Cx23, a connexin with only four extracellular‐loop cysteines, forms functional gap junction channels and hemichannels

Iovine, M. Kathryn; Gumpert, Anna M.; Falk, Matthias M.; Mendelson, Tamra C.

doi:10.1016/j.febslet.2007.11.079

Cited by 39 publications

(38 citation statements)

References 19 publications

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“…It is also widely believed that Cx43 can also form such structures in a variety of cell types (201,445,458,508). Other reports have proposed that this property is shared by several other connexin isoforms, including Cx23, Cx26, Cx30, Cx30.2, Cx31.9, Cx32, Cx35, Cx36, Cx37, Cx41.8, Cx45, Cx45.6, Cx55.5, and Cx56 (59,130,173,174,234,378,384,385,445,462,543,544,567). However, it has proven difficult to unambiguously demonstrate the presence of functionally open and unpaired connexons made by these proteins (458,508).…”

Section: The Assembly Into "Hemi-channels"mentioning

confidence: 99%

Connexins: Key Mediators of Endocrine Function

Bosco

Haefliger

Meda

2011

Physiological Reviews

158

185

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The appearance of multicellular organisms imposed the development of several mechanisms for cell-to-cell communication, whereby different types of cells coordinate their function. Some of these mechanisms depend on the intercellular diffusion of signal molecules in the extracellular spaces, whereas others require cell-to-cell contact. Among the latter mechanisms, those provided by the proteins of the connexin family are widespread in most tissues. Connexin signaling is achieved via direct exchanges of cytosolic molecules between adjacent cells at gap junctions, for cell-to-cell coupling, and possibly also involves the formation of membrane “hemi-channels,” for the extracellular release of cytosolic signals, direct interactions between connexins and other cell proteins, and coordinated influence on the expression of multiple genes. Connexin signaling appears to be an obligatory attribute of all multicellular exocrine and endocrine glands. Specifically, the experimental evidence we review here points to a direct participation of the Cx36 isoform in the function of the insulin-producing β-cells of the endocrine pancreas, and of the Cx40 isoform in the function of the renin-producing juxtaglomerular epithelioid cells of the kidney cortex.

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Section: The Assembly Into "Hemi-channels"mentioning

confidence: 99%

Connexins: Key Mediators of Endocrine Function

Bosco

Haefliger

Meda

2011

Physiological Reviews

158

185

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“…Unopposed hemichannels are present on RCs in the cortex of fetal rats (Elias et al, 2007). Other proteins such as the noncanonical connexin C23 (Iovine et al, 2008) or the TRPV1 (Chung et al, 2008) can also allow the permeation of small molecules. In that context, it is important to notice that flufenamic acid can block connexins (Weissman et al, 2004), P2X 7 receptors (Suadicani et al, 2006), and transient receptor potential (TRP) channels (for review, see Pedersen and Nilius, 2007).…”

Section: Nonvesicular Release Of Glycine From Rcsmentioning

confidence: 99%

“…Glycine release could alternatively result from the opening of large channels in response to membrane stretch such as hemichannels formed by connexins or pannexins, P2X 7 receptors, and/or the TRPV1 (Suadicani et al, 2006;Chung et al, 2008;Iovine et al, 2008). Unopposed hemichannels are present on RCs in the cortex of fetal rats (Elias et al, 2007).…”

Section: Nonvesicular Release Of Glycine From Rcsmentioning

confidence: 99%

“…Hemichannels are permeable to the small anionic fluorescent dye LY [molecular weight (MW) 457] or to the cationic Neurobiotin (MW 322). LY can pass through connexons or pannexons (Shestopalov and Panchin, 2008) as well as through P2X 7 receptors (Colomar and Amédée, 2001), and Neurobiotin can pass through hemichannels formed by connexin C23 (Iovine et al, 2008). In control conditions (325 mosmol/kg H 2 O), some cells (22.5 Ϯ 2.5 cells; n ϭ 12 slices; 4 lumbar slices per SC; 3 SCs) displayed a low LY staining.…”

Section: Nonvesicular Release Of Glycine From Rcsmentioning

confidence: 99%

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Glycine Release from Radial Cells Modulates the Spontaneous Activity and Its Propagation during Early Spinal Cord Development

Scain¹,

Corronc²,

Allain³

et al. 2010

J. Neurosci.

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Rhythmic electrical activity is a hallmark of the developing embryonic CNS and is required for proper development in addition to genetic programs. Neurotransmitter release contributes to the genesis of this activity. In the mouse spinal cord, this rhythmic activity occurs after embryonic day 11.5 (E11.5) as waves spreading along the entire cord. At E12.5, blocking glycine receptors alters the propagation of the rhythmic activity, but the cellular source of the glycine receptor agonist, the release mechanisms, and its function remain obscure. At this early stage, the presence of synaptic activity even remains unexplored. Using isolated embryonic spinal cord preparations and whole-cell patch-clamp recordings of identified motoneurons, we find that the first synaptic activity develops at E12.5 and is mainly GABAergic. Using a multiple approach including direct measurement of neurotransmitter release (i.e., outside-out sniffer technique), we also show that, between E12.5 and E14.5, the main source of glycine in the embryonic spinal cord is radial cell progenitors, also known to be involved in neuronal migration. We then demonstrate that radial cells can release glycine during synaptogenesis. This spontaneous non-neuronal glycine release can also be evoked by mechanical stimuli and occurs through volume-sensitive chloride channels. Finally, we find that basal glycine release upregulates the propagating spontaneous rhythmic activity by depolarizing immature neurons and by increasing membrane potential fluctuations. Our data raise the question of a new role of radial cells as secretory cells involved in the modulation of the spontaneous electrical activity of embryonic neuronal networks.

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“…Cx46 and Cx50 co-localize at gap junctional plaques and form mixed hexamers (60,116). Recently, transcripts for another connexin, Cx23, have been detected in the zebrafish embryo lens (56) and in the mouse lens (121). Based on its pattern of expression and the lack of proper elongation of fiber cells in mice expressing a missense mutation of Cx23, Puk et al (121) have proposed that Cx23 is involved in fiber cell differentiation.…”

Section: Gap Junctions and Intercellular Communication In The Lensmentioning

confidence: 99%

Oxidative Stress, Lens Gap Junctions, and Cataracts

Berthoud

Beyer

2009

Antioxidants & Redox Signaling

217

141

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The eye lens is constantly subjected to oxidative stress from radiation and other sources. The lens has several mechanisms to protect its components from oxidative stress and to maintain its redox state, including enzymatic pathways and high concentrations of ascorbate and reduced glutathione. With aging, accumulation of oxidized lens components and decreased efficiency of repair mechanisms can contribute to the development of lens opacities or cataracts. Maintenance of transparency and homeostasis of the avascular lens depend on an extensive network of gap junctions. Communication through gap junction channels allows intercellular passage of molecules (up to 1 kDa) including antioxidants. Lens gap junctions and their constituent proteins, connexins (Cx43, Cx46, and Cx50), are also subject to the effects of oxidative stress. These observations suggest that oxidative stress-induced damage to connexins (and consequent altered intercellular communication) may contribute to cataract formation. Antioxid. Redox Signal. 11, 339-353. 339The Eye Lens

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Cx23, a connexin with only four extracellular‐loop cysteines, forms functional gap junction channels and hemichannels

Cited by 39 publications

References 19 publications

Connexins: Key Mediators of Endocrine Function

Connexins: Key Mediators of Endocrine Function

Glycine Release from Radial Cells Modulates the Spontaneous Activity and Its Propagation during Early Spinal Cord Development

Oxidative Stress, Lens Gap Junctions, and Cataracts

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