Intercellular calcium signaling via gap junctions in glioma cells.

Charles, Andrew; Naus, Christian C.; Zhu, Daguang; Kidder, Gerald M.; Dirksen, Ellen R.; Sanderson, Michael J.

doi:10.1083/jcb.118.1.195

Cited by 290 publications

(179 citation statements)

References 27 publications

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“…Thus, the Ca 2+ responses in neighboring cells were primarily induced by Ca 2+ release via ATP-dependent generation of Ins(1,4,5)P 3 . Although in some cell types gap junctions reportedly contribute to the intercellular Ca 2+ wave in neighboring cells (Boitano et al, 1992;Charles et al, 1992;Felix et al, 1998;Hansen et al, 1995;Sneyd et al, 1995;StrahonjaPackard and Sanderson, 1999), the gap junction inhibitors 1-octanol and 16-DSA had no effect on Ca 2+ responses in neighboring cells in the present study. Given that intercellular Ca 2+ waves are mediated by released ATP, we anticipated that ATP would have autocrine actions on the mechanical-stimulation-induced Ins(1,4,5)P 3 generation and subsequent Ca 2+ release in stimulated cells.…”

Section: +contrasting

confidence: 46%

Visualization of Ins(1,4,5)P3 dynamics in living cells: two distinct pathways for Ins(1,4,5)P3 generation following mechanical stimulation of HSY-EA1 cells

Nezu

Tanimura

Mitsui

et al. 2010

Journal of Cell Science

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Section: +contrasting

confidence: 46%

Visualization of Ins(1,4,5)P3 dynamics in living cells: two distinct pathways for Ins(1,4,5)P3 generation following mechanical stimulation of HSY-EA1 cells

Nezu

Tanimura

Mitsui

et al. 2010

Journal of Cell Science

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“…Extracellular Ca 2ϩ and Mg 2ϩ may also be modulating these or other channels in astrocytes. However, the dependence of intercellular Ca 2ϩ signaling on both connexin expression and ATP release (Charles et al, 1992;Cotrina et al, 1998;Guthrie et al, 1999), as well as the effect of divalent cations on the flux of low-molecular-weight dyes (a characteristic property of connexin channels), is most directly explained by an effect of extracellular Ca 2ϩ and Mg 2ϩ on ATP release through connexin hemichannels. Release of other nucleotides through connexin hemichannels has also been found to be critically dependent on the extracellular concentrations of divalent cations (Bruzzone et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

“…Ca 2ϩ waves in astrocytes have been shown to be dependent on both expression of connexins and on diffusion of an extracellular signaling molecule, namely ATP (Charles et al, 1992;Cotrina et al, 1998Cotrina et al, , 2000Guthrie et al, 1999). We and others have recently provided evidence for a mechanism that reconciles roles for both connexins and ATP release in astrocyte Ca 2ϩ signaling, i.e., release of ATP through connexin hemichannels (Cotrina et al, 1998;Stout et al, 2002).…”

Section: Introductionmentioning

confidence: 94%

Modulation of intercellular calcium signaling in astrocytes by extracellular calcium and magnesium

Stout

Charles

2003

Glia

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The extracellular concentrations of Ca 2ϩ and Mg 2ϩ are well known to play important roles in the function of the central nervous system. We examined the effects of extracellular Ca 2ϩ and Mg 2ϩ on ATP release and intercellular signaling in astrocytes. [Ca 2ϩ ] o -activated whole cell currents consistent with currents through connexin hemichannels. These currents were inhibited by extracellular Mg 2ϩ . We conclude that extracellular divalent cations modulate intercellular Ca 2ϩ signaling in astrocytes by modulating the release of ATP, possibly via connexin hemichannels.

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“…17,[39][40][41][42] When stimulated by an extracellular message, cells require direct communication between adjoining cells to promote rapid transmission of intercellular signals; that is, biologic signals are passed from stimulated cells to adjoining cells through GJIC. [43][44][45] Previous studies showed that disruption of GJIC between hepatocytes resulted in aberrant biologic signaling that contributed to neoplastic transformation and defective metabolic processes in vivo. 18,19 The vast majority of tumor promoters inhibit intercellular communication both in vivo [46][47][48][49] and in vitro, 8,46 and therefore, the modulation of gap junctional communication may play a role in tumorigenesis.…”

Section: Discussionmentioning

confidence: 99%

Gap Junction–Mediated Intercellular Communication in A Long–Term Primary Mouse Hepatocyte Culture System

Stoehr

Isom

2003

Hepatology

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Gap junction-mediated intercellular communication (GJIC) is critical for maintaining integral cellular processes including differentiation and growth control. The disruption of GJIC has been correlated with aberrant function in many cell types, including hepatocytes in vivo; therefore it is imperative that cellular model systems support intercellular communication to simulate normal cellular functions. Functional GJIC has been shown in long-term primary rat hepatocyte cultures, which have been implemented widely to study various aspects of hepatocellular function; however, the onset of transgenic technology in murine species has necessitated the development of a primary mouse hepatocyte system. In this report, we analyze GJIC in a dimethylsulfoxide (DMSO)-containing long-term primary mouse hepatocyte culture system. The cells retain morphologic and biochemical characteristics of differentiated hepatocytes through day 30 post plating, including liver-specific gene expression. We further show that connexin32 and connexin26 expression and gap junction plaque formation increase over time in culture concomitant with an increase in GJIC between adjoining primary mouse hepatocytes. In conclusion, the findings described in this study make it possible to maintain differentiated primary mouse hepatocytes that also show GJIC in long-term culture for 30 days. In addition, this system has the potential to be extended to study primary mouse hepatocytes isolated from genetically engineered mice. T he development of in vitro systems to study hepatocellular function largely has been impaired by the inability to maintain hepatocytes in a differentiated state in long-term culture. Previous reports have shown that primary rat hepatocytes, plated on collagencoated dishes and cultured in a chemically defined, serum-free medium supplemented with dimethylsulfoxide (DMSO), retain morphologic and biochemical characteristics of differentiated hepatocytes in long-term culture. 1 DMSO maintains primary rat hepatocytes in a differentiated state over long periods of time (Ͼ60 days), negating the need to coculture the hepatocytes with another cell type. 1 Although the rat system has been invaluable for studying various facets of liver biology in vitro, 1-7 the onset of transgenic technology in murine species has necessitated the development of a primary mouse hepatocyte culture system. Thus, the establishment of a long-term culture system for studying primary mouse hepatocytes (PMHs) would be highly important because hepatocytes could be isolated from genetically engineered mice as well as wild-type mice. Many laboratories have attempted to establish PMH culture systems. Short-term cultures using PMHs have been developed, but these cultures typically are maintained for 24 to 72 hours and therefore either are recovering from cellular isolation procedures or in the process of dedifferentiation. Importantly, gap junctionmediated intercellular communication (GJIC) rapidly declines within the first few days of hepatocyte culture. 8 Previous attempt...

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Intercellular calcium signaling via gap junctions in glioma cells.

Cited by 290 publications

References 27 publications

Visualization of Ins(1,4,5)P3 dynamics in living cells: two distinct pathways for Ins(1,4,5)P3 generation following mechanical stimulation of HSY-EA1 cells

Visualization of Ins(1,4,5)P3 dynamics in living cells: two distinct pathways for Ins(1,4,5)P3 generation following mechanical stimulation of HSY-EA1 cells

Modulation of intercellular calcium signaling in astrocytes by extracellular calcium and magnesium

Gap Junction–Mediated Intercellular Communication in A Long–Term Primary Mouse Hepatocyte Culture System

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