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Hormones in Malaria Infection: Influence on Disease Severity, Host Physiology, and Therapeutic Opportunities. 疟疾感染中的激素:对疾病严重程度、宿主生理学和治疗机会的影响。
IF 3.8 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-11-04 DOI: 10.1042/BSR20240482
Aleena Das, Mrutyunjay Suar, K Sony Reddy

Human malaria, caused by Plasmodium parasites, is a fatal disease that disrupts the host's physiological balance and affects the neuroendocrine system. This review explores how malaria influences and is influenced by hormones. Malaria activates the Hypothalamus-Pituitary-Adrenal axis, leading to increased cortisol, aldosterone, and epinephrine. Cortisol, while reducing inflammation, aids parasite survival, whereas epinephrine helps manage hypoglycemia. The Hypothalamus-Pituitary-Gonad and Hypothalamus-Pituitary-Thyroid axes are also impacted, resulting in lower sex and thyroid hormone levels. Malaria disrupts the renin-angiotensin-aldosterone system (RAAS), causing higher angiotensin-II and aldosterone levels, contributing to edema, hyponatremia and hypertension. Malaria-induced anemia is exacerbated by increased hepcidin, which impairs iron absorption, reducing both iron availability for the parasite and red blood cell formation, despite elevated erythropoietin. Hypoglycemia is common due to decreased glucose production and hyperinsulinemia, although some cases show hyperglycemia due to stress hormones and inflammation. Hypocalcemia, and hypophosphatemia are associated with low Vitamin D3 and parathyroid hormone but high calcitonin. Hormones such as DHEA, melatonin, PTH, Vitamin D3, hepcidin, progesterone, and erythropoietin protects against malaria. Furthermore, synthetic analogs, receptor agonists and antagonists or mimics of hormones like DHEA, melatonin, serotonin, PTH, vitamin D3, estrogen, progesterone, angiotensin, and somatostatin are being explored as potential antimalarial treatments or adjunct therapies. Additionally, hormones like leptin and PCT are being studied as probable markers of malaria infection.

由疟原虫引起的人类疟疾是一种致命疾病,它会破坏宿主的生理平衡并影响神经内分泌系统。本综述探讨疟疾如何影响激素以及激素如何影响疟疾。疟疾会激活下丘脑-垂体-肾上腺轴,导致皮质醇、醛固酮和肾上腺素增加。皮质醇在减少炎症的同时有助于寄生虫存活,而肾上腺素则有助于控制低血糖。下丘脑-垂体-性腺轴和下丘脑-垂体-甲状腺轴也会受到影响,导致性激素和甲状腺激素水平降低。疟疾会破坏肾素-血管紧张素-醛固酮系统(RAAS),导致血管紧张素-II 和醛固酮水平升高,造成水肿、低钠血症和高血压。尽管促红细胞生成素升高,但血红素增加会影响铁的吸收,减少寄生虫对铁的利用和红细胞的形成,从而加剧疟疾引起的贫血。由于葡萄糖生成减少和高胰岛素血症,低血糖症很常见,但有些病例会因应激激素和炎症而出现高血糖症。低钙血症和低磷血症与维生素 D3 和甲状旁腺激素偏低但降钙素偏高有关。DHEA、褪黑激素、PTH、维生素 D3、促红细胞生成素、黄体酮和促红细胞生成素等激素可预防疟疾。此外,DHEA、褪黑激素、5-羟色胺、PTH、维生素 D3、雌激素、孕酮、血管紧张素和体节蛋白等激素的合成类似物、受体激动剂和拮抗剂或模拟物正被探索用作潜在的抗疟治疗或辅助疗法。此外,还在研究瘦素和 PCT 等激素作为疟疾感染的可能标志物。
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引用次数: 0
YAP signaling orchestrates the endothelin-1-guided invadopodia formation in high-grade serous ovarian cancer. YAP信号在高级别浆液性卵巢癌中协调内皮素-1引导的内生树突形成。
IF 3.8 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-11-04 DOI: 10.1042/BSR20241320
Piera Tocci, Valentina Caprara, Celia Roman, Rosanna Sestito, Laura Rosanò, Anna Bagnato

