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Angiotensin II: Role in oxidative stress, endothelial dysfunction, and diseases 血管紧张素 II:在氧化应激、内皮功能障碍和疾病中的作用
IF 4.1 3区 医学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-06-08 DOI: 10.1016/j.mce.2024.112309
Amir Ajoolabady , Domenico Pratico , Jun Ren

Angiotensin II (Ang II) is a protein hormone capable of physiologically regulating blood pressure through diverse mechanisms. Ang II is mainly produced by the liver at homeostatic levels. However, excessive production of Ang II is closely associated with a series of pathological events in the body. The endothelial dysfunction is one of these pathological events that can drive vascular anomalies. The excessive exposure of endothelial cells (ECs) to Ang II may induce endothelial dysfunction via diverse mechanisms. One of these mechanisms is Ang II-mediated mitochondrial oxidative stress. In this mini-review, we aimed to discuss the molecular mechanisms of Ang II-mediated endothelial dysfunction through mitochondrial oxidative stress and the protective role of nitric oxide in ECs. Deciphering these mechanisms may disclose novel therapeutic strategies to prevent endothelial dysfunction and associated diseases induced by elevated leves of Ang II in the blood.

血管紧张素 II(Ang II)是一种蛋白质激素,能够通过多种机制对血压进行生理调节。血管紧张素 II 主要由肝脏产生,处于平衡状态。然而,Ang II 的过量产生与体内一系列病理事件密切相关。内皮功能障碍就是其中一种可导致血管异常的病理事件。内皮细胞(ECs)过度暴露于 Ang II 可通过多种机制诱发内皮功能障碍。其中一种机制是 Ang II 介导的线粒体氧化应激。在这篇微型综述中,我们旨在讨论 Ang II 通过线粒体氧化应激介导的内皮功能障碍的分子机制以及一氧化氮在 EC 中的保护作用。破译这些机制可能会发现新的治疗策略,以预防血液中 Ang II 浓度升高引起的内皮功能障碍和相关疾病。
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引用次数: 0
Corrigendum to “Polypeptide N-Acetylgalactosaminyl transferase 14 is a novel mediator in pancreatic β-cell function and growth” [Mol. Cell. Endocrinol., 591(2024) 112269-112278, 0303–7207] 多肽 N-乙酰半乳糖氨基转移酶 14 是胰腺 β 细胞功能和生长的新型介质》[Mol.Cell.Endocrinol.,591(2024) 112269-112278, 0303-7207] 更正
IF 4.1 3区 医学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-06-04 DOI: 10.1016/j.mce.2024.112291
Tingting Shu , Yan Zhang , Tong Sun , Yunxia Zhu
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引用次数: 0
Melatonin changes energy metabolism and reduces oncogenic signaling in ovarian cancer cells 褪黑激素改变卵巢癌细胞的能量代谢并减少致癌信号传导
IF 4.1 3区 医学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-06-04 DOI: 10.1016/j.mce.2024.112296
Henrique Spaulonci Silveira , Roberta Carvalho Cesário , Renan Aparecido Vígaro , Leticia Barbosa Gaiotte , Maira Smaniotto Cucielo , Fernando Guimarães , Fábio Rodrigues Ferreira Seiva , Debora Aparecida P.C. Zuccari , Russel J. Reiter , Luiz Gustavo de Almeida Chuffa

Ovarian cancer (OC) adjusts energy metabolism in favor of its progression and dissemination. Because melatonin (Mel) has antitumor actions, we investigated its impact on energy metabolism and kinase signaling in OC cells (SKOV-3 and CAISMOV-24). Cells were divided into control and Mel-treated groups, in the presence or absence of the antagonist luzindole. There was a decrease in the levels of HIF-1α, G6PDH, GAPDH, PDH, and CS after Mel treatment even in the presence of luzindole in both OC cells. Mel treatment also reduced the activity of OC-related enzymes including PFK-1, G6PDH, LDH, CS, and GS whereas PDH activity was increased. Lactate and glutamine levels dropped after Mel treatment. Mel further promoted a reduction in the concentrations of CREB, JNK, NF-kB, p-38, ERK1/2, AKT, P70S6K, and STAT in both cell lines. Mel reverses Warburg-type metabolism and possibly reduces glutaminolysis, thereby attenuating various oncogenic molecules associated with OC progression and invasion.

