Enhanced Neurite Outgrowth in PC12 Cells Mediated by Connexin Hemichannels and ATP

Belliveau, Daniel J.; Bani‐Yaghoub, Mahmud; McGirr, Becky; Naus, Christian C.; Rushlow, Walter

doi:10.1074/jbc.m600026200

Cited by 69 publications

(56 citation statements)

References 60 publications

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“…But argument continues, partly due to different experimental models, leading to different and even opposing results and conclusions [34][35][36] .…”

Section: Discussionmentioning

confidence: 99%

Protective effects of carbenoxolone are associated with attenuation of oxidative stress in ischemic brain injury

Zhang

Jing

et al. 2013

Neurosci. Bull.

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Accumulating evidence has suggested that the gap junction plays an important role in the determination of cerebral ischemia, but the underlying mechanisms remain to be elucidated. In this study, we assessed the effect of a gap-junction blocker, carbenoxolone (CBX), on ischemia/reperfusion-induced brain injury and the possible mechanisms. By using the transient cerebral ischemia model induced by occlusion of the middle cerebral artery for 30 min followed by reperfusion for 24 h, we found that pre-administration of CBX (25 mg/kg, intracerebroventricular injection, 30 min before cerebral ischemic surgery) diminished the infarction size in rats. And this was associated with a decrease of reactive oxygen species generation and inhibition of the activation of astrocytes and microglia. In PC12 cells, H 2 O 2 treatment induced more coupling and apoptosis, while CBX partly inhibited the opening of gap junctions and improved the cell viability. These results suggest that cerebral ischemia enhances the opening of gap junctions. Blocking the gap junction with CBX may attenuate the brain injury after cerebral ischemia/reperfusion by partially contributing to amelioration of the oxidative stress and apoptosis.

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“…But argument continues, partly due to different experimental models, leading to different and even opposing results and conclusions [34][35][36] .…”

Section: Discussionmentioning

confidence: 99%

Protective effects of carbenoxolone are associated with attenuation of oxidative stress in ischemic brain injury

Zhang

Jing

et al. 2013

Neurosci. Bull.

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“…Because Ngn2 is expressed in both the INPs and the new generated postmitotic neurons (15), and there is no specific marker to distinguish the INPs and the early stage postmitotic neurons, our results could not exclude the possibility that the BrdU ϩ cells in the VZ included the new generated postmitotic neurons. In addition, recent study has shown that ATP signaling might play a role in the neuronal differentiation and process outgrowth (40), both of which are essential for the initiation of radial migration of the postmitotic neurons. The proliferative SVZ in the forebrain has a uniquely important role during the second half of intrauterine development in the human brain (5,10).…”

Section: Discussionmentioning

confidence: 99%

The role of ATP signaling in the migration of intermediate neuronal progenitors to the neocortical subventricular zone

Liu

Hashimoto-Torii

Torii

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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P2Y1 ͉ calcium transient ͉ embryonic neocortex ͉ SVZ F or almost four decades we have known that neurons destined for the cerebral cortex in all mammalian species, including the human, are generated in the primary and secondary proliferative layers situated near the embryonic cerebral ventricle, respectively called the ventricular (VZ) and subventricular zones (SVZ) (1, 2). It is also generally recognized that the SVZ is formed by a subclass of neuronal progenitors that lose their attachment to the ventricular surface and translocate their nucleus and surrounding somatic cytoplasm to the SVZ, where they continue to divide and produce neurons destined predominantly for the upper cortical layers (3-5). The use of in vitro imaging has revealed that the SVZ progenitors (recently renamed the intermediate neuronal progenitors or INPs, to emphasize their continuous proliferation), originate in the VZ by asymmetric mitotic division of the neuroepithelial cells (6). After translocation of their soma to the SVZ, INPs amplify production of cortical neurons via asymmetrical and symmetric modes of mitotic divisions (6-9). The relative large size of the SVZ in primates, particularly in humans, has inspired suggestions that cells in this zone contribute to the expansion and elaboration of the neocortex during evolution (2, 10, 11). Furthermore, genetic and environmental disturbances of neuronal production in the SVZ affect the development and function of the cerebral cortex (5,(12)(13)(14).Considering the developmental and clinical significance of the SVZ, surprisingly little is known about its origin and how INPs are distinguished from other proliferative neural precursors and postmitotic migrating neurons. Similar to the postmitotic neurons, INPs leave the VZ by extending their basal processes toward the cortical plate (CP) along radial glia (RG) shafts and translocating their nuclei within the growing leading processes (1, 6). However, they stop migration after reaching the level of the SVZ, where they re-enter the cell cycle. It has been found that genes, such as p27, Ngn2, FLNa, and MEKK4 are involved in the final mitotic division and onset of migration from the VZ via modulation of the actin cytoskeleton (15-17). Reelin (18) and the neurotransmitters GABA and glutamate and their receptors might also contribute to this process (19,20). However, the nature of the complex intercellular signaling involved in the migration and settlement of INPs in the SVZ remains unexplored.We started with the assumption that Ca 2ϩ , a ubiquitous secondary messenger, and ATP released via gap junctions and hemichannels in the VZ might be involved in the cell-cell communication and the initiation of INP migration. Our hypothesis was based on the previous findings that Ca 2ϩ signaling influences the mitosis of neuronal progenitors and their nuclear interkinetic translocation in the embryonic retina (21), and that [Ca 2ϩ ] fluctuations also affect cellular migration in cerebellar granular cells (22-24), cultured neuronal progenitors (25), and p...

