Interleukin-13 and its receptor are synaptic proteins involved in plasticity and neuroprotection.
Interleukin-13 and its receptor are synaptic proteins involved in plasticity and neuroprotection.
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DOI：
10.1038/s41467-023-35806-8
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发表时间：
2023-01-13
影响因子：
16.6
通讯作者：
Roselli, Francesco
中科院分区：
文献类型：
--
作者：
Li, Shun;Heuvel, Florian Olde;Rehman, Rida;Aousji, Oumayma;Froehlich, Albrecht;Li, Zhenghui;Jark, Rebecca;Zhang, Wanhong;Conquest, Alison;Woelfle, Sarah;Schoen, Michael;O'Meara, Caitlin C. C.;Reinhardt, Richard Lee;Voehringer, David;Kassubek, Jan;Ludolph, Albert;Huber-Lang, Markus;Knoell, Bernd;Morganti-Kossmann, Maria Cristina;Brockmann, Marisa M.;Boeckers, Tobias;Roselli, Francesco
免疫系统分子是由神经元表达的，但它们的功能通常是未知的。我们已经确定IL-13及其受体IL-13Ra1是小鼠、大鼠和人类大脑中的神经元和突触蛋白，其参与上调NMDAR和AMPAR亚基的磷酸化，进而增加突触活性和creb介导的转录。我们证明IL-13的增加是雄性小鼠以及两组不同的人类患者创伤性脑损伤（TBI）的标志。我们还提供了IL-13上调保护神经元免于兴奋性毒性死亡的证据。我们显示IL-13上调发生在几个队列的人脑样本和脑脊液（CSF）。因此，IL-13是神经元来源的突触生理学的生理调节剂，与突触可塑性的建立和损伤条件下神经元的存活有关。此外，我们认为通过上调IL-13提供的神经保护代表了干预TBI病理生理的切入点。Il-13在神经元中表达，Il-13 ko引起记忆障碍。本文作者发现IL-13及其受体IL-13Ra1分别是突触前蛋白和突触后蛋白，参与突触信号传导、可塑性和神经保护。
Immune system molecules are expressed by neurons, yet their functions are often unknown. We have identified IL-13 and its receptor IL-13Ra1 as neuronal, synaptic proteins in mouse, rat, and human brains, whose engagement upregulates the phosphorylation of NMDAR and AMPAR subunits and, in turn, increases synaptic activity and CREB-mediated transcription. We demonstrate that increased IL-13 is a hallmark of traumatic brain injury (TBI) in male mice as well as in two distinct cohorts of human patients. We also provide evidence that IL-13 upregulation protects neurons from excitotoxic death. We show IL-13 upregulation occurring in several cohorts of human brain samples and in cerebrospinal fluid (CSF). Thus, IL-13 is a physiological modulator of synaptic physiology of neuronal origin, with implications for the establishment of synaptic plasticity and the survival of neurons under injury conditions. Furthermore, we suggest that the neuroprotection afforded through the upregulation of IL-13 represents an entry point for interventions in the pathophysiology of TBI. Il-13 is expressed in neurons and IL-13 ko causes memory impairment. Here, authors show that IL-13 and its receptor IL-13Ra1 are pre- and post-synaptic proteins, respectively, involved in synaptic signaling, plasticity and neuroprotection.
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影响因子：
5.6
作者：
De Benedictis CA;Haffke C;Hagmeyer S;Sauer AK;Grabrucker AM
通讯作者：
Grabrucker AM
影响因子：
5.6
作者：
Abboud A;Mi Q;Puccio A;Okonkwo D;Buliga M;Constantine G;Vodovotz Y
通讯作者：
Vodovotz Y
影响因子：
6.3
作者：
Catanese, Alberto;Garrido, Debora;Boeckers, Tobias M.
通讯作者：
Boeckers, Tobias M.
影响因子：
4.4
作者：
Brombacher, Tiroyaone M.;Nono, Justin K.;Brombacher, Frank
通讯作者：
Brombacher, Frank
在中度创伤性脑损伤小鼠模型中，自噬激活通过 IL-13 和 JAK1/STAT1 途径抑制细胞焦亡
影响因子：
5
作者：
Gao, Cheng;Yan, Ya'nan;Tao, Luyang
通讯作者：
Tao, Luyang