卵巢癌(OC)会调整能量代谢以促进其发展和扩散。由于褪黑激素(Mel)具有抗肿瘤作用,我们研究了它对卵巢癌细胞(SKOV-3 和 CAISMOV-24)能量代谢和激酶信号转导的影响。细胞被分为对照组和 Mel 处理组,在有或没有拮抗剂吕吲哚的情况下。即使在有吕吲哚存在的情况下,两种 OC 细胞中的 HIF-1α、G6PDH、GAPDH、PDH 和 CS 水平在经 Mel 处理后都有所下降。梅尔处理还降低了与 OC 相关的酶的活性,包括 PFK-1、G6PDH、LDH、CS 和 GS,而 PDH 的活性则有所增加。经 Mel 处理后,乳酸和谷氨酰胺水平下降。Mel 进一步促进了两种细胞系中 CREB、JNK、NF-kB、p-38、ERK1/2、AKT、P70S6K 和 STAT 浓度的降低。Mel能逆转沃伯格型新陈代谢,并可能减少谷氨酰胺溶解,从而抑制与OC进展和侵袭相关的各种致癌分子。
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引用次数: 0
Multiple androgen pathways contribute to the steroid signature of adrenarche 多种雄激素途径促成了肾上腺皮质发育的类固醇特征
IF 4.1 3区 医学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-06-03 DOI: 10.1016/j.mce.2024.112293
Jani Liimatta , Therina du Toit , Clarissa D. Voegel , Jarmo Jääskeläinen , Timo A. Lakka , Christa E. Flück

Context

Adrenarche is a normal developmental event in mid-childhood characterized by increasing adrenal androgen secretion. The role of the classic androgen pathway has been well described in adrenarche, but the role of newer active androgens and additional androgen pathways is less clear.

Objective

To study the contribution of novel androgens and related steroid biosynthesis pathways to the development of adrenarche, and to identify additional steroid biomarkers of adrenarche.

Design

A longitudinal study of children aged 6–8 years at baseline, followed up at ages 8–10 and 14–16 years. A total of 34 children (20 girls) with clinical and/or biochemical signs of adrenarche (cases) and 24 children (11 girls) without these signs (controls) at age 8–10 years were included. Serum steroid profiling was performed by liquid chromatography high-resolution mass spectrometry.

Main outcome measures

Thirty-two steroids compartmentalized in progestagens, gluco- and mineralocorticoid pathways, and four androgen related pathways, including the classic, backdoor, 11-oxy, and 11-oxy backdoor pathways.

Results

The classic and 11-oxy androgen pathways were more active, and serum concentrations of main androgens in the classic (dehydroepiandrosterone, dehydroepiandrosterone sulfate, androstenedione and androsterone) and 11-oxy (11β-hydroxyandrostenedione, 11β-hydroxytestosterone, 11-ketoandrostenedione, and 11-ketotestosterone) pathways were higher in cases at ages 6–8 and 8–10 years. Pregnenolone concentrations at adrenarchal age (8–10 years) and cortisol concentrations at adolescence (14–16 years) were higher in cases. 11β-hydroxyandrosterone and 11-ketoandrosterone tended to be higher in cases with clinical signs compared to cases who had only biochemical evidence of adrenarche, albeit they were detected at low levels. In biomarker analyses, calculated steroid ratios with cortisol, cortisone, or 11-deoxycortisone as dividers were better classifiers for adrenarche than single steroids. Among these ratios, androstenedione/cortisone was the best.

