Premium
Isoforms of VEGF‐A in the Developing Feline Placenta
Author(s) -
Weerakoon Shaneke,
Frydman Galit,
Martin Cassandra,
Gudenschwager Kristobal,
Huckle William
Publication year - 2015
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.29.1_supplement.lb622
Subject(s) - gene isoform , biology , placenta , messenger rna , gestation , alternative splicing , medicine , vascular endothelial growth factor , andrology , endocrinology , vegf receptors , microbiology and biotechnology , fetus , pregnancy , gene , cancer research , genetics
Development of the placental vasculature is crucial for successful gestation. Previous studies have suggested a significant role for VEGF‐A during placental vascularization, but distribution of VEGF‐A protein isoforms and their distinct biological activities over the course of placental development have not been thoroughly characterized. We aimed to determine the temporal distribution of expressed VEGF‐A mRNA splice variants during feline placental development. We hypothesize that observed dynamics of isoform expression will reflect their postulated angiogenic roles–promoting neo‐vessel branching or enlargement–at the appropriate period during gestation. cDNAs, prepared from feline placental RNAs in tissue removed during elective ovariohysterectomies, contained VEGF isoforms VEGF‐A 163 and VEGF‐A 181 , which were subcloned as assay controls. Isoform‐specific qRT‐PCR revealed that temporal distribution of both isoforms at the mRNA level followed patterns similar to that of the panVEGF‐A pool, with a trend upward in expression early in gestation, followed by a steady decline toward full term. However, mRNA encoding VEGF‐A 181 remained elevated over time relative to either the panVEGF‐A pool or VEGF‐A 163 . Preferential expression of VEGF‐A 181 earlier in gestation is consistent with its postulated role in vessel branching. VEGF‐A 163 , a potentially vessel‐enlarging isoform, was not preferentially expressed later in gestation as predicted. Future work will quantify additional known VEGF‐A isoforms and elucidate the biochemical mechanisms underlying the shifts in relative mRNA splice variant abundance during gestation.