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Defining Cytokine Responsive and Non-responsive Human β-cells. 定义细胞因子反应性和非反应性人 β 细胞
IF 5.1 Q2 CELL BIOLOGY Pub Date : 2024-09-10 DOI: 10.1093/function/zqae039
Samuel B Stephens
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引用次数: 0
The P2X7 Receptor is a Master Regulator of Microparticle and Mitochondria Exchange in Mouse Microglia. P2×7 受体是小鼠小胶质细胞微粒和线粒体交换的主调节器。
IF 5.1 Q2 CELL BIOLOGY Pub Date : 2024-07-11 DOI: 10.1093/function/zqae019
Simonetta Falzoni, Valentina Vultaggio-Poma, Paola Chiozzi, Mario Tarantini, Elena Adinolfi, Paola Boldrini, Anna Lisa Giuliani, Giampaolo Morciano, Yong Tang, Dariusz C Gorecki, Francesco Di Virgilio

Microparticles (MPs) are secreted by all cells, where they play a key role in intercellular communication, differentiation, inflammation, and cell energy transfer. P2X7 receptor (P2X7R) activation by extracellular ATP (eATP) causes a large MP release and affects their contents in a cell-specific fashion. We investigated MP release and functional impact in microglial cells from P2X7R-WT or P2X7R-KO mice, as well as mouse microglial cell lines characterized for high (N13-P2X7RHigh) or low (N13-P2X7RLow) P2X7R expression. P2X7R stimulation promoted release of a mixed MP population enriched with naked mitochondria. Released mitochondria were taken up and incorporated into the mitochondrial network of the recipient cells in a P2X7R-dependent fashion. NLRP3 and the P2X7R itself were also delivered to the recipient cells. Microparticle transfer increased the energy level of the recipient cells and conferred a pro-inflammatory phenotype. These data show that the P2X7R is a master regulator of intercellular organelle and MP trafficking in immune cells.

微颗粒(MPs)由所有细胞分泌,在细胞间通信、分化、炎症和细胞能量转移中发挥着关键作用。细胞外 ATP(eATP)激活 P2×7 受体(P2×7R)会导致大量 MP 释放,并以细胞特异的方式影响其内容。我们研究了来自 P2×7R-WT 或 P2×7R-KO 小鼠以及高(N13-P2×7RHigh)或低(N13-P2×7RLow)P2×7R 表达的小鼠小胶质细胞系的 MP 释放和功能影响。P2×7R 刺激促进了富含裸线粒体的混合 MP 群体的释放。释放的线粒体以 P2×7R 依赖性方式被吸收并整合到受体细胞的线粒体网络中。NLRP3 和 P2×7R 本身也被输送到受体细胞。MP 转移提高了受体细胞的能量水平,并产生了促炎表型。这些数据表明,P2×7R 是免疫细胞中细胞器间和 MP 转运的主调控因子。
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引用次数: 0
Megalin Knockout Reduces SGLT2 Expression and Sensitizes to Western Diet-induced Kidney Injury. Megalin基因敲除可减少SGLT2的表达,并对西方饮食诱导的肾损伤敏感。
IF 5.1 Q2 CELL BIOLOGY Pub Date : 2024-07-11 DOI: 10.1093/function/zqae026
Elynna B Youm, Katherine E Shipman, Wafaa N Albalawy, Amber M Vandevender, Ian J Sipula, Youssef Rbaibi, Allison E Marciszyn, Jared A Lashway, Emma E Brown, Corry B Bondi, Cary R Boyd-Shiwarski, Roderick J Tan, Michael J Jurczak, Ora A Weisz

Megalin (Lrp2) is a multiligand receptor that drives endocytic flux in the kidney proximal tubule (PT) and is necessary for the recovery of albumin and other filtered proteins that escape the glomerular filtration barrier. Studies in our lab have shown that knockout (KO) of Lrp2 in opossum PT cells leads to a dramatic reduction in sodium-glucose co-transporter 2 (SGLT2) transcript and protein levels, as well as differential expression of genes involved in mitochondrial and metabolic function. SGLT2 transcript levels are reduced more modestly in Lrp2 KO mice. Here, we investigated the effects of Lrp2 KO on kidney function and health in mice fed regular chow (RC) or a Western-style diet (WD) high in fat and refined sugar. Despite a modest reduction in SGLT2 expression, Lrp2 KO mice on either diet showed increased glucose tolerance compared to control mice. Moreover, Lrp2 KO mice were protected against WD-induced fat gain. Surprisingly, renal function in male Lrp2 KO mice on WD was compromised, and the mice exhibited significant kidney injury compared with control mice on WD. Female Lrp2 KO mice were less susceptible to WD-induced kidney injury than male Lrp2 KO. Together, our findings reveal both positive and negative contributions of megalin expression to metabolic health, and highlight a megalin-mediated sex-dependent response to injury following WD.

