ATP Release through Connexin Hemichannels in Corneal Endothelial Cells

Gomes, Priya Martina; Srinivas, Sangly P.; Driessche, Willy Van; Vereecke, Johan; Himpens, Bernard

doi:10.1167/iovs.04-1181

Cited by 183 publications

(219 citation statements)

References 71 publications

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“…A Px1 mimetic peptide with apparent specific blocking effect was also recently reported ( 110 pxn1) (Pelegrin and Surprenant 2006). A large number of publications demonstrate specific effects of some of these peptides on connexin hemichannels by using in parallel scrambled peptide versions, additional hemichannel blockers and/or studies of their effects on connexin-specific expression systems (Braet et al 2003a(Braet et al , 2003bPearson et al 2005;Gomes et al 2005;Eltzschig et al 2006;Takeuchi et al 2006;DeVuyst et al 2006;De Vuyst et al 2007;Retamal et al 2006Retamal et al , 2007bShintani-Ishida et al 2007). However, it was recently reported that some Cx32, Cx43, and Px1 mimetic peptides cause non-specific blockade of hemichannels formed by Px1, Cx46, and a connexin Cx32 chimera carrying the first extracellular loop of Cx43 (Cx32E143) in the oocyte expression system (Wang et al 2007).…”

Section: Pharmacology Of Hemichannelsmentioning

confidence: 88%

Currently Used Methods for Identification and Characterization of Hemichannels

Schalper

Palacios-Prado

Orellana

et al. 2008

Cell Communication & Adhesion

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Connexins and pannexins are vertebrate transmembrane proteins that form hexameric conduits termed hemichannels. Functional hemichannels allow the diffusional transport of ions and small molecules across the plasma membrane and serve as paracrine and autocrine communication pathways. During the last decade, interest in the hemichannel field increased substantially. Today, there is evidence for the existence of connexin hemichannels in vertebrate cells and bulk of information supports their function in diverse physiological and pathological responses. Controversy regarding the molecular identity of the hemichannel type mediating many responses arose recently with the identification of pannexin-based hemichannels. Here, the authors describe the most frequently used methods for studying hemichannels in living mammalian cells and focus on those with which they have more experience. Although the available in vitro evidence is substantial, further studies and possibly new experimental approaches are required to understand the role and properties of connexin and pannexin hemichannels in vivo.

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Section: Pharmacology Of Hemichannelsmentioning

confidence: 88%

Currently Used Methods for Identification and Characterization of Hemichannels

Schalper

Palacios-Prado

Orellana

et al. 2008

Cell Communication & Adhesion

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“…These interfere with GJ formation and inhibit hemichannel activity (Evans and Boitano, 2001; Leybaert et al, 2003). Because their initial characterization (Dahl, Nonner, & Werner, 1994), a series of “Gap” peptides with specificity for certain CX were developed (Abudara et al, 2014; Chaytor, Evans, & Griffith, 1997; Evans and Boitano 2001; Gomes, Srinivas, Van Driessche, Vereecke, & Himpens, 2005; Leybaert et al, 2003). A promising new report shows that Gap19, a nonapeptide derived from the cytoplasmic loop of CX43, inhibits astroglial CX43 hemichannels, while not affecting GJ channels (Abudara et al, 2014).…”

Section: Potential Therapeutic Targets In Astrocytesmentioning

confidence: 99%

Astroglia as a cellular target for neuroprotection and treatment of neuro‐psychiatric disorders

