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鉴定新型 RIP1/RIP3 双重抑制剂,抑制小鼠腹主动脉瘤模型中的细胞死亡和炎症。

Identification of a novel class of RIP1/RIP3 dual inhibitors that impede cell death and inflammation in mouse abdominal aortic aneurysm models.

机构信息

Department of Surgery, School of Medicine and Public Health, University of Wisconsin, Madison, WI, 53705, USA.

Department of Cancer Biology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, 02215, USA.

出版信息

Cell Death Dis. 2019 Mar 6;10(3):226. doi: 10.1038/s41419-019-1468-6.

Abstract

Receptor interacting protein kinase-1 and -3 (RIP1 and RIP3) are essential mediators of cell death processes and participate in inflammatory responses. Our group recently demonstrated that gene deletion of Rip3 or pharmacological inhibition of RIP1 attenuated pathogenesis of abdominal aortic aneurysm (AAA), a life-threatening degenerative vascular disease characterized by depletion of smooth muscle cells (SMCs), inflammation, negative extracellular matrix remodeling, and progressive expansion of aorta. The goal of this study was to develop drug candidates for AAA and other disease conditions involving cell death and inflammation. We screened 1141 kinase inhibitors for their ability to block necroptosis using the RIP1 inhibitor Necrostatin-1s (Nec-1s) as a selection baseline. Positive compounds were further screened for cytotoxicity and virtual binding to RIP3. A cluster of top hits, represented by GSK2593074A (GSK'074), displayed structural similarity to the established RIP3 inhibitor GSK'843. In multiple cell types including mouse SMCs, fibroblasts (L929), bone marrow derived macrophages (BMDM), and human colon epithelial cells (HT29), GSK'074 inhibited necroptosis with an IC50 of ~3 nM. Furthermore, GSK'074, but not Nec-1s, blocked cytokine production by SMCs. Biochemical analyses identified both RIP1 and RIP3 as the biological targets of GSK'074. Unlike GSK'843 which causes profound apoptosis at high doses (>3 µM), GSK'074 showed no detectable cytotoxicity even at 20 µM. Daily intraperitoneal injection of GSK'074 at 0.93 mg/kg significantly attenuated aortic expansion in two mouse models of AAA (calcium phosphate: DMSO 66.06 ± 9.17% vs GSK'074 27.36 ± 8.25%, P < 0.05; Angiotensin II: DMSO 85.39 ± 15.76% vs GSK'074 36.28 ± 5.76%, P < 0.05). Histologically, GSK'074 treatment diminished cell death and macrophage infiltration in aneurysm-prone aortae. Together, our data suggest that GSK'074 represents a new class of necroptosis inhibitors with dual targeting ability to both RIP1 and RIP3. The high potency and minimum cytotoxicity make GSK'074 a desirable drug candidate of pharmacological therapies to attenuate AAA progression and other necroptosis related diseases.

摘要

受体相互作用蛋白激酶-1 和 -3(RIP1 和 RIP3)是细胞死亡过程和参与炎症反应的必要介质。我们的研究小组最近表明,Rip3 的基因缺失或 RIP1 的药理学抑制减弱了腹主动脉瘤(AAA)的发病机制,AAA 是一种危及生命的退行性血管疾病,其特征是平滑肌细胞(SMC)耗竭、炎症、负细胞外基质重塑和主动脉进行性扩张。本研究的目的是开发用于 AAA 和其他涉及细胞死亡和炎症的疾病的药物候选物。我们使用 RIP1 抑制剂 Necrostatin-1s(Nec-1s)作为选择基线,筛选了 1141 种激酶抑制剂以抑制坏死性凋亡的能力。阳性化合物进一步进行细胞毒性和虚拟结合 RIP3 的筛选。以 GSK2593074A(GSK'074)为代表的一组顶级化合物显示出与已建立的 RIP3 抑制剂 GSK'843 的结构相似性。在多种细胞类型中,包括小鼠 SMC、成纤维细胞(L929)、骨髓来源的巨噬细胞(BMDM)和人结肠上皮细胞(HT29),GSK'074 的抑制坏死性凋亡的 IC50 约为 3 nM。此外,GSK'074 而非 Nec-1s 可阻断 SMC 产生细胞因子。生化分析鉴定 RIP1 和 RIP3 均为 GSK'074 的生物学靶标。与 GSK'843 不同,GSK'843 在高剂量(>3 µM)时会引起明显的细胞凋亡,而 GSK'074 即使在 20 µM 时也没有检测到细胞毒性。每天腹腔注射 GSK'074(0.93mg/kg)可显著减轻两种 AAA 小鼠模型的主动脉扩张(磷酸钙:DMSO 66.06±9.17%比 GSK'074 27.36±8.25%,P<0.05;血管紧张素 II:DMSO 85.39±15.76%比 GSK'074 36.28±5.76%,P<0.05)。组织学上,GSK'074 治疗可减少易发生动脉瘤的主动脉中的细胞死亡和巨噬细胞浸润。总的来说,我们的数据表明,GSK'074 代表了一类新的坏死性凋亡抑制剂,对 RIP1 和 RIP3 具有双重靶向能力。高效力和最小的细胞毒性使 GSK'074 成为减弱 AAA 进展和其他坏死性凋亡相关疾病的药理学治疗的理想药物候选物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d06f/6403222/17ded4e95187/41419_2019_1468_Fig1_HTML.jpg

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