关键词: SLC22A16 abdominal adipocytes chicken lncRNA

Mesh : Animals Adipocytes / metabolism cytology Chickens / genetics Adipogenesis / genetics RNA, Long Noncoding / genetics Cell Differentiation / genetics Cell Proliferation / genetics

来  源:   DOI:10.3390/genes15060758   PDF(Pubmed)

Abstract:
The excessive deposition of abdominal adipocytes in chickens is detrimental to poultry production. However, the regulatory factors that affect abdominal adipogenesis in chickens are still poorly understood. SLC22A16 is differentially expressed in abdominal preadipocytes and 10-day differentiated adipocytes in chickens, but its role in regulating chicken adipogenesis has not been reported. In this study, the function of SLC22A16 in chicken abdominal preadipocytes was investigated. SLC22A16 is significantly upregulated during abdominal adipocyte differentiation. The overexpression of SLC2A16 upregulated the expression of adipogenic marker genes and proliferation-related genes, and promoted the proliferation of adipocytes and the accumulation of triglycerides. The knockdown of SLC22A16 downregulated the expression of adipogenic marker genes and proliferation-related genes, inhibited the proliferation of adipocytes, and impaired the accumulation of triglycerides in adipocytes. In addition, LNC6302 was differentially expressed in abdominal preadipocytes and mature adipocytes, and was significantly positively correlated with the expression of SLC22A16. Interference with LNC6302 inhibits the expression of adipogenic marker genes and proliferation-related genes. The data supported the notion that LNC6302 promotes the differentiation of chicken abdominal adipocytes by cis-regulating the expression of SLC22A16. This study identified the role of SLC22A16 in the differentiation and proliferation of chicken adipocytes, providing a potential target for improving abdominal adipogenesis in chickens.
摘要:
鸡腹部脂肪细胞的过度沉积对家禽生产有害。然而,影响鸡腹部脂肪形成的调节因素仍然知之甚少。SLC22A16在鸡的腹部前脂肪细胞和10天分化脂肪细胞中差异表达,但其在调节鸡脂肪生成中的作用尚未见报道。在这项研究中,研究了SLC22A16在鸡腹部前脂肪细胞中的功能。SLC22A16在腹部脂肪细胞分化过程中显著上调。SLC2A16过表达上调成脂标记基因和增殖相关基因的表达,并促进脂肪细胞的增殖和甘油三酯的积累。SLC22A16基因敲除下调成脂标记基因和增殖相关基因的表达,抑制脂肪细胞的增殖,并损害甘油三酸酯在脂肪细胞中的积累。此外,LNC6302在腹前脂肪细胞和成熟脂肪细胞中差异表达,与SLC22A16的表达呈显著正相关。干扰LNC6302抑制成脂标记基因和增殖相关基因的表达。数据支持LNC6302通过顺式调节SLC22A16的表达促进鸡腹部脂肪细胞分化的观点。本研究确定了SLC22A16在鸡脂肪细胞分化和增殖中的作用。为改善鸡腹部脂肪形成提供了潜在的靶标。
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