The high-grade serous ovarian cancer (HG-SOC) is a notoriously challenging disease, characterized by a rapid peritoneal dissemination. HG-SOC cells leverage actin-rich membrane protrusions, known as invadopodia, to degrade the surrounding extracellular matrix (ECM) and invade, initiating the metastatic cascade. In HG-SOC, the endothelin-1 (ET-1)/endothelin A receptor (ETAR)-driven signaling coordinates invadopodia activity, however how this axis integrates pro-oncogenic signaling routes, as YAP-driven one, impacting on the invadopodia-mediated ECM degradation and metastatic progression, deserves a deeper investigation. Herein, we observed that downstream of the ET-1/ET-1R axis, the RhoC and Rac1 GTPases, acting as signaling intermediaries, promote the de-phosphorylation and nuclear accumulation of YAP. Conversely, the treatment with the dual ETA/ETB receptor antagonist, macitentan, inhibits the ET-1-driven YAP activity. Similarly, RhoC silencing, or cell transfection with a dominant inactive form of Rac1, restore the YAP phosphorylated and inhibited state. Mechanistically, the ET-1R/YAP signal alliance coordinates invadopodia maturation into ECM-degrading structures, indicating how such ET-1R-guided protein network represents a route able to enhance the HG-SOC invasive potential. At functional level, we found that the interconnection between the ET-1R/RhoC and YAP signals is required for MMP-2 and MMP-9 proteolytic functions, cell invasion, and cytoskeleton architecture changes, supporting the HG-SOC metastatic strength. In HG-SOC patient-derived xenografts (PDX) macitentan, turning-off the invadopodia regulators RhoC/YAP, halt the metastatic colonization. ET-1R targeting, hindering the YAP activity, weakens the invadopodia machinery, embodying a promising therapeutic avenue to prevent peritoneal dissemination in HG-SOC.

高级别浆液性卵巢癌(HG-SOC)是一种臭名昭著的挑战性疾病,其特点是腹膜扩散迅速。HG-SOC细胞利用富含肌动蛋白的膜突起(即侵袭体)来降解周围的细胞外基质(ECM)并进行侵袭,从而启动转移级联反应。在HG-SOC中,内皮素-1(ET-1)/内皮素A受体(ETAR)驱动的信号转导协调着内生型突起的活动,但这一轴心如何与YAP驱动的促致癌信号途径相结合,从而影响内生型突起介导的ECM降解和转移进程,值得深入研究。在此,我们观察到,在 ET-1/ET-1R 轴的下游,RhoC 和 Rac1 GTPases 作为信号中间体,促进了 YAP 的去磷酸化和核积累。相反,ETA/ETB 双受体拮抗剂马西替坦可抑制 ET-1 驱动的 YAP 活性。同样,RhoC 沉默或细胞转染显性无活性形式的 Rac1 可恢复 YAP 的磷酸化和抑制状态。从机理上讲,ET-1R/YAP 信号联盟协调了内吸附体成熟为 ECM 降解结构的过程,表明这种由 ET-1R 引导的蛋白质网络是如何代表了一种能够增强 HG-SOC 侵袭潜力的途径。在功能层面,我们发现 ET-1R/RhoC 和 YAP 信号之间的相互联系是 MMP-2 和 MMP-9 蛋白分解功能、细胞侵袭和细胞骨架结构变化所必需的,从而支持了 HG-SOC 的转移强度。在 HG-SOC 患者衍生异种移植物(PDX)中,马基坦能关闭侵袭性调控因子 RhoC/YAP,阻止转移性定植。以 ET-1R 为靶点,阻碍 YAP 的活性,从而削弱内生癌细胞的内生机制,为防止 HG-SOC 的腹膜扩散提供了一条很有前景的治疗途径。
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引用次数: 0
Causal Effects of Gut Microbiota on Gout and Hyperuricemia: Insights from Genome-Wide Mendelian Randomization, RNA-Sequencing, 16S rRNA Sequencing, and Metabolomes. 肠道微生物群对痛风和高尿酸血症的因果效应:全基因组孟德尔随机化、RNA测序、16S rRNA测序和代谢组的启示。
IF 3.8 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-11-04 DOI: 10.1042/BSR20240595
Xia Liu, Zhe Feng, Fenglian Zhang, Bo Wang, Zhijuan Wei, Nanqing Liao, Min Zhang, Jian Liang, Lisheng Wang

Background: This study investigated the causal relationship between gut microbiota (GM), serum metabolome, and host transcriptome in the development of gout and hyperuricemia (HUA) using genome-wide association studies (GWAS) data and HUA mouse model experiments.  Methods: Mendelian randomization (MR) analysis of GWAS summary statistics was performed using an inverse variance weighted (IVW) approach to determine predict the causal role of the gut microbiota on gout. The HUA mouse model was used to characterize changes in the gut microbiome, host metabolome, and host kidney transcriptome by integrating cecal 16S rRNA sequencing, untargeted serum metabolomics, and host mRNA sequencing.

 Results: Our analysis demonstrated causal effects of seven gut microbiota taxa on gout, including genera of Ruminococcus, Odoribacter, and Bacteroides. Thirty-eight, immune cell traits were associated with gout. Dysbiosis of Dubosiella, Lactobacillus,Bacteroides, Alloprevotella, and Lachnospiraceae_NK4A136_group genera were associated with changes in the serum metabolites and kidney transcriptome of the HUA model mice. The changes in the gut microbiome of the HUA model mice correlated significantly with alterations in the levels of serum metabolites such as taurodeoxycholic acid, phenylacetylglycine, vanylglycol, methyl hexadecanoic acid, carnosol, 6-aminopenicillanic acid, sphinganine, p-hydroxyphenylacetic acid, pyridoxamine, and de-o-methylsterigmatocystin, and expression of kidney genes such as CNDP2, SELENOP, TTR, CAR3, SLC12A3, SCD1, PIGR, CD74, MFSD4B5, and NAPSA.

