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Interaction between thyrocytes and adipose tissue in vitro

机译:甲状腺细胞与脂肪组织之间的相互作用

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Adipose tissue (AT)-thyrocyte interaction is largely unknown. Here we described the interaction in a co-culture system, in which thyrocytes were cultured on AT fragment (ATF)-embedded collagen gel, using electron microscopy, immunocytochemistry, real-time reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA). ATFs promoted the hypertrophy, polarization and lipid accumulation of thyrocytes. ATFs did not affect the growth of thyroyctes, and inhibited their apoptosis. ATFs increased the protein expression of thyroglobulin (Tg) and paired box gene 8 (PAX8) in thyrocytes. In turn, thyrocytes decreased the concentration of leptin and adiponectin, and increased the expression of these mRNAs in ATFs. Thyrotropin (TSH) enhanced the ATF-induced nuclear hypertrophy and Tg protein expression in thyrocytes, while TSH enhanced the thyrocyte-induced expression of leptin and adiponectin mRNAs in ATFs. Finally, leptin promoted the hypertrophy and Tg protein expression in thyrocytes. TSH enhanced these leptin-induced effects. The data indicate an active interaction between thyrocytes and AT, suggesting that (i) ATFs may serve to regulate the morphology, survival and differentiation of thyrocytes probably through lipid accumulation partly in a TSH-synergistic way; (ii) thyrocytes may affect adipokine production from ATFs in a TSH-independent manner; and (3) leptin may be related to the hypertrophy and differentiation of thyrocytes in a TSH-synergistic way.
机译:脂肪组织(AT)与甲状腺细胞的相互作用在很大程度上是未知的。在这里,我们描述了在共培养系统中的相互作用,在该系统中,使用电子显微镜,免疫细胞化学,实时逆转录聚合酶链反应(RT-PCR)和酶将甲状腺细胞培养在嵌入AT片段(ATF)的胶原蛋白凝胶上联免疫吸附测定(ELISA)。 ATF促进甲状腺细胞的肥大,极化和脂质蓄积。 ATF不影响甲状腺细胞的生长,并抑制其凋亡。 ATFs增加了甲状腺细胞中甲状腺球蛋白(Tg)和配对框基因8(PAX8)的蛋白表达。反过来,甲状腺细胞降低了瘦素和脂联素的浓度,并增加了这些mRNA在ATF中的表达。促甲状腺素(TSH)增强了ATF诱导的甲状腺细胞核肥大和Tg蛋白表达,而TSH增强了TTF诱导的甲状腺细胞瘦素和脂联素mRNA表达。最终,瘦素促进了甲状腺细胞中的肥大和Tg蛋白表达。 TSH增强了这些瘦素诱导的作用。数据表明,甲状腺细胞与AT之间存在活跃的相互作用,这表明(i)ATF可能部分通过TSH协同方式通过脂质蓄积来调节甲状腺细胞的形态,存活和分化。 (ii)甲状腺细胞可能以与TSH无关的方式影响ATF产生的脂肪因子; (3)瘦素可能以TSH协同方式与甲状腺细胞肥大和分化有关。

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