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首页> 外文OA文献 >Species Specificity of ADAM10 and ADAM17 Proteins in Interleukin-6 (IL-6) Trans-signaling and Novel Role of ADAM10 in Inducible IL-6 Receptor Shedding*
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Species Specificity of ADAM10 and ADAM17 Proteins in Interleukin-6 (IL-6) Trans-signaling and Novel Role of ADAM10 in Inducible IL-6 Receptor Shedding*

机译：白介素6（IL-6）信号转导中ADAM10和ADAM17蛋白的物种特异性以及ADAM10在诱导性IL-6受体脱落中的新作用*

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Hypomorphic ADAM17ex/ex mice showed defects in mucosal regeneration due to inefficient enhanced GFR shedding. ADAM17 is the main sheddase of interleukin-6 receptor (IL-6R) to induce IL-6 trans-signaling. However, serum levels of soluble murine IL-6R were not reduced in ADAM17ex/ex mice, and murine ADAM17 was not the major sheddase of murine IL-6R. Shedding of murine IL-6R by murine ADAM17 was rescued in chimeric murine IL-6R proteins containing any extracellular domain but not the transmembrane and intracellular domain of human IL-6R. Apoptosis is a physiological stimulus of ADAM17-mediated shedding of human IL-6R. Even though apoptosis induced IL-6R shedding in mice, the responsible protease was identified as ADAM10. ADAM10 also was identified as protease responsible for ionomycin-induced shedding of murine and human IL-6R. However, in ADAM10-deficient murine embryonic fibroblasts, compensatory shedding of human IL-6R was mediated by ADAM17, but loss of ADAM10-mediated shedding of murine IL-6R was compensated by an as-yet-unidentified protease. Finally, we identified physiological purinergic P2X7 receptor stimulation as a novel inducer of murine and human IL-6R shedding solely mediated by ADAM10. In conclusion, we describe an unexpected species specificity of ADAM10 and ADAM17 and identified ADAM10 as novel inducible sheddase of IL-6R in mice and humans, which might have consequences for the interpretation of phenotypes from ADAM17- and ADAM10-deficient mice.
机译：亚型ADAM17ex / ex小鼠由于缺乏有效的GFR脱落而显示出粘膜再生缺陷。 ADAM17是白介素6受体（IL-6R）诱导IL-6反式信号转导的主要产物。但是，ADAM17ex / ex小鼠的可溶性鼠IL-6R血清水平并未降低，鼠ADAM17并不是鼠IL-6R的主要脱落酶。在含有人IL-6R的任何胞外域但不包含跨膜和胞内域的嵌合鼠IL-6R蛋白中，挽救了鼠ADAM17对鼠IL-6R的脱落。凋亡是ADAM17介导的人IL-6R脱落的生理刺激。即使凋亡诱导小鼠中IL-6R脱落，其负责的蛋白酶也被鉴定为ADAM10。 ADAM10也被确定为蛋白酶，可引起离子霉素诱导的鼠类和人IL-6R脱落。然而，在ADAM10缺陷的鼠胚胎成纤维细胞中，人IL-6R的补偿性脱落是由ADAM17介导的，但ADAM10介导的鼠IL-6R的脱落的丧失是由至今尚未鉴定的蛋白酶补偿的。最后，我们确定了生理嘌呤P2X7受体刺激是仅由ADAM10介导的鼠类和人IL-6R脱落的新型诱导剂。总之，我们描述了ADAM10和ADAM17的意外物种特异性，并将ADAM10鉴定为小鼠和人类中IL-6R的新型诱导型脱氢酶，这可能对解释ADAM17和ADAM10缺陷型小鼠的表型有影响。

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