Megalin(Lrp2)是一种多配体受体,可驱动肾近曲小管(PT)中的内细胞通量,是回收白蛋白和其他逃逸肾小球滤过屏障的滤过蛋白所必需的。我们实验室的研究表明,在负鼠近端肾小管细胞中敲除(KO)Lrp2 会导致钠葡萄糖共转运体 2(SGLT2)转录物和蛋白质水平的急剧下降,以及线粒体和代谢功能相关基因的差异表达。在 Lrp2 KO 小鼠中,SGLT2 转录物水平的降低幅度较小。在这里,我们研究了 Lrp2 KO 对喂食普通饲料(RC)或高脂肪、高精制糖的西式饮食(WD)的小鼠肾功能和健康的影响。尽管 SGLT2 的表达略有减少,但与对照组小鼠相比,两种饮食中 Lrp2 KO 小鼠的葡萄糖耐受性都有所提高。此外,Lrp2 KO 小鼠对 WD 诱导的脂肪增加有保护作用。令人惊讶的是,与服用 WD 的对照组小鼠相比,服用 WD 的雄性 Lrp2 KO 小鼠的肾功能受损,表现出明显的肾损伤。与雄性 Lrp2 KO 小鼠相比,雌性 Lrp2 KO 小鼠不易受到 WD 引起的肾损伤的影响。总之,我们的研究结果揭示了巨球蛋白表达对代谢健康的积极和消极贡献,并强调了巨球蛋白介导的对WD损伤的性别依赖性反应。
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引用次数: 0
Sex-Specific Effects of Cholesteryl Ester Transfer Protein (CETP) on the Perivascular Adipose Tissue. 胆固醇酯转移蛋白 (CETP) 对血管周围脂肪组织的性别特异性影响
IF 5.1 Q2 CELL BIOLOGY Pub Date : 2024-07-11 DOI: 10.1093/function/zqae024
C M Lazaro, I N Freitas, V S Nunes, D M Guizoni, J A Victorio, H C F Oliveira, A P Davel

Cholesteryl ester transfer protein (CETP) increases the atherosclerosis risk by lowering HDL-cholesterol levels. It also exhibits tissue-specific effects independent of HDL. However, sexual dimorphism of CETP effects remains largely unexplored. Here, we hypothesized that CETP impacts the perivascular adipose tissue (PVAT) phenotype and function in a sex-specific manner. PVAT function, gene and protein expression, and morphology were examined in male and female transgenic mice expressing human or simian CETP and their non-transgenic counterparts (NTg). PVAT exerted its anticontractile effect in aortas from NTg males, NTg females, and CETP females, but not in CETP males. CETP male PVAT had reduced NO levels, decreased eNOS and phospho-eNOS levels, oxidative stress, increased NOX1 and 2, and decreased SOD2 and 3 expressions. In contrast, CETP-expressing female PVAT displayed increased NO and phospho-eNOS levels with unchanged NOX expression. NOX inhibition and the antioxidant tempol restored PVAT anticontractile function in CETP males. Ex vivo estrogen treatment also restored PVAT function in CETP males. Moreover, CETP males, but not female PVAT, show increased inflammatory markers. PVAT lipid content increased in CETP males but decreased in CETP females, while PVAT cholesterol content increased in CETP females. CETP male PVAT exhibited elevated leptin and reduced Prdm16 (brown adipocyte marker) expression. These findings highlight CETP sex-specific impact on PVAT. In males, CETP impaired PVAT anticontractile function, accompanied by oxidative stress, inflammation, and whitening. Conversely, in females, CETP expression increased NO levels, induced an anti-inflammatory phenotype, and preserved the anticontractile function. This study reveals sex-specific vascular dysfunction mediated by CETP.

