Inhibition of Ca2+ influx by pentoxifylline in NR8383 alveolar macrophages

Sun, Xiuhua; Martinez, J. Ricardo; Zhang, Guo H.

doi:10.1016/s0162-3109(99)00042-9

Cited by 11 publications

(5 citation statements)

References 48 publications

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“…NCS 613) were potent and selective PDE4 inhibitors (18). The aim of the present study was to evaluate the effect of new more potent PDE4 inhibitors belonging to the same chemical series on TNF-␣ as well as on interleukin (IL)-1␤, IL-6 and IL-8 production by lipopolysaccharide (LPS) activated peripheral blood mononuclear cells (PBMCs) from healthy subjects, and to compare them to two selective PDE4 inhibitors, RP 73401 (Piclamilast) (19,20) and Denbufylline (21), as well as a non-selective PDE inhibitor, Pentoxifylline (22).…”

mentioning

confidence: 99%

Anti-TNF-α Properties of New 9-Benzyladenine Derivatives with Selective Phosphodiesterase-4- Inhibiting Properties

Reimund

Raboisson

Pinna

et al. 2001

Biochemical and Biophysical Research Communications

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mentioning

confidence: 99%

Anti-TNF-α Properties of New 9-Benzyladenine Derivatives with Selective Phosphodiesterase-4- Inhibiting Properties

Reimund

Raboisson

Pinna

et al. 2001

Biochemical and Biophysical Research Communications

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“…[Ca 2ϩ ] i was measured using the Ca 2ϩ sensitive fluorescent probe fura-2 as previously described [Zhang et al, 1997;Mörk et al, 1998a;Sun et al, 1999]. NR8383 AMs were loaded with fura-2 by incubation with 2 M fura-2/AM for 20 min at 37°C.…”

Section: Measurement Of [Ca 2؉ ] Imentioning

confidence: 99%

“…Excitation wavelengths used were 340 and 380 nm and emission wavelength was 505 nm. Calibration of [Ca 2ϩ ] i was performed for each measurement trace as previously described [Zhang et al, 1997;Mörk et al, 1998a;Sun et al, 1999]. Fluorescence ratios of the 340/380 nm excitation and 505 nm emission were converted to [Ca 2ϩ ] i according to Grynkiewicz et al [1985] using 224 nM as the K d of fura-2 at 37°C for Ca 2ϩ .…”

Section: Measurement Of [Ca 2؉ ] Imentioning

confidence: 99%

“…We have previously demonstrated that exposure to particulate (1-3)-␤-glucan agonists such as zymosan, induces an increase in [Ca 2ϩ ] i in NR8383 AMs [Zhang et al, 1997;Mörk et al, 1998a;Sun et al, 1999]. The (1-3)-␤-glucan receptor mediated increase in [Ca 2ϩ ] i was due to Ca 2ϩ influx via receptoroperated channels since the increase was abolished by the removal of extracellular Ca 2ϩ or by SK&F96365, a specific inhibitor of receptoroperated Ca 2ϩ channels [Zhang et al, 1997;M ork et al, 1998a;Sun et al, 1999]. Currently, little information exists on the intracellular signaling pathway regulating the receptor-operated Ca 2ϩ influx in AMs.…”

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confidence: 99%

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Regulation of (1-3)-?-glucan-stimulated Ca2+ influx by protein kinase C in NR8383 alveolar macrophages

