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Atypical protein kinase C is essential for embryonic vascular development in mice
Author(s) -
Chen Zee,
Duan Yaoyun,
Wang Hong,
Tang Huayuan,
Wang Shijia,
Wang Xinru,
Liu Jie,
Fang Xi,
Ouyang Kunfu
Publication year - 2021
Publication title -
genesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.093
H-Index - 110
eISSN - 1526-968X
pISSN - 1526-954X
DOI - 10.1002/dvg.23412
Subject(s) - protein kinase c , embryonic stem cell , microbiology and biotechnology , biology , gene isoform , embryogenesis , embryo , angiogenesis , apoptosis , yolk sac , kinase , cancer research , genetics , gene
Summary The atypical PKC (aPKC) subfamily constitutes PKCζ and PKCλ in mice, and both aPKC isoforms have been proposed to be involved in regulating various endothelial cell (EC) functions. However, the physiological function of aPKC in ECs during embryonic development has not been well understood. To address this question, we utilized Tie2‐Cre to delete PKCλ alone (PKCλ‐SKO) or both PKCλ and PKCζ (DKO) in ECs, and found that all DKO mice died at around the embryonic day 11.5 (E11.5), whereas a small proportion of PKCλ‐SKO mice survived till birth. PKCλ‐SKO embryos also exhibited less phenotypic severity than DKO embryos at E10.5 and E11.5, suggesting a potential compensatory role of PKCζ for PKCλ in embryonic ECs. We then focused on DKO embryos and investigated the effects of aPKC deficiency on embryonic vascular development. At E9.5, deletion of both aPKC isoforms reduced the diameters of vitelline artery and vein, and decreased branching from both vitelline vessels in yolk sac. Ablation of both aPKC isoforms also disrupted embryonic angiogenesis in head and trunk at the same stage, increasing apoptosis of both ECs and non‐ECs. Taken together, our results demonstrated that aPKC in ECs plays an essential role in regulating cell apoptosis, angiogenesis, and embryonic survival.

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