胆固醇酯转移蛋白(CETP)会降低高密度脂蛋白胆固醇水平,从而增加动脉粥样硬化的风险。它还表现出与高密度脂蛋白无关的组织特异性效应。然而,CETP 作用的性双态性在很大程度上仍未得到研究。在这里,我们假设 CETP 以性别特异性的方式影响血管周围脂肪组织(PVAT)的表型和功能。我们对表达人或猿CETP的雌雄转基因小鼠及其非转基因小鼠(NTg)的PVAT功能、基因和蛋白表达以及形态进行了研究。PVAT在NTg雄性、NTg雌性和CETP雌性小鼠的主动脉中发挥了抗收缩作用,但在CETP雄性小鼠中却没有。CETP雄性PVAT的NO水平降低,eNOS和磷酸化-eNOS水平降低,氧化应激增加,NOX1和2表达增加,SOD2和3表达减少。相反,表达 CETP 的雌性 PVAT 的 NO 和磷酸化-eNOS 水平升高,NOX 表达量不变。抑制 NOX 和抗氧化剂 tempol 恢复了 CETP 雄性 PVAT 的抗收缩功能。体内外雌激素处理也恢复了 CETP 雄性 PVAT 的功能。此外,CETP 雄性而非雌性 PVAT 显示出炎症标记物的增加。CETP 雄性 PVAT 的脂质含量增加,而 CETP 雌性 PVAT 的脂质含量减少,而 CETP 雌性 PVAT 的胆固醇含量增加。CETP 雄性 PVAT 表现出瘦素升高和 Prdm16(棕色脂肪细胞标志物)表达降低。这些发现凸显了 CETP 性别特异性对 PVAT 的影响。在男性中,CETP 会损害 PVAT 的抗收缩功能,并伴有氧化应激、炎症和白化。相反,在女性中,CETP 的表达会增加 NO 水平,诱导抗炎表型,并保持抗收缩功能。这项研究揭示了 CETP 介导的具有性别特异性的血管功能障碍。
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引用次数: 0
Single Cell RNAseq Analysis of Cytokine-Treated Human Islets: Association of Cellular Stress with Impaired Cytokine Responsiveness. 细胞因子处理的人类胰岛的单细胞 RNAseq 分析:细胞压力与细胞因子反应能力受损的关系
IF 5.1 Q2 CELL BIOLOGY Pub Date : 2024-07-11 DOI: 10.1093/function/zqae015
Jennifer S Stancill, Moujtaba Y Kasmani, Weiguo Cui, John A Corbett

Pancreatic β-cells are essential for survival, being the only cell type capable of insulin secretion. While they are believed to be vulnerable to damage by inflammatory cytokines such as interleukin-1 beta (IL-1β) and interferon-gamma, we have recently identified physiological roles for cytokine signaling in rodent β-cells that include the stimulation of antiviral and antimicrobial gene expression and the inhibition of viral replication. In this study, we examine cytokine-stimulated changes in gene expression in human islets using single-cell RNA sequencing. Surprisingly, the global responses of human islets to cytokine exposure were remarkably blunted compared to our previous observations in the mouse. The small population of human islet cells that were cytokine responsive exhibited increased expression of IL-1β-stimulated antiviral guanylate-binding proteins, just like in the mouse. Most human islet cells were not responsive to cytokines, and this lack of responsiveness was associated with high expression of genes encoding ribosomal proteins. We further correlated the expression levels of RPL5 with stress response genes, and when expressed at high levels, RPL5 is predictive of failure to respond to cytokines in all endocrine cells. We postulate that donor causes of death and isolation methodologies may contribute to stress of the islet preparation. Our findings indicate that activation of stress responses in human islets limits cytokine-stimulated gene expression, and we urge caution in the evaluation of studies that have examined cytokine-stimulated gene expression in human islets without evaluation of stress-related gene expression.

