Louisiana State University, Department of Biological Sciences, 202 Life Sciences Bldg., Baton Rouge, LA 70803, USA.
Biochem Biophys Res Commun. 2010 Apr 23;395(1):48-50. doi: 10.1016/j.bbrc.2010.03.132. Epub 2010 Mar 28.
Neuropoietin (NP) is a member of the gp130 cytokine family that is closely related to cardiotrophin-1(CT-1) and shares functional and structural features with other family members, including ciliary neurotrophic factor (CNTF) and cardiotrophin-like cytokine (CLC). Studies have shown that NP can play a role in the development of the nervous system, as well as affect adipogenesis and fat cell function. However, the signaling mechanisms utilized by NP in adipocytes have not been examined. In our present studies, we demonstrate that NP-induced activation of STAT3 tyrosine phosphorylation is independent of leukemia inhibitory factor receptor (LIFR) phosphorylation and degradation. Although it is widely accepted that NP signals via the LIFR, our studies reveal that NP results in phosphorylation of gp130, but not LIFR. These observations suggest that the profound effects that NP has on adipocytes are not mediated via LIFR signaling.
神经细胞营养素（NP）是 gp130 细胞因子家族的一员，与心营养素-1（CT-1）密切相关，并与其他家族成员（包括睫状神经营养因子（CNTF）和心营养素样细胞因子（CLC））具有功能和结构特征。研究表明，NP 可以在神经系统的发育中发挥作用，并且可以影响脂肪生成和脂肪细胞功能。然而，NP 在脂肪细胞中利用的信号机制尚未被研究。在我们目前的研究中，我们证明 NP 诱导的 STAT3 酪氨酸磷酸化的激活不依赖于白血病抑制因子受体（LIFR）的磷酸化和降解。尽管人们普遍认为 NP 通过 LIFR 信号传递，但我们的研究表明 NP 导致 gp130 的磷酸化，而不是 LIFR。这些观察结果表明，NP 对脂肪细胞的深远影响不是通过 LIFR 信号传递介导的。
