Involvement of protein kinase Cα (PKCα) in the early action of Angiotensin II type 2 (AT) effects on neurite outgrowth in NG108-15 cells: AT-receptor inhibits PKCα and p21 activity
Endocrinology, ISSN: 0013-7227, Vol: 147, Issue: 9, Page: 4263-4272
2006
- 19Citations
- 14Captures
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Metrics Details
- Citations19
- Citation Indexes19
- 19
- CrossRef15
- Captures14
- Readers14
- 14
Article Description
The aim of the present study was to investigate whether protein kinase C (PKC) isoforms may be among the putative candidates implicated in the primary effects of the Ang II type 2 (AT) receptor. Western blot analyses revealed the presence of PKCα,ε, ι, and ζ in NG108-15 cells. After a 3-d treatment with 3 nM Gö6976, a specific inhibitor of classical PKC isoforms, cells were characterized by the presence of one elongated process similar to that observed after treatment with Ang II or with CGP42112, a selective AT receptor agonist. Similar findings were observed in cells expressing a dominant-negative mutant of PKCα (K368A). Inhibition of PKCα in NG108-15 cells also decreased cell number and proliferation. In conditions of acute stimulation, Ang II induced a time-dependent and transient inhibition of PKCα activity, as well as a decrease in PKCα levels associated with the membrane. Treatment of cells with Gö6976 was also found to inhibit p21 (between 1-10 min) but stimulated Rap1 activity (1-5 min) in a timecourse similar to that of Ang II. Incubation of NG108-15 cells with Gö6976 (3 nM) inhibited basal p42/p44 phosphorylation, but failed to interfere with its activation by the AT receptor, indicating that inhibition of PKCα is not directly involved in the Rap1-MEK-p42/p44 cascade. Taken together, these results indicate that PKCα is a primary target of the AT receptor. Inhibition of PKCα leads to a decrease in both p21 activity and cell proliferation, which may facilitate AT receptor signaling through p42/p44, thereby leading to neurite outgrowth. Copyright © 2006 by The Endocrine Society.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=33747591655&origin=inward; http://dx.doi.org/10.1210/en.2006-0411; http://www.ncbi.nlm.nih.gov/pubmed/16740968; https://academic.oup.com/endo/article/147/9/4263/2528332; https://dx.doi.org/10.1210/en.2006-0411; https://academic.oup.com/endo/article-abstract/147/9/4263/2528332?redirectedFrom=fulltext
The Endocrine Society
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