Conclusions

The classic and 11-oxy androgen pathways are active in adrenarche. Children with earlier timing of adrenarche have higher serum cortisol levels at late pubertal age, suggesting that early adrenarche might have long-term effects on adrenal steroidogenesis by increasing the activity of the glucocorticoid pathway. Future studies should employ comprehensive steroid profiling to define novel classifiers and biomarkers for adrenarche and premature adrenarche.

背景肾上腺初潮是儿童中期的正常发育过程,其特点是肾上腺雄激素分泌增加。研究新型雄激素和相关类固醇生物合成途径对肾上腺皮质发育的作用,并确定肾上腺皮质发育的其他类固醇生物标志物。设计对基线年龄为 6-8 岁的儿童进行纵向研究,并在 8-10 岁和 14-16 岁时进行随访。研究共纳入了 34 名(20 名女孩)8-10 岁时有肾上腺皮质激素临床和/或生化征兆的儿童(病例)和 24 名(11 名女孩)无这些征兆的儿童(对照组)。血清类固醇分析采用液相色谱高分辨质谱法进行。主要结果指标32种类固醇分为孕激素、糖皮质激素和矿皮质激素途径,以及四种雄激素相关途径,包括经典途径、后门途径、11-氧途径和11-氧后门途径。结果 6-8岁和8-10岁的病例中,经典雄激素途径和11-氧雄激素途径更为活跃,血清中经典途径(脱氢表雄酮、硫酸脱氢表雄酮、雄烯二酮和雄甾酮)和11-氧途径(11β-羟基雄烯二酮、11β-羟基睾酮、11-酮雄烯二酮和11-酮睾酮)的主要雄激素浓度较高。病例在肾上腺年龄(8-10 岁)的孕烯醇酮浓度和青春期(14-16 岁)的皮质醇浓度较高。有临床症状的病例中,11β-羟基雄酮和 11-酮基雄酮的含量往往高于仅有肾上腺皮质发育生化证据的病例,尽管这两种激素的检测水平较低。在生物标志物分析中,以皮质醇、可的松或 11-脱氧可的松为分界线计算出的类固醇比率比单一类固醇更能对肾上腺皮质发育不良进行分类。在这些比率中,雄烯二酮/可的松是最好的。肾上腺初潮时间较早的儿童在青春期晚期的血清皮质醇水平较高,这表明肾上腺初潮过早可能会增加糖皮质激素途径的活性,从而对肾上腺类固醇的生成产生长期影响。未来的研究应采用全面的类固醇分析方法来确定肾上腺皮质激素初潮和过早肾上腺皮质激素初潮的新型分类指标和生物标志物。
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引用次数: 0
Dopamine-mediated autocrine inhibition of insulin secretion 多巴胺介导的胰岛素分泌自分泌抑制。
IF 4.1 3区 医学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-06-03 DOI: 10.1016/j.mce.2024.112294
Edoardo Ferrero , Matilde Masini , Marco Carli , Stefania Moscato , Pascale Beffy , Francesca Vaglini , Letizia Mattii , Alessandro Corti , Marco Scarselli , Michela Novelli , Vincenzo De Tata

The aim of the present research was to explore the mechanisms underlying the role of dopamine in the regulation of insulin secretion in beta cells. The effect of dopamine on insulin secretion was investigated on INS 832/13 cell line upon glucose and other secretagogues stimulation. Results show that dopamine significantly inhibits insulin secretion stimulated by both glucose and other secretagogues, while it has no effect on the basal secretion. This effect requires the presence of dopamine during incubation with the various secretagogues. Both electron microscopy and immunohistochemistry indicate that in beta cells the D2 dopamine receptor is localized within the insulin granules. Blocking dopamine entry into the insulin granules by inhibiting the VMAT2 transporter with tetrabenazine causes a significant increase in ROS production. Our results confirm that dopamine plays an important role in the regulation of insulin secretion by pancreatic beta cells through a regulated and precise compartmentalization mechanisms.