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“…Recently, studies using Cx43cKO and Cx43k258stop mice have indicated that the C terminus is required for cortical neuronal migration (30). In addition, independent regulation of the gap junction channel or C-terminal domain in neurite outgrowth (31,32) and cellular motility (33)(34)(35)(36)(37) have been demonstrated in various cell types, indicating that they may affect the neocortical development (38).…”

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confidence: 99%

Connexin 43 controls the multipolar phase of neuronal migration to the cerebral cortex

Liu

Sun

Torii

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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The prospective pyramidal neurons, migrating from the proliferative ventricular zone to the overlaying cortical plate, assume multipolar morphology while passing through the transient subventricular zone. Here, we show that this morphogenetic transformation, from the bipolar to the mutipolar and then back to bipolar again, is associated with expression of connexin 43 (Cx43) and, that knockdown of Cx43 retards, whereas its overexpression enhances, this morphogenetic process. In addition, we have observed that knockdown of Cx43 reduces expression of p27, whereas overexpression of p27 rescues the effect of Cx43 knockdown in the multipolar neurons. Furthermore, functional gap junction/ hemichannel domain, and the C-terminal domain of Cx43, independently enhance the expression of p27 and promote the morphological transformation and migration of the multipolar neurons in the SVZ/IZ. Collectively, these results indicate that Cx43 regulates the passage of migrating neurons through their multipolar stage via p27 signaling and that interference with this process, by either genetic and/or environmental factors, may cause cortical malformations.T he laminated structure of the mammalian cerebral cortex is an end product of coordinated generation, migration, and deposition of neurons to their final locations during the embryonic period (1). All prospective cortical pyramidal neurons are generated in either the ventricular (VZ) or subventricular (SVZ) zones and, after their final division, migrate radially to the cortical plate (CP) situated beneath the pial surface (2). Although it has been observed long ago that cells in the SVZ and intermediate zone (IZ) display multiple processes as they choose and translocate between adjacent radial glial fibers (3, 4), it has been only until recently possible to study this transient process by live imaging combined with genetic introduction of GFP (5-9). The newly generated neurons usually undergo transient multipolar transformation before assuming radial migration (8, 10). Based on these observations, it has been proposed that many developmental disorders, such as periventricular nodular heterotopia, subcortical band heterotopia, and doublecortex syndrome are related to migration abnormalities including its multipolar stage at SVZ/VZ (11-13).The molecular mechanisms controlling directly and/or indirectly the multipolar stage of neuronal migration have just begun to be recognized (7,(14)(15)(16)(17). For example, knockdown or inactivation of Filamin A or LIS1 accumulated the multipolar neurons in the VZ and SVZ, whereas knockdown or inactivation of Doublecortin (DCX) accumulated these cells in the IZ (18,19). Conversely, increasing filamin A activity by siRNA of Filamin A-interacting protein accelerated the transition to a bipolar shape in the SVZ, and overexpression of DCX increased the number of bipolar cells in the IZ (20,21). In addition, Cdk5 has also been shown to control the multipolar-to-bipolar transition during radial migration (7,18,20). Recently, it has been reported that t...

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Enhanced Neurite Outgrowth in PC12 Cells Mediated by Connexin Hemichannels and ATP

Cited by 69 publications

References 60 publications

Protective effects of carbenoxolone are associated with attenuation of oxidative stress in ischemic brain injury

Protective effects of carbenoxolone are associated with attenuation of oxidative stress in ischemic brain injury

The role of ATP signaling in the migration of intermediate neuronal progenitors to the neocortical subventricular zone

Connexin 43 controls the multipolar phase of neuronal migration to the cerebral cortex

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