 Conclusion: Our study demonstrated a causal relationship between GM, immune cells, and gout. HUA development involved alterations in the vitamin B6 metabolism because of gut microbiota dysbiosis that resulted in altered pyridoxamine and pyridoxal levels, dysregulated sphingolipid metabolism, and excessive inflammation.

.

研究背景本研究利用全基因组关联研究(GWAS)数据和HUA小鼠模型实验,研究了痛风和高尿酸血症(HUA)发病过程中肠道微生物群(GM)、血清代谢组和宿主转录组之间的因果关系:采用反方差加权法(IVW)对全基因组关联研究(GWAS)摘要统计进行孟德尔随机化(MR)分析,以确定预测肠道微生物群对痛风的因果作用。通过整合盲肠 16S rRNA 测序、非靶向血清代谢组学和宿主 mRNA 测序,利用 HUA 小鼠模型描述了肠道微生物组、宿主代谢组和宿主肾脏转录组的变化:我们的分析表明,七个肠道微生物群分类群对痛风有因果影响,其中包括反刍球菌属、Odoribacter 和 Bacteroides。38种免疫细胞特征与痛风有关。Dubosiella、Lactobacillus、Bacteroides、Alloprevotella和Lachnospiraceae_NK4A136_group等菌属的菌群失调与HUA模型小鼠血清代谢物和肾脏转录组的变化有关。6-氨基青霉烷酸、鞘氨醇、对羟基苯乙酸、吡哆胺和去甲基异麦角胱氨酸等肾脏代谢产物,以及 CNDP2、SELENOP、TTR、CAR3、SLC12A3、SCD1、PIGR、CD74、MFSD4B5 和 NAPSA 等肾脏基因的表达。 结论:我们的研究证明了 GM、免疫细胞和痛风之间的因果关系。由于肠道微生物群失调导致吡哆胺和吡哆醛水平改变、鞘脂代谢失调和过度炎症,HUA 的发生涉及维生素 B6 代谢的改变。
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引用次数: 0
Simulated ischaemia/reperfusion impairs trophoblast function through divergent oxidative stress- and MMP-9-dependent mechanisms. 模拟缺血/再灌注通过不同的氧化应激和 MMP-9 依赖性机制损害滋养层功能。
IF 3.8 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-10-30 DOI: 10.1042/BSR20240763
Aaron Barron, Jetro Tuulari, Linnea Karlsson, Hasse Karlsson, Gerard W O'Keeffe, Cathal M McCarthy

Early-onset pre-eclampsia is believed to arise from defective placentation in the 1st trimester, leading to placental ischaemia/reperfusion (I/R) and oxidative stress. However, our current understanding of the effects of I/R and oxidative stress on trophoblast function is ambiguous in part due to studies exposing trophoblasts to hypoxia instead of I/R, and which report conflicting results. Here we present a model of simulated ischaemia/reperfusion (SI/R) to recapitulate the pathophysiological events of early-onset PE, by exposing 1st trimester cytotrophoblast HTR-8/SVneo cells to a simulated ischaemia buffer followed by reperfusion. We examined different ischaemia and reperfusion times and observed that 1h ischaemia and 24h reperfusion induced an increase in reactive oxygen species (ROS) production (p < 0.0001) and oxygen consumption rate (p < 0.01). SI/R-exposed trophoblast cells exhibited deficits in migration, proliferation and invasion (p < 0.01). While the deficits in migration and proliferation were rescued by antioxidants, suggesting a ROS-dependent mechanism, the loss of invasion was not affected by antioxidants, which suggests a divergent ROS-independent pathway. In line with this, we observed a decrease in MMP-9, the key regulatory enzyme necessary for trophoblast invasion (p < 0.01), which was similarly unaffected by antioxidants, and pharmacological inhibition of MMP-9 replicated the phenotype of deficient invasion (p < 0.01). Collectively, these data demonstrate that I/R impairs trophoblast migration and proliferation via a ROS-dependent mechanism, and invasion via a ROS-independent loss of MMP-9, disambiguating the role of oxidative stress and providing insights into the response of trophoblasts to I/R in the context of early-onset PE.