胰岛β细胞是唯一能够分泌胰岛素的细胞类型,对胰岛β细胞的存活至关重要。虽然人们认为它们容易受到白细胞介素-1β(IL-1β)和γ干扰素(IFN-γ)等炎症细胞因子的损害,但我们最近发现细胞因子信号在啮齿动物β细胞中的生理作用包括刺激抗病毒和抗微生物基因表达以及抑制病毒复制。在本研究中,我们利用单细胞 RNA 测序技术研究了细胞因子刺激下人类胰岛基因表达的变化。令人惊讶的是,与我们之前在小鼠体内观察到的结果相比,人类胰岛细胞对细胞因子暴露的整体反应明显减弱。对细胞因子有反应的一小部分人胰岛细胞表现出IL-1β刺激的抗病毒鸟苷酸结合蛋白的表达增加,就像在小鼠中一样。大多数人的胰岛细胞对细胞因子没有反应,这种缺乏反应与核糖体蛋白编码基因的高表达有关。我们进一步将 RPL5 的表达水平与应激反应基因相关联,当 RPL5 高水平表达时,可预测所有内分泌细胞对细胞因子的反应失败。我们推测,供体的死因和分离方法可能会导致胰岛制备过程中的应激反应。我们的研究结果表明,人类胰岛中应激反应的激活限制了细胞因子刺激基因的表达,因此我们呼吁在评估那些未评估应激相关基因表达就检测人类胰岛中细胞因子刺激基因表达的研究时要谨慎。
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引用次数: 0
Brain Ballet: The Choreography of Left-Right Neuroendocrine Signals in Injury. 大脑芭蕾:损伤中左右神经内分泌信号的编排。
IF 5.1 Q2 CELL BIOLOGY Pub Date : 2024-07-11 DOI: 10.1093/function/zqae022
Marshall T Holland, Bryan Becker
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引用次数: 0
Society Note - 'How Do We Clean Up the Scientific Record?' 社会说明--"我们如何清理科学记录?
IF 5.1 Q2 CELL BIOLOGY Pub Date : 2024-06-11 eCollection Date: 2024-01-01 DOI: 10.1093/function/zqae028
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引用次数: 0
Rethinking Ischemic Acute Kidney Injury as Nephrotoxicity. 将缺血性急性肾损伤视为肾毒性的再思考
Q2 CELL BIOLOGY Pub Date : 2024-04-17 eCollection Date: 2024-01-01 DOI: 10.1093/function/zqae020
David M Pollock
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引用次数: 0
High Salt Remodels Kidney Metabolism: Metabolite Fuel, Fate, and Signals. 高盐重塑肾脏代谢:代谢物燃料、命运和信号
Q2 CELL BIOLOGY Pub Date : 2024-01-29 eCollection Date: 2024-01-01 DOI: 10.1093/function/zqae006
Moritz Lassé, Markus M Rinschen
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引用次数: 0
Epigenetic Regulation of Autophagy in Bone Metabolism. 骨代谢中自噬的表观遗传调控
Q2 CELL BIOLOGY Pub Date : 2024-01-27 eCollection Date: 2024-01-01 DOI: 10.1093/function/zqae004
Yazhou Zhang, Qianqian Wang, Hongjia Xue, Yujin Guo, Shanshan Wei, Fengfeng Li, Linqiang Gong, Weiliang Pan, Pei Jiang

The skeletal system is crucial for supporting bodily functions, protecting vital organs, facilitating hematopoiesis, and storing essential minerals. Skeletal homeostasis, which includes aspects such as bone density, structural integrity, and regenerative processes, is essential for normal skeletal function. Autophagy, an intricate intracellular mechanism for degrading and recycling cellular components, plays a multifaceted role in bone metabolism. It involves sequestering cellular waste, damaged proteins, and organelles within autophagosomes, which are then degraded and recycled. Autophagy's impact on bone health varies depending on factors such as regulation, cell type, environmental cues, and physiological context. Despite being traditionally considered a cytoplasmic process, autophagy is subject to transcriptional and epigenetic regulation within the nucleus. However, the precise influence of epigenetic regulation, including DNA methylation, histone modifications, and non-coding RNA expression, on cellular fate remains incompletely understood. The interplay between autophagy and epigenetic modifications adds complexity to bone cell regulation. This article provides an in-depth exploration of the intricate interplay between these two regulatory paradigms, with a focus on the epigenetic control of autophagy in bone metabolism. Such an understanding enhances our knowledge of bone metabolism-related disorders and offers insights for the development of targeted therapeutic strategies.

骨骼系统对于支持身体机能、保护重要器官、促进造血和储存必需矿物质至关重要。骨骼平衡包括骨密度、结构完整性和再生过程等方面,对骨骼功能的正常发挥至关重要。自噬是一种降解和回收细胞成分的复杂细胞内机制,在骨代谢中发挥着多方面的作用。它将细胞废物、受损蛋白质和细胞器封存在自噬体中,然后进行降解和再循环。自噬对骨骼健康的影响因调节、细胞类型、环境线索和生理背景等因素而异。尽管自噬传统上被认为是一个细胞质过程,但它在细胞核内受到转录和表观遗传的调控。然而,表观遗传调控(包括 DNA 甲基化、组蛋白修饰和非编码 RNA 表达)对细胞命运的确切影响仍不完全清楚。自噬和表观遗传修饰之间的相互作用增加了骨细胞调控的复杂性。本文深入探讨了这两种调控模式之间错综复杂的相互作用,重点是自噬在骨代谢中的表观遗传调控。这种认识增强了我们对骨代谢相关疾病的了解,并为开发有针对性的治疗策略提供了启示。
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引用次数: 0
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Function (Oxford, England)
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