本研究旨在探索多巴胺在调节β细胞胰岛素分泌中的作用机制。研究人员在 INS 832/13 细胞系上研究了多巴胺在葡萄糖和其他促泌剂刺激下对胰岛素分泌的影响。结果表明,多巴胺能明显抑制葡萄糖和其他促泌剂刺激下的胰岛素分泌,而对基础分泌没有影响。这种作用需要在与各种分泌物一起孵育期间多巴胺的存在。电子显微镜和免疫组化都表明,在β细胞中,D2多巴胺受体位于胰岛素颗粒内。用四苯巴嗪抑制 VMAT2 转运体,阻止多巴胺进入胰岛素颗粒,会导致 ROS 生成显著增加。我们的研究结果证实,多巴胺通过调节和精确的分区机制在调节胰岛β细胞分泌胰岛素的过程中发挥着重要作用。
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引用次数: 0
YTHDF2 regulates MSS51 expression contributing to mitochondria dysfunction of granulosa cells in polycystic ovarian syndrome patients YTHDF2调节MSS51的表达,导致多囊卵巢综合征患者颗粒细胞线粒体功能障碍
IF 3.8 3区 医学 Q2 CELL BIOLOGY Pub Date : 2024-06-01 DOI: 10.1016/j.mce.2024.112292
Yun-Yun Jiao , Ning Song , Xing-Yu Fang , Xiao-Tong Lu, Ning Sun, Hai-Xia Jin, Lei Chen, Xian-Ju Huang, Shuang Wen, Zhao-Ting Wu, Xiao-Peng Wang, Ting-Ting Cheng, Gui-Dong Yao, Wen-Yan Song

Research question

Granulosa cells (GCs) dysfunction plays a crucial role in the pathogenesis of polycystic ovary syndrome (PCOS). It is reported that YTH domain-containing family protein 2 (YTHDF2) is upregulated in mural GCs of PCOS patients. What effect does the differential expression of YTHDF2 have in PCOS patients?

Design

Mural GCs and cumulus GCs from 15 patients with PCOS and 15 ovulatory controls and 4 cases of pathological sections in each group were collected. Real-time PCR, Western Blot, immunohistochemistry, and immunofluorescence experiments were conducted to detect gene and protein expression. RNA immunoprecipitation assay was performed to evaluate the binding relationship between YTHDF2 and MSS51. Mitochondrial morphology, cellular ATP and ROS levels and glycolysis-related gene expression were detected after YTHDF2 overexpression or MSS51 inhibition.

Results

In the present study, we found that YTHDF2 was upregulated in GCs of PCOS patients while MSS51 was downregulated. YTHDF2 protein can bind to MSS51 mRNA and affect MSS51 expression. The reduction of MSS51 expression or the increase in YTHDF2 expression can lead to mitochondrial damage, reduced ATP levels, increased ROS levels and reduced expression of LDHA, PFKP and PKM.

Conclusions

YTHDF2 may regulate the expression of MSS51, affecting the structure and function of mitochondria in GCs and interfering with cellular glycolysis, which may disturb the normal biological processes of GCs and follicle development in PCOS patients.

