediated via a dysregulated Ca2+/PKC/p38 MAPK/NF‐κB cascade

Toxic effects of TiO2 nanoparticles in primary cultured rat sertoli cells are mediated via a dysregulated Ca2+/PKC/p38 MAPK/NF‐κB cascade

Maintenance of intracellular Ca2+ basal concentration in airway smooth muscle (Review)

Resveratrol inhibits plasma membrane Ca 2+ -ATPase inducing an increase in cytoplasmic calcium

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Toxic effects of TiO₂ nanoparticles in primary cultured rat sertoli cells are mediated via a dysregulated Ca²⁺/PKC/p38 MAPK/NF‐κB cascade

Toxic effects of TiO₂ nanoparticles in primary cultured rat sertoli cells are mediated via a dysregulated Ca²⁺/PKC/p38 MAPK/NF‐κB cascade