Energy status determines hindbrain signal transduction pathway transcriptional reactivity to AMPK in the estradiol-treated ovariectomized female rat.
Energy status determines hindbrain signal transduction pathway transcriptional reactivity to AMPK in the estradiol-treated ovariectomized female rat.
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DOI：
10.1016/j.neuroscience.2014.10.068
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发表时间：
2015-01-22
期刊：
影响因子：
3.3
通讯作者：
Briski, K. P.
中科院分区：
文献类型：
--
作者：
Ibrahim, B. A.;Alenazi, F. S. H.;Briski, K. P.
雌激素处理的卵巢切除（OVX）雌性大鼠的背迷走神经复合体（DVC）AMPK对摄食的调节是能量状态依赖性的。在这里，RT-PCR阵列技术被用来确定雌二醇敏感的AMPK调节的DVC信号转导途径，表现出不同的反应性，传感器激活过程中的能量平衡与不平衡。AMP模拟物AICAR相应地减少或刺激了全饲（F）和禁食12小时（D）雌二醇治疗的卵巢切除（OVX）大鼠中的cDVC磷酸化AMPK（pAMPK）和雌激素受体β（ERβ）蛋白，但仅在F中升高ER α（ERα）。与OVX对照组相比，雌二醇抑制DVC ERβ蛋白和缺氧、NFκB、STAT 3、STAT 6和Hedgehog信号通路标记基因。与F+S相比，F +（A）ICAR和D +（S）aline组均进一步抑制了NFκB、STAT 3和Hedgehog通路基因，并减少了PPAR、Notch和STAT 5转录。相反，AICAR处理D.结果表明，在该动物模型中，急性AMP增加或喂养停止各自抑制pAMPK和ERβ表达，但组合增加这些蛋白质谱。在F和D状态下，AICAR分别平行下调或上调pAMPK蛋白和DVC TNF（NFκB）、SOCS 3（JAK/STAT）、WNT 6（Hedgehog）和FABP 1（PPAR）mRNA。需要进一步的研究来确定ERβ对这些反应的相反方向性的影响，并表征上述信号通路在急性进食中断期间雌性动物对AICAR诱导的DVC AMPK激活的过度吞噬反应中的作用。
Dorsal vagal complex (DVC) AMPK regulation of food intake in the estradiol-treated ovariectomized (OVX) female rat is energy state-dependent. Here, RT-PCR array technology was used to identify estradiol-sensitive AMPK-regulated DVC signal transduction pathways that exhibit differential reactivity to sensor activation during energy balance versus imbalance. The AMP mimetic AICAR correspondingly reduced or stimulated cDVC phosphoAMPK (pAMPK) and estrogen receptor-beta (ERβ) proteins in full-fed (F) versus 12 hr food-deprived (D) estradiol-treated ovariectomized (OVX) rats, but elevated ER-alpha (ERα) in F only. Estradiol suppressed DVC ERβ protein and hypoxia, NFκB, STAT3, STAT6, and Hedgehog signaling pathway marker genes against oil-implanted OVX controls. F + (A)ICAR and D + (S)aline groups each exhibited further inhibition of NFκB, STAT3, and Hedgehog pathway genes, and diminished PPAR, Notch, and STAT5 transcripts versus F+S. Conversely, genes in these six pathways were up-regulated by AICAR treatment of D. Results show that in this animal model, acute AMP augmentation or feeding cessation each inhibit both pAMPK and ERβ expression, but in combination increase these protein profiles. pAMPK protein and DVC TNF (NFκB), SOCS3 (JAK/STAT), WNT6 (Hedgehog), and FABP1 (PPAR) mRNAs were down- or upregulated in parallel by AICAR in F versus D states, respectively. Further research is needed to determine the impact of ERβ on opposing directionality of these responses, and to characterize the role of the aforementioned signaling pathways in hyperphagic responses in the female to AICAR-induced DVC AMPK activation during acute interruption of feeding.
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影响因子：
3.2
作者：
Briski, K. P.;Nedungadi, T. P.
通讯作者：
Nedungadi, T. P.
影响因子：
4.1
作者：
Briski, KP;Marshall, ES;Sylvester, PW
通讯作者：
Sylvester, PW
影响因子：
5.3
作者：
Nilsen, Jon;Irwin, Ronald W.;Brinton, Roberta Diaz
通讯作者：
Brinton, Roberta Diaz
影响因子：
4.1
作者：
Antonenkov, VD;Sormunen, RI;Hiltunen, JK
通讯作者：
Hiltunen, JK
DOI：
10.1016/j.molbrainres.2004.09.025
发表时间：
2005-01-05
期刊：
MOLECULAR BRAIN RESEARCH
影响因子：
--
作者：
Lindblom, J;Haitina, T;Schiöth, HB
通讯作者：
Schiöth, HB