研究问题颗粒细胞(GCs)功能障碍在多囊卵巢综合征(PCOS)的发病机制中起着至关重要的作用。据报道,含YTH结构域的家族蛋白2(YTHDF2)在多囊卵巢综合征患者的壁层GC中上调。设计收集15例多囊卵巢综合征患者和15例排卵对照组的壁细胞和积液细胞,每组4例病理切片。采用实时 PCR、Western Blot、免疫组织化学和免疫荧光实验检测基因和蛋白质的表达。通过 RNA 免疫沉淀实验评估 YTHDF2 与 MSS51 的结合关系。结果 在本研究中,我们发现 YTHDF2 在 PCOS 患者的 GC 中上调,而 MSS51 则下调。YTHDF2蛋白可与MSS51 mRNA结合并影响MSS51的表达。结论YTHDF2可能调控MSS51的表达,影响GCs中线粒体的结构和功能,干扰细胞糖酵解,从而干扰PCOS患者GCs的正常生物学过程和卵泡发育。
{"title":"YTHDF2 regulates MSS51 expression contributing to mitochondria dysfunction of granulosa cells in polycystic ovarian syndrome patients","authors":"Yun-Yun Jiao ,&nbsp;Ning Song ,&nbsp;Xing-Yu Fang ,&nbsp;Xiao-Tong Lu,&nbsp;Ning Sun,&nbsp;Hai-Xia Jin,&nbsp;Lei Chen,&nbsp;Xian-Ju Huang,&nbsp;Shuang Wen,&nbsp;Zhao-Ting Wu,&nbsp;Xiao-Peng Wang,&nbsp;Ting-Ting Cheng,&nbsp;Gui-Dong Yao,&nbsp;Wen-Yan Song","doi":"10.1016/j.mce.2024.112292","DOIUrl":"10.1016/j.mce.2024.112292","url":null,"abstract":"<div><h3>Research question</h3><p>Granulosa cells (GCs) dysfunction plays a crucial role in the pathogenesis of polycystic ovary syndrome (PCOS). It is reported that YTH domain-containing family protein 2 (YTHDF2) is upregulated in mural GCs of PCOS patients. What effect does the differential expression of YTHDF2 have in PCOS patients?</p></div><div><h3>Design</h3><p>Mural GCs and cumulus GCs from 15 patients with PCOS and 15 ovulatory controls and 4 cases of pathological sections in each group were collected. Real-time PCR, Western Blot, immunohistochemistry, and immunofluorescence experiments were conducted to detect gene and protein expression. RNA immunoprecipitation assay was performed to evaluate the binding relationship between YTHDF2 and MSS51. Mitochondrial morphology, cellular ATP and ROS levels and glycolysis-related gene expression were detected after YTHDF2 overexpression or MSS51 inhibition.</p></div><div><h3>Results</h3><p>In the present study, we found that YTHDF2 was upregulated in GCs of PCOS patients while MSS51 was downregulated. YTHDF2 protein can bind to MSS51 mRNA and affect MSS51 expression. The reduction of MSS51 expression or the increase in YTHDF2 expression can lead to mitochondrial damage, reduced ATP levels, increased ROS levels and reduced expression of <em>LDHA, PFKP</em> and <em>PKM</em>.</p></div><div><h3>Conclusions</h3><p>YTHDF2 may regulate the expression of MSS51, affecting the structure and function of mitochondria in GCs and interfering with cellular glycolysis, which may disturb the normal biological processes of GCs and follicle development in PCOS patients.</p></div>","PeriodicalId":18707,"journal":{"name":"Molecular and Cellular Endocrinology","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141235621","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Dual inhibition of AKT and ERK1/2 pathways restores the expression of progesterone Receptor-B in endometriotic lesions through epigenetic mechanisms 通过表观遗传机制双重抑制 AKT 和 ERK1/2 通路可恢复子宫内膜异位症病灶中孕酮受体-B 的表达
IF 3.8 3区 医学 Q2 CELL BIOLOGY Pub Date : 2024-05-31 DOI: 10.1016/j.mce.2024.112290
Sudipta Dutta , JeHoon Lee , Sakhila K. Banu, Joe A. Arosh

