科学家通过针对蝌蚪的实验,发现在蝌蚪的心脏发育完成之后,移除蝌蚪体内的IGFBP-4蛋白质，蝌蚪的心脏变得越来越小最后竟然消失了。
研究人员目前尚不清楚IGFBP-4蛋白质是否能在人体胚胎干细胞分化过程中起到作用。但是实验表明IGFBP-4蛋白质在维护心脏健康发育方面能起到非常重要的作用。
IGFBP-4蛋白质是由肝脏产生的。胎儿首先形成的是心脏,然后等生长到中期阶段时,IGFBP-4蛋白质才开始起作用,它对心脏的发育很重要。心脏长成之后,如果IGFBP-4蛋白质被移除,心脏就会慢慢消失。蝌蚪实验证实了这一理论。
原始出处：
IGFBP-4 is an inhibitor of canonical Wnt signalling required for cardiogenesis
Weidong Zhu1,8, Ichiro Shiojima1,8, Yuzuru Ito2,8, Zhi Li1, Hiroyuki Ikeda1, Masashi Yoshida1, Atsuhiko T. Naito1, Jun-ichiro Nishi1, Hiroo Ueno3, Akihiro Umezawa4, Tohru Minamino1, Toshio Nagai1, Akira Kikuchi5, Makoto Asashima2,6,7 & Issei Komuro1
- Department of Cardiovascular Science and Medicine, Chiba University Graduate School of Medicine, Chiba 260-8670, Japan
- ICORP Organ Regeneration Project, Japan Science and Technology Agency (JST), Tokyo 153-8902, Japan
- Institute of Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, California 94305, USA
- Department of Reproductive Biology, National Institute for Child Health and Development, Tokyo 157-8535, Japan
- Department of Biochemistry, Graduate School of Biomedical Sciences, Hiroshima University, Hiroshima 734-8551, Japan
- Department of Life Sciences (Biology), Graduate School of Arts and Science, The University of Tokyo, Tokyo 153-8902, Japan
- National Institute of Advanced Industrial Sciences and Technology (AIST), Ibaraki 305-8562, Japan
- These authors contributed equally to this work.
Correspondence to: Issei Komuro1 Correspondence and requests for materials should be addressed to I.K. (Email: komuro-tky@umin.ac.jp).
Insulin-like growth-factor-binding proteins (IGFBPs) bind to and modulate the actions of insulin-like growth factors (IGFs)1. Although some of the actions of IGFBPs have been reported to be independent of IGFs, the precise mechanisms of IGF-independent actions of IGFBPs are largely unknown1, 2. Here we report a previously unknown function for IGFBP-4 as a cardiogenic growth factor. IGFBP-4 enhanced cardiomyocyte differentiation in vitro, and knockdown of Igfbp4 attenuated cardiomyogenesis both in vitro and in vivo. The cardiogenic effect of IGFBP-4 was independent of its IGF-binding activity but was mediated by the inhibitory effect on canonical Wnt signalling. IGFBP-4 physically interacted with a Wnt receptor, Frizzled 8 (Frz8), and a Wnt co-receptor, low-density lipoprotein receptor-related protein 6 (LRP6), and inhibited the binding of Wnt3A to Frz8 and LRP6. Although IGF-independent, the cardiogenic effect of IGFBP-4 was attenuated by IGFs through IGFBP-4 sequestration. IGFBP-4 is therefore an inhibitor of the canonical Wnt signalling required for cardiogenesis and provides a molecular link between IGF signalling and Wnt signalling.
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