Liu

Teschemacher

Kasparov

2017

Glia

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Astrocytes are key homeostatic cells of the central nervous system. They cooperate with neurons at several levels, including ion and water homeostasis, chemical signal transmission, blood flow regulation, immune and oxidative stress defense, supply of metabolites and neurogenesis. Astroglia is also important for viability and maturation of stem‐cell derived neurons. Neurons critically depend on intrinsic protective and supportive properties of astrocytes. Conversely, all forms of pathogenic stimuli which disturb astrocytic functions compromise neuronal functionality and viability. Support of neuroprotective functions of astrocytes is thus an important strategy for enhancing neuronal survival and improving outcomes in disease states. In this review, we first briefly examine how astrocytic dysfunction contributes to major neurological disorders, which are traditionally associated with malfunctioning of processes residing in neurons. Possible molecular entities within astrocytes that could underpin the cause, initiation and/or progression of various disorders are outlined. In the second section, we explore opportunities enhancing neuroprotective function of astroglia. We consider targeting astrocyte‐specific molecular pathways which are involved in neuroprotection or could be expected to have a therapeutic value. Examples of those are oxidative stress defense mechanisms, glutamate uptake, purinergic signaling, water and ion homeostasis, connexin gap junctions, neurotrophic factors and the Nrf2‐ARE pathway. We propose that enhancing the neuroprotective capacity of astrocytes is a viable strategy for improving brain resilience and developing new therapeutic approaches.

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“…Adenosine triphosphate disodium salt (Na 2 ATP), 2Ј(3Ј)-O-(4-benzoylbenzoyl) adenosine 5Ј-triphosphate triethylammonium salt (bzATP), ␣,␤-methylene ATP (␣,␤-Me-ATP), Brilliant Blue G (BBG), 4,4Ј-diisothiocyanatostilbene-2,2Ј-disulfonic acid disodium salt hydrate (DIDS), and the hemichannel blocker CBX (Gomes et al, 2005;Ma et al, 2009) were purchased from Sigma-Aldrich. CuCl 2 and ZnCl 2 (0.1 M stock solution) were also purchased from Sigma-Aldrich.…”

Section: Introductionmentioning

confidence: 99%

Microglia Proliferation Is Controlled by P2X7 Receptors in a Pannexin-1-Independent Manner during Early Embryonic Spinal Cord Invasion

et al. 2012

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Microglia are known to invade the mammalian spinal cord (SC) at an early embryonic stage. While the mechanisms underlying this early colonization of the nervous system are still unknown, we recently found that it is associated, at least partially, with the ability of microglia to proliferate at the onset of motoneuron developmental cell death and of synaptogenesis in mouse embryo (E13.5). In vitro studies have shown that the proliferation and activation of adult microglia can be influenced by the purinergic ionotropic receptor P2X7 via a coupling with Pannexin-1. By performing patch-clamp recordings in situ using a whole-mouse embryonic SC preparation, we show here that embryonic microglia already express functional P2X7R. P2X7R activation evoked a biphasic current in embryonic microglia, which is supposed to reflect large plasma membrane pore opening. However, although embryonic microglia express pannexin-1, this biphasic current was still recorded in microglia of pannexin-1 knock-out embryos, indicating that it rather reflected P2X7R intrinsic pore dilatation. More important, we found that proliferation of embryonic SC microglia, but not their activation state, depends almost entirely on P2X7R by comparing wild-type and P2X7RϪ/Ϫ embryos. Absence of P2X7R led also to a decrease in microglia density. Pannexin-1Ϫ/Ϫ embryos did not exhibit any difference in microglial proliferation, showing that the control of embryonic microglial proliferation by P2X7R does not depend on pannexin-1 expression. These results reveal a developmental role of P2X7R by controlling embryonic SC microglia proliferation at a critical developmental state in the SC of mouse embryos.

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ATP Release through Connexin Hemichannels in Corneal Endothelial Cells

Abstract: Hemichannels contribute to ATP release on mechanical stimulation in BCECs. The released ATP contributes to propagation of the Ca(2+) wave.

Cited by 183 publications

References 71 publications

Currently Used Methods for Identification and Characterization of Hemichannels

Currently Used Methods for Identification and Characterization of Hemichannels

Astroglia as a cellular target for neuroprotection and treatment of neuro‐psychiatric disorders

Microglia Proliferation Is Controlled by P2X7 Receptors in a Pannexin-1-Independent Manner during Early Embryonic Spinal Cord Invasion

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