Endometriosis is an estrogen-dependent and progesterone-resistant gynecological inflammatory disease of reproductive-age women. Progesterone resistance, loss of progesterone receptor -B (PR-B) in the stromal cells of the endometrium, is one of the hallmarks of endometriosis and a major contributing factor for infertility in endometriosis patients. Loss of PR-B in the stromal cells of the endometriotic lesions poses resistance to the success of progesterone-based therapy. The working hypothesis is that PR-B is hypermethylated and epigenetically silenced, and inhibition of AKT and ERK1/2 pathways will decrease the hypermethylation, reverse the epigenetic silencing, and restore the expression of PR-B via DNA methylation and histone modification mechanisms in the endometriotic lesions. The objectives are to (i) determine the effects of dual inhibition of AKT and ERK1/2 pathways on the expression of PR-B and DNA methylation and histone modification protein machinery in the endometriotic lesions and (ii) identify the underlying epigenetic mechanisms of PR-B restoration in the endometriotic lesions. The results indicate that dual inhibition of AKT and ERK1/2 pathways decreases the hypermethylation, reverses the epigenetic silencing, and restores the expression of PR-B via DNA methylation and H3K9 and H3K27 methylation mechanisms in the endometriotic lesions or endometriotic stromal cells of human origin. These results support the novel concept that restored expression of PR-B in the endometriotic lesions and endometrium may improve the clinical outcome of progesterone therapy in endometriosis patients.

子宫内膜异位症是育龄妇女的一种雌激素依赖性和孕激素抵抗性妇科炎症。孕激素抵抗,即子宫内膜基质细胞中孕激素受体-B(PR-B)的缺失,是子宫内膜异位症的特征之一,也是导致子宫内膜异位症患者不孕的主要因素。子宫内膜异位症病灶基质细胞中 PR-B 的缺失对孕激素治疗的成功构成了阻力。研究假设 PR-B 存在高甲基化和表观遗传沉默,而抑制 AKT 和 ERK1/2 通路将减少高甲基化,逆转表观遗传沉默,并通过 DNA 甲基化和组蛋白修饰机制恢复 PR-B 在子宫内膜异位症病灶中的表达。研究目的是:(i) 确定 AKT 和 ERK1/2 通路双重抑制对子宫内膜异位症病灶中 PR-B 的表达以及 DNA 甲基化和组蛋白修饰蛋白机制的影响;(ii) 找出子宫内膜异位症病灶中 PR-B 恢复的潜在表观遗传学机制。结果表明,双重抑制 AKT 和 ERK1/2 通路可降低高甲基化,逆转表观遗传沉默,并通过 DNA 甲基化、H3K9 和 H3K27 甲基化机制恢复 PR-B 在子宫内膜异位症病灶或人源子宫内膜异位症基质细胞中的表达。这些结果支持了一个新概念,即恢复 PR-B 在子宫内膜异位症病灶和子宫内膜中的表达可改善子宫内膜异位症患者接受黄体酮治疗的临床效果。
{"title":"Dual inhibition of AKT and ERK1/2 pathways restores the expression of progesterone Receptor-B in endometriotic lesions through epigenetic mechanisms","authors":"Sudipta Dutta ,&nbsp;JeHoon Lee ,&nbsp;Sakhila K. Banu,&nbsp;Joe A. Arosh","doi":"10.1016/j.mce.2024.112290","DOIUrl":"10.1016/j.mce.2024.112290","url":null,"abstract":"<div><p>Endometriosis is an estrogen-dependent and progesterone-resistant gynecological inflammatory disease of reproductive-age women. Progesterone resistance, loss of progesterone receptor -B (PR-B) in the stromal cells of the endometrium, is one of the hallmarks of endometriosis and a major contributing factor for infertility in endometriosis patients. Loss of PR-B in the stromal cells of the endometriotic lesions poses resistance to the success of progesterone-based therapy. The working hypothesis is that PR-B is hypermethylated and epigenetically silenced, and inhibition of AKT and ERK1/2 pathways will decrease the hypermethylation, reverse the epigenetic silencing, and restore the expression of PR-B via DNA methylation and histone modification mechanisms in the endometriotic lesions. The objectives are to (i) determine the effects of dual inhibition of AKT and ERK1/2 pathways on the expression of PR-B and DNA methylation and histone modification protein machinery in the endometriotic lesions and (ii) identify the underlying epigenetic mechanisms of PR-B restoration in the endometriotic lesions. The results indicate that dual inhibition of AKT and ERK1/2 pathways decreases the hypermethylation, reverses the epigenetic silencing, and restores the expression of PR-B via DNA methylation and H3K9 and H3K27 methylation mechanisms in the endometriotic lesions or endometriotic stromal cells of human origin. These results support the novel concept that restored expression of PR-B in the endometriotic lesions and endometrium may improve the clinical outcome of progesterone therapy in endometriosis patients.</p></div>","PeriodicalId":18707,"journal":{"name":"Molecular and Cellular Endocrinology","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2024-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141200385","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Legumain-deficient macrophages regulate inflammation and lipid metabolism in adipose tissues to protect against diet-induced obesity 缺失豆豆蛋白酶的巨噬细胞能调节脂肪组织中的炎症和脂质代谢,从而防止饮食引起的肥胖。
IF 4.1 3区 医学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-05-28 DOI: 10.1016/j.mce.2024.112283
Wanyu Zhang , Shuowen Wang , Zhuo Liu , Ping Qian , Yuanyuan Li , Jianxin Wu

