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PRR activates canonical Wnt signaling pathway during pregnancy‐induced hypertension in rats
Author(s) -
Lopez Pedro,
RamirezMontero Claudia,
AnguianoRobledo Liliana,
AvilaRamirez Massiel A.,
HernandezCampos Maria Elena
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.942.9
Subject(s) - wnt signaling pathway , medicine , endocrinology , signal transduction , renin–angiotensin system , receptor , blood pressure , downregulation and upregulation , kidney , biology , microbiology and biotechnology , biochemistry , gene
Pregnancy is a physiological condition with profound hemodynamic changes. Pregnancy‐induced hypertension (PIH) is a common and severe complication. There is no a clear cause, but several systems have been involved. Renin Angiotensin Aldosterone System (RAAS) is one of them. Prorrenin renin receptor (PRR) a component of this system could play a role in PIH physiopathology. This receptor has been associated to Wnt signaling pathway, both canonical and non‐canonical. In this work we studied the posible activation of Wnt pathway by PRR in a PIH model in rats. We submitted female Wistar rats to sub‐renal aortic coarctation (SRAC) to induce PIH, set in control, pregnant‐non SRAC and pregnant‐SRAC groups. We measured blood pressure, proteinuria and offspring weight and size. We determined b‐catenin, DVL‐1, HDA4, JNK‐1and PKCa in aorta, heart, and kidney by immunoblot. We found and increased expression of PRR, b‐catenin, HDA4 and DVL‐1 in cardiac, renal and aortic tissue from PIH animals. Similar findings were shown using immunohistochemistry on same tissues. No significant changes were found in JNK‐1 and PKCa in any tissue. These results suggest that canonical Wnt pathway seems to be activated in the studied tissues during PIH, whereas non‐canonical pathway seems not to have a role in it. Support or Funding Information Supported by SIP20150457 grant