Ac¹,

X²,

Liu³

et al. 2000

J. Cell. Biochem.

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Stimulation of (1-3)-beta-glucan receptors results in Ca(2+) influx through receptor-operated channels in alveolar macrophages (AMs), but the mechanism(s) regulating Ca(2+) influx is still undefined. In this study we investigated the role of protein kinase C (PKC) regulation of Ca(2+) influx in the NR8383 AM cell line using the particulate (1-3)-beta-glucan receptor agonist zymosan. PKC inhibition with calphostin C (CC) or bisindolymaleimide I (BSM) significantly reduced zymosan-induced Ca(2+) influx, whereas activation of PKC with phorbol-12-myristate 13-acetate (PMA) or 1, 2-dioctanoyl-sn-glycerol (DOG) mimicked zymosan, inducing a concentration-dependent Ca(2+) influx. This influx was dependent on extracellular Ca(2+) and inhibited by the receptor-operated Ca(2+) channel blocker SK&F96365, indicating that zymosan and PKC activate Ca(2+) influx through a similar pathway. NR8383 AMs expressed one new PKC isoform (delta) and two atypical PKC isoforms (iota and lambda), but conventional PKC isoforms were not present. Stimulation with zymosan resulted in a translocation of PKC-delta from the cytosol to the membrane fraction. Furthermore, inhibition of protein tyrosine kinases (PTKs) with genistein prevented zymosan-stimulated Ca(2+) influx and PKC-delta translocation. These results suggest that PKC-delta plays a critical role in regulating (1-3)-beta-glucan receptor activated Ca(2+) influx in NR8383 AMs and PKC-delta translocation is possibly dependent on PTK activity.

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“…In Xenopus oocytes, acute stimulation of PKC with a phorbol ester initially enhanced thapsigarginevoked Ca 2ϩ entry (via SOC), as indicated by the endogenous Ca 2ϩ -dependent Clcurrent(40). In NR8383 alveolar macrophages, stimulation of PKC corresponded to activation of Ca 2ϩ influx(41). In whole-cell patch-clamp experiments with RBL-2H3 cells, Parekh and Penner (42) demonstrated that inward Ca 2ϩ current through SOC was accelerated by PMA and prevented by inhibitors of PKC.This study is seemingly in conflict with at least two studies that have demonstrated that PKC mediates SOC inhibition.…”

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confidence: 97%

Epidermal Growth Factor Activates Store-Operated Calcium Channels in Human Glomerular Mesangial Cells

Sansom

2001

Journal of the American Society of Nephrology

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Abstract. A cellular influx of Ca2+ is critical for initiating and maintaining growth in a variety of cell types. Experiments were performed to determine whether epidermal growth factor (EGF), which is known to initiate a proliferative response in mesangial cells, could regulate by intracellular signal transduction the store-operated Ca2+ channels (SOC) of human mesangial cells (HMC) in culture. The cell-attached patch configuration was used to monitor the activity of SOC, with 90 mM Ba2+ in the pipette and physiologic saline solution in the bath. Under control conditions, the mean NPo value was 1.06 at a holding potential of -80 mV. When 100 nM EGF was added to the bath, SOC were activated by 53%. The EGF-evoked response was dose-dependent, with a half-maximal activation concentration of 4.8 nM. An inhibitor of tyrosine kinase, i.e., tyrphostin A23 (100 μM), completely abolished EGF-evoked channel activation. EGF combined with the inactive control compound tyrphostin A1 (100 μM) elicited significant (85%) activation of SOC. Calphostin C, an inhibitor of protein kinase C (PKC), did not affect the baseline activity of SOC but abolished the EGF-evoked enhancement of SOC activity. The PKC activator phorbol-12-myristate-13-acetate (PMA) significantly activated SOC. However, the effects of PMA were duplicative rather than additive or potentiating with maximal concentrations (100 nM) of EGF, suggesting that PMA and EGF activate SOC through a common PKC pathway. In addition, downregulation of PKC via incubation of HMC with PMA for 1 to 20 h depressed both basal activity and EGF-induced activation of SOC. It is concluded that EGF stimulates SOC in HMC through an intracellular signaling mechanism involving tyrosine kinase and PKC.

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Inhibition of Ca2+ influx by pentoxifylline in NR8383 alveolar macrophages

Cited by 11 publications

References 48 publications

Anti-TNF-α Properties of New 9-Benzyladenine Derivatives with Selective Phosphodiesterase-4- Inhibiting Properties

Anti-TNF-α Properties of New 9-Benzyladenine Derivatives with Selective Phosphodiesterase-4- Inhibiting Properties

Regulation of (1-3)-?-glucan-stimulated Ca2+ influx by protein kinase C in NR8383 alveolar macrophages

Epidermal Growth Factor Activates Store-Operated Calcium Channels in Human Glomerular Mesangial Cells

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