Adipose tissue macrophages (ATMs) are key players in the development of obesity and associated metabolic inflammation, which contributes to systemic metabolic dysfunction, and understanding the interaction between macrophages and adipocytes is crucial for developing novel macrophage-based strategies against obesity. Here, we found that Legumain (Lgmn), a well-known lysosomal cysteine protease, is expressed mainly in the ATMs of obese mice. To further define the potential role of Lgmn-expressing macrophages in the generation of an aberrant metabolic state, LgmnF/F; LysMCre mice, which do not express Lgmn in macrophages, were maintained on a high-fat diet (HFD), and metabolic parameters were assessed. Macrophage-specific Lgmn deficiency protects mice against HFD-induced obesity, diminishes the quantity of proinflammatory macrophages in obese adipose tissues, and alleviates hepatic steatosis and insulin resistance. By analysing the transcriptome and proteome of murine visceral white adipose tissue (vWAT) after HFD feeding, we determined that macrophage Lgmn deficiency causes changes in lipid metabolism and the inflammatory response. Furthermore, the reciprocity of macrophage-derived Lgmn with integrin α5β1 in adipocytes was tested via colocalization analyses. It is further demonstrated in macrophage and adipocyte coculture system that macrophage derived Lgmn bound to integrin α5β1 in adipocytes, therefore attenuating PKA activation, downregulating lipolysis-related proteins and eventually exacerbating obesity development. Overall, our study identified Lgmn as a previously unrecognized regulator involved in the interaction between ATMs and adipocytes contributing to diet-induced obesity and suggested that Lgmn is a potential target for treating metabolic disorders.

