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RACK1 促进心肌肥厚模型中胚胎基因的上调。

RACK1 contributes to the upregulation of embryonic genes in a model of cardiac hypertrophy.

机构信息

DEB, University of Tuscia, Viterbo, Italy.

DNHA, Catholic University of Sacred Heart, Rome, Italy.

出版信息

Sci Rep. 2024 Oct 28;14(1):25698. doi: 10.1038/s41598-024-76138-x.

DOI:10.1038/s41598-024-76138-x
PMID:39465301
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11514175/
Abstract

Receptors for activated C kinases (RACKs) have been shown to coordinate PKC-mediated hypertrophic signalling in mice. However, little information is available on its participation in embryonic gene expression. This study investigated the involvement of RACK1 in the expression of embryonic genes in a zebrafish (ZF) ex vivo heart culture model by using phenylephrine (PE) or a growth factors cocktail (GFs) as a prohypertrophic/regeneration stimulus. Blebbistatin (BL) inhibition has also been studied for its ability to block the signal transduction actions of some PEs. qRT‒PCR and immunoblot analyses confirmed the upregulation of RACK1 in the PE- and GFs-treated groups. BL administration counteracted PE-induced hypertrophy and downregulated RACK1 expression. Immunohistochemical analyses of the heart revealed the colocalization of RACK1 and embryonic genes, namely, Gata4, Wt1, and Nfat2, under stimulation, whereas these genes were expressed at lower levels in the BL treatment group. Culturing ZF heart cells activated via GFs treatment increased the expression of RACK1. The overexpression of RACK1 induced by the transfection of recombinant RACK1 cDNA in ZF heart cells increased the expression of embryonic genes, especially after one week of GFs treatment. In summary, these results support the involvement of RACK1 in the induction of embryonic genes during cardiac hypertrophy/GFs stimulation in a fish heart model, which can be used as an alternative study model for mammals.

摘要

已证实激活的 C 激酶受体 (RACKs) 可协调蛋白激酶 C (PKC) 介导的小鼠肥厚信号。然而，关于其在胚胎基因表达中的参与的信息很少。本研究通过使用苯肾上腺素 (PE) 或生长因子鸡尾酒 (GFs) 作为促肥厚/再生刺激物，在斑马鱼 (ZF) 离体心脏培养模型中研究了 RACK1 参与胚胎基因表达的情况。还研究了 blebbistatin (BL) 抑制阻断某些 PEs 的信号转导作用的能力。qRT-PCR 和免疫印迹分析证实了 RACK1 在 PE 和 GFs 处理组中的上调。BL 给药可拮抗 PE 诱导的肥大，并下调 RACK1 表达。心脏免疫组织化学分析显示，在刺激下，RACK1 与胚胎基因（即 Gata4、Wt1 和 Nfat2）发生共定位，而在 BL 处理组中这些基因的表达水平较低。通过 GFs 处理激活的 ZF 心脏细胞培养增加了 RACK1 的表达。转染重组 RACK1 cDNA 后 ZF 心脏细胞中 RACK1 的过表达增加了胚胎基因的表达，尤其是在 GFs 处理一周后。总之，这些结果支持 RACK1 参与心脏肥大/GFs 刺激期间鱼类心脏模型中胚胎基因的诱导，可作为哺乳动物的替代研究模型。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41dc/11514175/daa4820f678a/41598_2024_76138_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41dc/11514175/04800fb281d2/41598_2024_76138_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41dc/11514175/ad434131d355/41598_2024_76138_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41dc/11514175/fff91a1b6b73/41598_2024_76138_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41dc/11514175/dd263c07dea2/41598_2024_76138_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41dc/11514175/6d69f3e2cfa5/41598_2024_76138_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41dc/11514175/d02a2c83d758/41598_2024_76138_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41dc/11514175/883e8c795db3/41598_2024_76138_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41dc/11514175/daa4820f678a/41598_2024_76138_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41dc/11514175/04800fb281d2/41598_2024_76138_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41dc/11514175/ad434131d355/41598_2024_76138_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41dc/11514175/fff91a1b6b73/41598_2024_76138_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41dc/11514175/dd263c07dea2/41598_2024_76138_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41dc/11514175/6d69f3e2cfa5/41598_2024_76138_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41dc/11514175/d02a2c83d758/41598_2024_76138_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41dc/11514175/883e8c795db3/41598_2024_76138_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41dc/11514175/daa4820f678a/41598_2024_76138_Fig8_HTML.jpg

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