Abstract
Astrocytes form functional networks that participate in active signaling in which external stimuli are generated and amplified in many of the same ways as in neurons. Gap junctions between astrocytes offer the structural avenue by which the electrical and metabolic signals are propagated from one cell to another. Little is known about the trafficking, assembly, and degradation mechanisms of the major astrocytic gap junction protein connexin43. We have studied a glial cell line transfected with the C- erbB2/neu oncogene (neu+), finding severe interruption of gap junctional communication after stable transfection. Evidence from Western blotting and phosphorylation studies showed that the processing of connexin43 to its higher phosphorylated isoforms is disturbed. Confocal laser imaging indicates that the major deficit in the neu+ cells is attributable to a lack in plaque assembly of connexin43. Because the neu+ cells also lack N-CAM proteins and because work from others has indicated a close relationship between communication competence and constitutive CAM expression, our data suggest that expression of C-erbB2/neu oncogene alters cell-cell association via CAM proteins, which thereby affects gap junction plaque assembly and appropriate phosphorylation of connexin43.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 4311-4321 |
| Number of pages | 11 |
| Journal | Journal of Neuroscience |
| Volume | 16 |
| Issue number | 14 |
| State | Published - Jul 15 1996 |
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Keywords
- astrocytes
- connexin43
- gap junctions
- N-CAM
- oncogene
- phosphorylation
ASJC Scopus subject areas
- Neuroscience(all)
Cite this
C-erbB2/neu transfection induces gap junctional communication incompetence in glial cells. / Hofer, Andreas; Sáez, Juan C.; Chang, Chia Cheng; Trosko, James E.; Spray, David C.; Dermietzel, Rolf.
In: Journal of Neuroscience, Vol. 16, No. 14, 15.07.1996, p. 4311-4321.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - C-erbB2/neu transfection induces gap junctional communication incompetence in glial cells
AU - Hofer, Andreas
AU - Sáez, Juan C.
AU - Chang, Chia Cheng
AU - Trosko, James E.
AU - Spray, David C.
AU - Dermietzel, Rolf
PY - 1996/7/15
Y1 - 1996/7/15
N2 - Astrocytes form functional networks that participate in active signaling in which external stimuli are generated and amplified in many of the same ways as in neurons. Gap junctions between astrocytes offer the structural avenue by which the electrical and metabolic signals are propagated from one cell to another. Little is known about the trafficking, assembly, and degradation mechanisms of the major astrocytic gap junction protein connexin43. We have studied a glial cell line transfected with the C- erbB2/neu oncogene (neu+), finding severe interruption of gap junctional communication after stable transfection. Evidence from Western blotting and phosphorylation studies showed that the processing of connexin43 to its higher phosphorylated isoforms is disturbed. Confocal laser imaging indicates that the major deficit in the neu+ cells is attributable to a lack in plaque assembly of connexin43. Because the neu+ cells also lack N-CAM proteins and because work from others has indicated a close relationship between communication competence and constitutive CAM expression, our data suggest that expression of C-erbB2/neu oncogene alters cell-cell association via CAM proteins, which thereby affects gap junction plaque assembly and appropriate phosphorylation of connexin43.
AB - Astrocytes form functional networks that participate in active signaling in which external stimuli are generated and amplified in many of the same ways as in neurons. Gap junctions between astrocytes offer the structural avenue by which the electrical and metabolic signals are propagated from one cell to another. Little is known about the trafficking, assembly, and degradation mechanisms of the major astrocytic gap junction protein connexin43. We have studied a glial cell line transfected with the C- erbB2/neu oncogene (neu+), finding severe interruption of gap junctional communication after stable transfection. Evidence from Western blotting and phosphorylation studies showed that the processing of connexin43 to its higher phosphorylated isoforms is disturbed. Confocal laser imaging indicates that the major deficit in the neu+ cells is attributable to a lack in plaque assembly of connexin43. Because the neu+ cells also lack N-CAM proteins and because work from others has indicated a close relationship between communication competence and constitutive CAM expression, our data suggest that expression of C-erbB2/neu oncogene alters cell-cell association via CAM proteins, which thereby affects gap junction plaque assembly and appropriate phosphorylation of connexin43.
KW - astrocytes
KW - connexin43
KW - gap junctions
KW - N-CAM
KW - oncogene
KW - phosphorylation
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M3 - Article
VL - 16
SP - 4311
EP - 4321
JO - Journal of Neuroscience
JF - Journal of Neuroscience
SN - 0270-6474
IS - 14
ER -