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In zvadfmk to Masckauchan et al., we did not detect proliferative nor promigratory effects of Wnt5a on HUVEC. These results might be explained by the difference in receptor context since Masckauchan et al. detected FZD5 transcript in HUVEC, besides of FZD4 and FZD6 [17].
To uncover the receptor conveying the signal for Wnt3a-induced proliferation, we made use of purified Fzd4-cysteine rich domain (CRD). When added to HUVECs with Wnt3a, the Fzd4-CRD inhibited the proliferative effects of Wnt3a, suggesting that this receptor might transduce the Wnt3a proliferative signals.
In a search for the downstream pathway activated upon Wnt3a treatment, we detected stabilization of β-catenin, indicating activation of the canonical Wnt pathway. The upregulation of the transcript from the known canonical Wnt target gene c-MYC upon treatment with Wnt3a ligand is in line with incomplete flower observation. However, we also detected an upregulation of the TIE-2 transcript, a gene that has previously been shown to be downstream of non-canonical Wnt signaling in HUVECs [17]. Taken together with the observation that addition of the CamKII inhibitor, which blocks a branch of the Wnt–calcium pathway, suppresses Wnt3a-induced proliferation, these results suggest that Wnt3a may affect HUVEC biology through both canonical and non-canonical Wnt signaling.