Calcium waves and oscillations driven by an intercellular gradient of inositol (1,4,5)-trisphosphate

Sneyd, James; Wilkins, Matthew M.; Strahonja, Andreja; Sanderson, Michael J.

doi:10.1016/s0301-4622(98)00126-4

Cited by 50 publications

(67 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Modeling predicts that the IP 3 concentration in these cells is in the correct range to support Ca 2ϩ oscillations. This concept was subsequently confirmed by examining the responses of an individual glial cell to ICWs initiated in other cells at different distances from the observed cell (331,344). When the initiating cell was close or far away, the Ca 2ϩ increase was transient in keeping with the expected high or low diffusion concentration of IP 3 .…”

Section: Which Messenger: Ip 3 or Ca 2ϩ ?mentioning

confidence: 79%

Intercellular Ca²⁺Waves: Mechanisms and Function

Leybaert

Sanderson

2012

Physiological Reviews

Self Cite

285

290

View full text Add to dashboard Cite

Intercellular calcium (Ca 2ϩ ) waves (ICWs) represent the propagation of increases in intracellular Ca 2ϩ through a syncytium of cells and appear to be a fundamental mechanism for coordinating multicellular responses. ICWs occur in a wide diversity of cells and have been extensively studied in vitro. More recent studies focus on ICWs in vivo. ICWs are triggered by a variety of stimuli and involve the release of Ca 2ϩ from internal stores. The propagation of ICWs predominately involves cell communication with internal messengers moving via gap junctions or extracellular messengers mediating paracrine signaling. ICWs appear to be important in both normal physiology as well as pathophysiological processes in a variety of organs and tissues including brain, liver, retina, cochlea, and vascular tissue. We review here the mechanisms of initiation and propagation of ICWs, the key intra-and extracellular messengers (inositol 1,4,5-trisphosphate and ATP) mediating ICWs, and the proposed physiological functions of ICWs.

show abstract

Section: Which Messenger: Ip 3 or Ca 2ϩ ?mentioning

confidence: 79%

Intercellular Ca²⁺Waves: Mechanisms and Function

Leybaert

Sanderson

2012

Physiological Reviews

Self Cite

285

290

View full text Add to dashboard Cite

show abstract

“…In other cases it appears that junctional Ca flux is a major factor (Sáez et al, 1989;Boitano et al, 1992;Christ et al, 1992). Computational modeling has supported both scenarios, and delineated synergistic roles for both (Sneyd et al, 1994;Sneyd et al, 1998;Höfer, 1999;Höfer et al 2001;Höfer et al, 2002;Iacobas et al, 2006).…”

Section: Junctional Channelsmentioning

confidence: 92%

Connexin channel permeability to cytoplasmic molecules

Harris¹

2007

Progress in Biophysics and Molecular Biology

414

346

View full text Add to dashboard Cite

Connexin channels are known to be permeable to a variety of cytoplasmic molecules. The first observation of second messenger junctional permeability, made ∼30 years ago, sparked broad interest in gap junction channels as mediators of intercellular molecular signaling. Since then, much has been learned about the diversity of connexin channels with regard to isoform diversity, tissue and developmental distribution, modes of channel regulation, assembly and expression, biochemical modification and permeability, all of which appear to be dynamically regulated. This information has expanded the potential roles of connexin channels in development, physiology and disease, and made their elucidation much more complex -30 years ago such an orchestra of junctional dynamics was unanticipated. Only recently, however, have investigators been able to directly address, in this more complex framework, the key issue: What specific biological molecules, second messengers and others, are able to permeate the various types of connexin channels, and how well? An important related issue, given the ever-growing list of connexin-related pathologies, is how these permeabilities are altered by disease-causing connexin mutations. Together, many studies show that a variety of cytoplasmic molecules can permeate the different types of connexin channels. A few studies reveal differences in permeation by different molecules through a particular type of connexin channel, and differences in permeation by a particular molecule through different types of connexin channels. This article describes and evaluates the various methods used to obtain these data, presents an annotated compilation of the results, and discusses the findings in the context of what can be inferred about mechanism of selectivity and potential relevance to signaling. The data strongly suggest that highly specific interactions take place between connexin pores and specific biological molecular permeants, and that those interactions determine which cytoplasmic molecules can permeate and how well. At this time, the nature of those interactions is unclear. One hopes that with more detailed permeability and structural information, the specific molecular mechanisms of the selectivity can be elucidated.

show abstract

“…nucleotide variants, IP 3 , sugars, glutathione, etc. (Bevans et al, 1998;Sneyd et al, 1998;Goldberg et al, 1999)], gating responses (Harris and Contreras, 2014), regulation by different kinases (Lampe and Lau, 2000;Mitra et al, 2012;Solan and Lampe, 2014) and association with various cytoplasmic and membrane proteins (Giepmans, 2004;Laird, 2010). In addition, connexins form hexameric hemichannels (connexons) that, prior to docking, form intercellular gap junction channels and can mediate release of larger molecules to the extracellular space (Goodenough and Paul, 2003;Sáez and Leybaert, 2014).…”

Section: Introductionmentioning

confidence: 99%

Cell coupling mediated by connexin 26 selectively contributes to reduced adhesivity and increased migration

Polusani

Kalmykov

Chandrasekhar

et al. 2016

Journal of Cell Science

View full text Add to dashboard Cite

Gap junction proteins (connexins) have crucial effects on cell motility in many systems, from migration of neural crest cells to promotion of metastatic invasiveness. Here, we show that expression of Cx26 (also known as GJB2) in HeLa cells specifically enhances cell motility in scrape wounding and sparse culture models. This effect is dependent on gap junction channels and is isotype specific [Cx26 enhances motility, whereas Cx43 (also known as GJA1) does not and Cx32 (also known as GJB1) has an intermediate effect]. The increased motility is associated with reduced cell adhesiveness, caused by loss of N-cadherin protein and RNA at the wound edge. This in turn causes a redistribution of N-cadherin-binding proteins ( p120 catenin and β-catenin) to the cytosol and nucleus, respectively. The former activates Rac-1, which mediates cytoskeletal rearrangements needed for filopod extension. The latter is associated with increased expression of urokinase plasminogen activating receptor (an activator of extracellular proteases) and secretion of extracellular matrix components like collagen. Although these effects were dependent on Cx26-mediated coupling of the cells, they are not mediated by the same signal (i.e. cAMP) through which Cx26 has been shown to suppress proliferation in the same system.

show abstract

Calcium waves and oscillations driven by an intercellular gradient of inositol (1,4,5)-trisphosphate

Cited by 50 publications

References 16 publications

Intercellular Ca²⁺Waves: Mechanisms and Function

Intercellular Ca²⁺Waves: Mechanisms and Function

Connexin channel permeability to cytoplasmic molecules

Cell coupling mediated by connexin 26 selectively contributes to reduced adhesivity and increased migration

Contact Info

Product

Resources

About

Calcium waves and oscillations driven by an intercellular gradient of inositol (1,4,5)-trisphosphate

Cited by 50 publications

References 16 publications

Intercellular Ca2+Waves: Mechanisms and Function

Intercellular Ca2+Waves: Mechanisms and Function

Connexin channel permeability to cytoplasmic molecules

Cell coupling mediated by connexin 26 selectively contributes to reduced adhesivity and increased migration

Contact Info

Product

Resources

About

Intercellular Ca²⁺Waves: Mechanisms and Function

Intercellular Ca²⁺Waves: Mechanisms and Function