Changes in gap junction organization and decreased coupling during induced apoptosis in lens epithelial and NIH-3T3 cells

Theiß, Carsten; Mazur, Antonina Joanna; Meller, Karl; Mannherz, Hans Georg

doi:10.1016/j.yexcr.2006.09.029

Cited by 22 publications

(17 citation statements)

References 41 publications

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“…We found that GJIC between cultured hepatocytes drastically decreases upon progression of the FasL/CHX-induced cell death response. This outcome is in line with the recent study of Theiss et al [33], showing strongly reduced cell-cell coupling between primary lens epithelial cells upon exposure to a number of apoptosis-inducing chemicals, including CHX. Kalvelyte et al [17] reported that abrogation of GJIC during apoptosis results from the removal of gap junctions and not from their functional closure.…”

Section: Discussionsupporting

confidence: 91%

Connexin32 hemichannels contribute to the apoptotic-to-necrotic transition during Fas-mediated hepatocyte cell death

Vinken

Decrock

Vuyst

et al. 2009

Cell. Mol. Life Sci.

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The present study was set up to investigate the fate of connexin32 and its channels in hepatocellular apoptosis. Primary hepatocyte cultures were exposed to Fas ligand and cycloheximide, and modifications in connexin32 expression and localization, and gap junction functionality were studied. We found that gap junction functionality rapidly declined upon progression of cell death, which was associated with a decay of the gap junctional connexin32 protein pool. Simultaneously, levels of newly synthesized connexin32 protein increased and gathered in a hemichannel configuration. This became particularly evident towards the end stages of the cell death process and was not reflected at the transcriptional level. We next either silenced connexin32 expression or inhibited connexin32 hemichannel activity prior to cell death induction. Both approaches resulted in a delayed termination of the cell death response. We conclude that connexin32 hemichannels facilitate the apoptotic-to-necrotic transition, which typically occurs in the final stage of hepatocellular apoptosis.

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Section: Discussionsupporting

confidence: 91%

Connexin32 hemichannels contribute to the apoptotic-to-necrotic transition during Fas-mediated hepatocyte cell death

Vinken

Decrock

Vuyst

et al. 2009

Cell. Mol. Life Sci.

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“…Indeed, in the WB-F344 rat liver epithelial cell model, serum deprivation 91 and exposure to the histone deacetylase inhibitor suberoylanilide hydroxamic acid 97 enhanced GJIC, particularly during the early phases of apoptosis, and simultaneously increased Cx43 phosphorylation. Inversely, inhibition of GJIC in primary bovine lens epithelial cells and primary human corneal fibroblasts by staurosporine 92 and TNFa 98 was accompanied by a decrease in the Cx43 phosphorylation status. Of note, alterations in Cx phosphorylation are frequently allied with modifications in cellular localization.…”

Section: Connexin-based Gap Junction Channels and Cell Deathmentioning

confidence: 94%

“…The abolishment of GJIC thus coincides with the typical morphological transformations that occur in apoptosis and results from an increased removal of GJ channels from the PM and not from their functional closure. 70 In a recent study, Theiss et al 92 exposed primary bovine lens epithelial cells and mouse NIH-3T3 fibroblasts to a number of well-established apoptosis-inducing agents. The authors noticed a decrease in GJIC that was associated with caspase 3-mediated degradation of Cx43.…”

Section: Connexin-based Gap Junction Channels and Cell Deathmentioning

confidence: 99%

Connexin-related signaling in cell death: to live or let die?

et al. 2009

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“…300 mg) as previously described [Theiss et al, 2007]. In short, tissue was homogenized in radioimmunoprecipitation assay buffer by rotor-stator treatment (UltraTurrax T8 homogenizer, IKA Labortechnik, Staufen, Germany) and centrifugated (15 min, 7000 rpm).…”

Section: Western Blottingmentioning

confidence: 99%

VEGF-Induced Growth Cone Enhancement Is Diminished by Inhibiting Tyrosine-Residue 1214 of VEGFR-2

Foehring

Brand‐Saberi

Theiß³

2012

Cells Tissues Organs

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Axonal outgrowth is of paramount significance for establishing the intricate neuronal network both during embryogenesis and nerve regeneration. Vascular endothelial growth factor (VEGF), which is known for its essential role in vascular sprouting and its involvement in cancer, has recently been found to exert a trophic activity on neurons leading to an increased axonal outgrowth. Although two receptors, VEGFR-2 and neuropilin-1, were identified on neurons, the signaling pathways associated with them are not well understood. The aim of this study was to analyze the influence of VEGF on the growth cone morphology and motility of dorsal root ganglia (DRG) neurons. Moreover, we aimed for a deeper understanding of VEGFR-2 on growth cones that potentially mediates the stimulating and attractive effects. We cultivated chicken DRG in medium containing mouse VEGF and analyzed growth cone size. The data presented here show a positive effect of VEGF on growth cone size. Furthermore, we interrupted the activity of VEGFR-2 by either blocking the tyrosine residue 1214 (tyr1214) or by inhibiting the receptor phosphorylation with axitinib, a novel small molecule, which has recently entered phase III trials for cancer treatment. Disruption of the VEGFR-2 leads to a significantly diminished growth cone size. Based on these findings, we propose a positive effect of VEGF on peripheral nervous system growth cone size and show for the first time quantitative data to underline this hypothesis. Additionally, we propose that VEGFR-2 and especially the tyr1214-dependent pathway of VEGFR-2 are of importance in VEGF signaling in the growth cone of DRG neurons.

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Changes in gap junction organization and decreased coupling during induced apoptosis in lens epithelial and NIH-3T3 cells

Cited by 22 publications

References 41 publications

Connexin32 hemichannels contribute to the apoptotic-to-necrotic transition during Fas-mediated hepatocyte cell death

Connexin32 hemichannels contribute to the apoptotic-to-necrotic transition during Fas-mediated hepatocyte cell death

Connexin-related signaling in cell death: to live or let die?

VEGF-Induced Growth Cone Enhancement Is Diminished by Inhibiting Tyrosine-Residue 1214 of VEGFR-2

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