Wnt5a媒介による中性粒子の徴集は,圧力の過剰に起因する心臓機能不全において必須である

Ying Wang^1,2, Soichi Sano¹, Kosei Oshima³

¹Hematovascular Biology Center, Robert M. Berne Cardiovascular Research Center, University of Virginia School of Medicine, Charlottesville (Y. Wang, S.S., M.S., Y.Y., C.J., K.W.).

Circulation

|June 8, 2019

まとめ

中性粒子は圧力の過剰に起因する心不全に重要な役割を果たします. Wnt5aのシグナリングは中性粒子の浸透を調節し,心臓の過剰成長と機能に影響を与えます.

科学分野:

心臓病科
免疫学
分子生物学

背景:

心筋損傷におけるマクロファージの役割は知られているが,非発血性心疾患における中性粒子は十分に研究されていない.
圧力過負荷による心筋縮における中性粒子の機能の調査は,心不全を理解するために極めて重要です.

研究の目的:

圧力過負荷による心筋縮における中性粒子の役割と調節を解明する.
中性粒子の浸透と心臓病変に Wnt5a 信号の関与を決定する.

主な方法:

ネズミは,中性粒子を枯渇させるためのLy6G抗体で治療された.
ネズミは圧力の過負荷を誘導するために横動脈収縮 (TAC) を受けました.
Wnt5aの発現は骨髄細胞 (欠乏または過剰発現) で操作された.

主要な成果:

中性粒子の減少は,TAC誘発の心筋縮,炎症を緩和し,心筋機能を保ちました.
ミエロイドWnt5a欠乏症は中性粒子の浸透を抑制し,中性粒子の減少を模倣した.
骨髄細胞におけるWnt5aの過剰発現は,心臓の縮,炎症,機能障害を悪化させた.

結論:

Wnt5a調節された中性粒子の浸透は,圧力の過剰に起因する心不全において極めて重要です.
中性粒子の浸透をターゲットにすることで,心筋縮と心不全の治療策を提供することができる.

キーワード:

心臓ヘマトポエーシス炎症

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