Abstract
Increasing data suggest that glutamate might act as a cell-signaling molecule in non-neuronal tissues such as the skin. Here we demonstrate the presence of functional N-methyl-D-aspartate (NMDA)-type glutamate receptors in human keratinocytes. NMDA receptor expression strongly reflects the degree of cell-to-cell contact. Wounding polarizes the expression of NMDA receptors in keratinocytes involved in re-epithelialization, and the process of re-epithelialization is inhibited by NMDA receptor activation. We also demonstrate that squamous cell carcinomas lack NMDA receptors. Our data suggest that Ca2+ entry through NMDA receptors influences the cycle of keratinocyte proliferation, differentiation, and migration during epithelialization. Moreover, NMDA receptor activation might play a role in contact-mediated inhibition of growth, a process that is absent during neoplastic pathology. This receptor may serve as a pharmacological target for modulating keratinocyte behavior and treating cutaneous disorders.
| Original language | English |
|---|---|
| Pages (from-to) | 309-317 |
| Number of pages | 9 |
| Journal | Journal of Cellular Physiology |
| Volume | 200 |
| Issue number | 2 |
| DOIs | |
| State | Published - Aug 1 2004 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Clinical Biochemistry
- Cell Biology
- Physiology
Cite this
Significance of N-methyl-D-aspartate (NMDA) receptor-mediated signaling in human keratinocytes. / Nahm, Walter K.; Philpot, Benjamin D.; Adams, Michelle M.; Badiavas, Evangelos V; Zhou, Linda H.; Butmarc, Janet; Bear, Mark F.; Falanga, Vincent.
In: Journal of Cellular Physiology, Vol. 200, No. 2, 01.08.2004, p. 309-317.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Significance of N-methyl-D-aspartate (NMDA) receptor-mediated signaling in human keratinocytes
AU - Nahm, Walter K.
AU - Philpot, Benjamin D.
AU - Adams, Michelle M.
AU - Badiavas, Evangelos V
AU - Zhou, Linda H.
AU - Butmarc, Janet
AU - Bear, Mark F.
AU - Falanga, Vincent
PY - 2004/8/1
Y1 - 2004/8/1
N2 - Increasing data suggest that glutamate might act as a cell-signaling molecule in non-neuronal tissues such as the skin. Here we demonstrate the presence of functional N-methyl-D-aspartate (NMDA)-type glutamate receptors in human keratinocytes. NMDA receptor expression strongly reflects the degree of cell-to-cell contact. Wounding polarizes the expression of NMDA receptors in keratinocytes involved in re-epithelialization, and the process of re-epithelialization is inhibited by NMDA receptor activation. We also demonstrate that squamous cell carcinomas lack NMDA receptors. Our data suggest that Ca2+ entry through NMDA receptors influences the cycle of keratinocyte proliferation, differentiation, and migration during epithelialization. Moreover, NMDA receptor activation might play a role in contact-mediated inhibition of growth, a process that is absent during neoplastic pathology. This receptor may serve as a pharmacological target for modulating keratinocyte behavior and treating cutaneous disorders.
AB - Increasing data suggest that glutamate might act as a cell-signaling molecule in non-neuronal tissues such as the skin. Here we demonstrate the presence of functional N-methyl-D-aspartate (NMDA)-type glutamate receptors in human keratinocytes. NMDA receptor expression strongly reflects the degree of cell-to-cell contact. Wounding polarizes the expression of NMDA receptors in keratinocytes involved in re-epithelialization, and the process of re-epithelialization is inhibited by NMDA receptor activation. We also demonstrate that squamous cell carcinomas lack NMDA receptors. Our data suggest that Ca2+ entry through NMDA receptors influences the cycle of keratinocyte proliferation, differentiation, and migration during epithelialization. Moreover, NMDA receptor activation might play a role in contact-mediated inhibition of growth, a process that is absent during neoplastic pathology. This receptor may serve as a pharmacological target for modulating keratinocyte behavior and treating cutaneous disorders.
UR - http://www.scopus.com/inward/record.url?scp=3042818143&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=3042818143&partnerID=8YFLogxK
U2 - 10.1002/jcp.20010
DO - 10.1002/jcp.20010
M3 - Article
C2 - 15174101
AN - SCOPUS:3042818143
VL - 200
SP - 309
EP - 317
JO - Journal of Cellular Physiology
JF - Journal of Cellular Physiology
SN - 0021-9541
IS - 2
ER -