Role of miR29c in goose fatty liver is mediated by its target genes that are involved in energy homeostasis and cell growth.
Role of miR29c in goose fatty liver is mediated by its target genes that are involved in energy homeostasis and cell growth.
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miR29c 在鹅脂肪肝中的作用是由其参与能量稳态和细胞生长的靶基因介导的
DOI：
10.1186/s12917-018-1653-3
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发表时间：
2018-11-06
影响因子：
2.6
通讯作者：
Gong D
中科院分区：
文献类型：
--
作者：
Liu L;Wang Q;Wang Q;Zhao X;Zhao P;Geng T;Gong D
短时间的过度喂养会导致鹅发生严重的肝脏脂肪变性，这是生理性的，表明鹅作为迁徙祖先的后代，可能在进化上发展了一种独特的机制，与人类或其他哺乳动物的病理性脂肪肝机制相反。在这项研究中，我们报告说，与正常肝脏相比，在鹅脂肪肝中miR 29 c的抑制及其靶基因的上调可能是一种独特机制的一部分，这种机制有助于调节能量稳态和细胞生长。我们的数据表明，miR 29 c的表达被全面抑制的能量稳态相关的组织（肝脏，脂肪和肌肉）的过度喂养与正常喂养的鹅，这是不同的miR 29 c的诱导，发生在组织中的糖尿病大鼠。为了解决miR 29 c的功能，三个预测的靶基因（即，Insig 1、Sgk 1和Col 3a 1）参与能量稳态或细胞生长，并通过双荧光报告系统和其他体外试验进行了验证。重要的是，Insig 1，Sgk 1和Col 3a 1在鹅脂肪肝中的表达上调。与这些观察结果一致，用高葡萄糖或棕榈酸盐处理鹅肝细胞抑制了miR 29 c的表达，但诱导了靶基因的表达，这表明高血糖症和高脂血症至少部分有助于抑制miR 29 c和诱导鹅脂肪肝中的靶基因。此外，药理学分析表明RFX 1是参与miR 29 c表达的转录因子。这项研究表明，miR 29 c可能通过其靶基因在调节能量稳态和组织生长方面发挥作用，有助于鹅对严重肝脂肪变性的耐受性。本文的在线版本（10.1186/s12917-018-1653-3）包含补充材料，可供授权用户使用。
A short period of overfeeding can lead to severe hepatic steatosis in the goose, which is physiological, suggesting that geese, as a descendent of a migrating ancestor, may have evolutionally developed a unique mechanism that operates in contrast to the mechanism underlying pathological fatty liver in humans or other mammals. In this study, we report that suppression of miR29c and upregulation of its target genes in goose fatty liver vs. normal liver could be part of a unique mechanism that contributes to the regulation of energy homeostasis and cell growth. Our data showed that miR29c expression was comprehensively inhibited in energy homeostasis-related tissues (the liver, fat and muscle) of overfed vs. normally fed geese, which is different from miR29c induction that occurs in tissues of the diabetic rat. To address the function of miR29c, three predicted target genes (i.e., Insig1, Sgk1 and Col3a1) that participate in energy homeostasis or cell growth were validated by a dual-fluorescence reporter system and other in vitro assays. Importantly, expression of Insig1, Sgk1 and Col3a1 was upregulated in goose fatty liver. In line with these observations, treatment of goose hepatocytes with high glucose or palmitate suppressed the expression of miR29c but induced the expression of the target genes, suggesting that hyperglycemia and hyperlipidemia, at least partially, contribute to the suppression of miR29c and induction of the target genes in goose fatty liver. In addition, pharmacological assays indicated that RFX1 was a transcription factor involved in the expression of miR29c. This study suggests that miR29c may play a role in the regulation of energy homeostasis and tissue growth via its target genes, contributing to the tolerance of the goose to severe hepatic steatosis. The online version of this article (10.1186/s12917-018-1653-3) contains supplementary material, which is available to authorized users.
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