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Estrogen-induced cell signaling in the sexually dimorphic nucleus of the rat preoptic area: Potential involvement of cofilin in actin dynamics for cell migration
•E2-induced PKC-δ/Rac1/PAK1/LIMK1/cofilin signaling in SDN-POA.•SDN-POA does not involve pathways including RhoA/ROCK/LIMK2.•Dynamics of cofilin phosphorylation occurred at SDN during the critical period.•Cell migration is a cue to the formation of sexual dimorphism in SDN-POA. Estrogen is a key fac...
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Published in: | Biochemical and biophysical research communications 2013-05, Vol.434 (2), p.287-292 |
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Main Authors: | , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | •E2-induced PKC-δ/Rac1/PAK1/LIMK1/cofilin signaling in SDN-POA.•SDN-POA does not involve pathways including RhoA/ROCK/LIMK2.•Dynamics of cofilin phosphorylation occurred at SDN during the critical period.•Cell migration is a cue to the formation of sexual dimorphism in SDN-POA.
Estrogen is a key factor to induce the sexually dimorphic nucleus (SDN) in the preoptic area (POA) of the rat brain. Identification of estrogen-dependent signaling pathways at SDN in POA during the critical period is a prerequisite for elucidating the mechanism. In the present study, we treated female rats with/without 17β-estradiol (E2) at birth, designated as postnatal day 1 (P1), and prepared total RNA from brain slices containing SDN for DNA microarray analysis. Among the estrogen-responsive genes identified, protein kinase C-delta (PKC-δ) was significantly up-regulated by E2 at P5. We examined the downstream effectors of PKC-δ protein by Western blotting and found an E2-induced PKC-δ/Rac1/PAK1/LIMK1/cofilin pathway. In the pathway, E2 suppressed the phosphorylation (inactive form) of cofilin. This result was supported by immunohistochemistry, where the phosphorylation/dephosphorylation of cofilin occurred at SDN, which suggests that cell migration is a cue to create sexual dimorphism in POA. |
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ISSN: | 0006-291X 1090-2104 |
DOI: | 10.1016/j.bbrc.2013.02.117 |