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Effect of angiotensin II and angiotensin‐(1–7) on proliferation of stem cells from human dental apical papilla
Author(s) -
Macedo Larissa M.,
Ávila Renato I.,
Pedrino Gustavo R.,
Colugnati Diego B.,
Valadares Marize C.,
Lima Eliana M.,
Borges Clayton L.,
Kitten Gregory T.,
Gava Elisandra,
Castro Carlos H.
Publication year - 2021
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.29862
Subject(s) - angiotensin ii , microbiology and biotechnology , angiotensin ii receptor type 1 , renin–angiotensin system , cell growth , chemistry , stem cell , intracellular , receptor , phosphorylation , endocrinology , medicine , biology , biochemistry , blood pressure
Abstract The effects of the renin–angiotensin system (RAS) on stem cells isolated from human dental apical papilla (SCAPs) are completely unknown. Therefore, the aim of this study was to identify RAS components expressed in SCAPs and the effects of angiotensin (Ang) II and Ang‐(1–7) on cell proliferation. SCAPs were collected from third molar teeth of adolescents and maintained in cell culture. Messenger RNA expression and protein levels of angiotensin‐converting enzyme (ACE), ACE2, and Mas, Ang II type I (AT1) and type II (AT2) receptors were detected in SCAPs. Treatment with either Ang II or Ang‐(1–7) increased the proliferation of SCAPs. These effects were inhibited by PD123319, an AT2 antagonist. While Ang II augmented mTOR phosphorylation, Ang‐(1–7) induced ERK1/2 phosphorylation. In conclusion, SCAPs produce the main RAS components and both Ang II and Ang‐(1–7) treatments induced cell proliferation mediated by AT2 activation through different intracellular mechanisms.