脂肪组织巨噬细胞(ATMs)是肥胖症和相关代谢炎症发展过程中的关键角色,而肥胖症和相关代谢炎症会导致全身代谢功能障碍,因此了解巨噬细胞和脂肪细胞之间的相互作用对于开发基于巨噬细胞的新型肥胖症防治策略至关重要。在这里,我们发现著名的溶酶体半胱氨酸蛋白酶 Legumain (Lgmn) 主要在肥胖小鼠的 ATMs 中表达。为了进一步确定表达 Lgmn 的巨噬细胞在产生异常代谢状态中的潜在作用,我们将巨噬细胞中不表达 Lgmn 的 LgmnF/F; LysMCre 小鼠饲养在高脂饮食(HFD)中,并对代谢参数进行了评估。巨噬细胞特异性Lgmn的缺乏能保护小鼠免受饮食诱发的肥胖,减少肥胖脂肪组织中促炎巨噬细胞的数量,减轻肝脏脂肪变性和胰岛素抵抗。通过分析喂食高密度脂蛋白胆固醇(HFD)后小鼠内脏白色脂肪组织(vWAT)的转录组和蛋白质组,我们确定巨噬细胞 Lgmn 缺乏会引起脂质代谢和炎症反应的变化。此外,我们还通过共定位分析测试了巨噬细胞衍生的 Lgmn 与脂肪细胞中整合素 α5β1 的互作关系。在巨噬细胞和脂肪细胞共培养系统中进一步证实,巨噬细胞衍生的Lgmn与脂肪细胞中的整合素α5β1结合,从而减弱了PKA的激活,下调了脂肪分解相关蛋白,最终加剧了肥胖的发展。总之,我们的研究发现,Lgmn是一种以前未被发现的调节因子,它参与了ATMs与脂肪细胞之间的相互作用,导致饮食引起的肥胖,并表明Lgmn是治疗代谢紊乱的潜在靶点。
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引用次数: 0
Reduced hepatic AdipoR2 by increased glucocorticoid mediates effect of psychosocial stress to elevate serum cholesterol 糖皮质激素增加导致肝脏 AdipoR2 减少,从而介导了社会心理压力对血清胆固醇升高的影响。
IF 4.1 3区 医学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-05-28 DOI: 10.1016/j.mce.2024.112282
Qi Wei Guo , Jia Lin , Yi Lin Shen , Yan Jiang Zheng , Xu Chen , Mi Su , Ji Cheng Zhang , Jin Hua Wang , Hui Tang , Guo Ming Su , Zheng Ke Li , Ding Zhi Fang

Understanding the effects of psychosocial stress on serum cholesterol may offer valuable insights into the relationship between psychological disorders and endocrine diseases. However, these effects and their underlying mechanisms have not been elucidated yet. Here we show that serum corticosterone, total cholesterol and low-density lipoprotein cholesterol (LDL-C) are elevated in a mouse model of psychosocial stress. Furthermore, alterations occur in AdipoR2-mediated AMPK and PPARα signaling pathways in liver, accompanied by a decrease in LDL-C clearance and an increase in cholesterol synthesis. These changes are further verified in wild-type and AdipoR2 overexpression HepG2 cells incubated with cortisol and AdipoR agonist, and are finally confirmed by treating wild-type and hepatic-specific AdipoR2 overexpression mice with corticosterone. We conclude that increased glucocorticoid mediates the effects of psychosocial stress to elevate serum cholesterol by inhibiting AdipoR2-mediated AMPK and PPARα signaling to decrease LDL-C clearance and increase cholesterol synthesis in liver.

了解社会心理压力对血清胆固醇的影响可能会对心理障碍与内分泌疾病之间的关系提供有价值的见解。然而,这些影响及其内在机制尚未得到阐明。在这里,我们发现,在社会心理应激小鼠模型中,血清皮质酮、总胆固醇和低密度脂蛋白胆固醇(LDL-C)会升高。此外,肝脏中由 AdipoR2 介导的 AMPK 和 PPARα 信号通路也发生了改变,同时低密度脂蛋白胆固醇清除率降低,胆固醇合成增加。这些变化在用皮质醇和 AdipoR 激动剂培养的野生型和 AdipoR2 过表达 HepG2 细胞中得到了进一步验证,并最终通过用皮质酮处理野生型和肝特异性 AdipoR2 过表达小鼠得到了证实。我们的结论是,糖皮质激素的增加通过抑制 AdipoR2 介导的 AMPK 和 PPARα 信号传导来降低 LDL-C 的清除率并增加肝脏中胆固醇的合成,从而介导社会心理压力对血清胆固醇升高的影响。
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引用次数: 0
Microbial Endocrinology: Host metabolism and appetite hormones interaction with gut microbiome 微生物内分泌学:宿主新陈代谢和食欲激素与肠道微生物组的相互作用。
IF 4.1 3区 医学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-05-27 DOI: 10.1016/j.mce.2024.112281
Anam Ashraf, Md. Imtaiyaz Hassan
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引用次数: 0
期刊
Molecular and Cellular Endocrinology
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