Abstract:
:NG108-15 cells, which have a rounding-up morphology when cultured in serum-supplemented medium, extend neurites when stimulated for 3 d with angiotensin II (Ang II). The aim of the present study was to investigate whether growth factor receptors are necessary for mediating the effects of Ang II. A 3-d treatment with AG879, an inhibitor of nerve growth factor receptor TrkA, strongly affected neurite outgrowth and phosphorylation of p42/p44(mapk) induced by Ang II. PD168393, an inhibitor of epidermal growth factor (EGF) receptor slightly decreased Ang II-induced neurite outgrowth, whereas AG213, an inhibitor of both platelet-derived growth factor receptor and EGF receptor, stimulated neurite outgrowth and p42/p44(mapk) phosphorylation on its own, without affecting further stimulation with Ang II. Moreover, Ang II induced the phosphorylation of TrkA (maximum at 5 min of incubation in the presence of serum or at 20 min in cells depleted in serum for 2 h) and a rapid increase in Rap1 activity, both effects abolished in cells preincubated with 10 microm AG879. In summary, the present results demonstrate that AT(2) receptor-induced sustained activation of p42/p44(mapk) and corresponding neurite outgrowth are mediated by phosphorylation of the nerve growth factor TrkA receptor. However, the results also point out that the presence of other growth factors, such as EGF or PDFG, may interfere with the effect of Ang II. Altogether, the current findings clearly indicate that the effects of the AT(2) receptor on neurite outgrowth dynamics are modulated by the presence of growth factors in the culture medium.
journal_name
Endocrinologyjournal_title
Endocrinologyauthors
Plouffe B,Guimond MO,Beaudry H,Gallo-Payet Ndoi
10.1210/en.2005-1315subject
Has Abstractpub_date
2006-10-01 00:00:00pages
4646-54issue
10eissn
0013-7227issn
1945-7170pii
en.2005-1315journal_volume
147pub_type
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