早发型子痫前期被认为是由于妊娠头三个月胎盘功能缺陷导致胎盘缺血/再灌注(I/R)和氧化应激引起的。然而,我们目前对缺血再灌注和氧化应激对滋养细胞功能影响的认识并不明确,部分原因是有研究将滋养细胞暴露于缺氧而非缺血再灌注环境中,这些研究报告的结果相互矛盾。在这里,我们提出了一种模拟缺血/再灌注(SI/R)模型,通过将怀孕三个月的滋养层细胞 HTR-8/SVneo 暴露于模拟缺血缓冲液中,然后进行再灌注,来再现早期 PE 的病理生理事件。我们研究了不同的缺血和再灌注时间,观察到缺血1小时和再灌注24小时会导致活性氧(ROS)生成增加(p < 0.0001)和耗氧量增加(p < 0.01)。SI/R暴露的滋养层细胞在迁移、增殖和侵袭方面表现出缺陷(p < 0.01)。虽然迁移和增殖的缺陷能被抗氧化剂所挽救,这表明这是一种依赖于 ROS 的机制,但侵袭的丧失不受抗氧化剂的影响,这表明这是一种不同的 ROS 非依赖性途径。与此相一致,我们观察到滋养细胞侵袭所必需的关键调控酶 MMP-9 减少(p < 0.01),同样不受抗氧化剂的影响,药理抑制 MMP-9 复制了侵袭不足的表型(p < 0.01)。总之,这些数据证明了I/R通过ROS依赖性机制损害滋养细胞的迁移和增殖,并通过MMP-9的ROS依赖性损失损害侵袭,从而明确了氧化应激的作用,并为早期PE背景下滋养细胞对I/R的反应提供了见解。
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引用次数: 0
Expression of Concern: C1QTNF6 regulates cell proliferation and apoptosis of NSCLC in vitro and in vivo. 关注表达:C1QTNF6 在体外和体内调节 NSCLC 的细胞增殖和凋亡。
IF 3.8 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-10-30 DOI: 10.1042/BSR-2020-1541_EOC
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引用次数: 0
Correction: Therapeutic activity of green synthesized selenium nanoparticles from turmeric against cisplatin-induced oxido-inflammatory stress, and cell death in mice kidney. 更正:姜黄绿色合成硒纳米粒子对顺铂诱导的氧化-炎症应激和小鼠肾脏细胞死亡具有治疗活性。
IF 3.8 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-10-30 DOI: 10.1042/BSR-2023-1130_COR
{"title":"Correction: Therapeutic activity of green synthesized selenium nanoparticles from turmeric against cisplatin-induced oxido-inflammatory stress, and cell death in mice kidney.","authors":"","doi":"10.1042/BSR-2023-1130_COR","DOIUrl":"10.1042/BSR-2023-1130_COR","url":null,"abstract":"","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":null,"pages":null},"PeriodicalIF":3.8,"publicationDate":"2024-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11522953/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142520907","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Multiple ASC-dependent inflammasomes drive differential pro-inflammatory cytokine production in a mouse model of tendinopathy. 在小鼠肌腱病模型中,多种依赖于 ASC 的炎性体驱动着不同的促炎细胞因子的产生。
IF 3.8 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-10-29 DOI: 10.1042/BSR20241282
Alejandro Peñín-Franch, Laura Hurtado-Navarro, Jose Antonio García-Vidal, Pilar Escolar-Reina, Francesc Medina-Mirapeix, Pablo Pelegrin

Inflammasomes are multiprotein complexes that regulate the bioactive production of IL-1b and IL-18, being implicated in the inflammatory response of different diseases. The inflammasome formed by the cytosolic sensor NLRP3 is highly promiscuous, as it could be activated by different pathogen- and sterile-signals. However, few models have studied the implication of NLRP3 in tissue damage-induced inflammation, particularly the implication of NLRP3 in tendinopathies. Here we aimed to investigate the implication of NLRP3 in a mouse model of tendinopathy by collagenase degradation of the extracellular matrix in the Achilles' mice tendon. We found that NLRP3 was involved in the production of IL-1b and IL-6, but another ASC-dependent inflammasome was required to produce IL-18 during sterile tissue damage. Our study suggests that in the immune response to extracellular matrix degradation different inflammasomes, probably expressed in different cell compartments, were able to differentially control IL-1b and IL-18 production in vivo. These results suggest the potential use of therapies targeting ASC as beneficial in the treatment of tendinopathies.

炎症小体是一种多蛋白复合物,可调节 IL-1b 和 IL-18 的生物活性生成,与不同疾病的炎症反应有关。由细胞膜传感器 NLRP3 形成的炎症小体具有很强的混杂性,因为它可以被不同的病原体信号和无菌信号激活。然而,很少有模型研究过 NLRP3 在组织损伤诱导的炎症中的作用,尤其是 NLRP3 在肌腱病中的作用。在这里,我们旨在通过跟腱小鼠细胞外基质的胶原酶降解研究 NLRP3 在小鼠腱鞘炎模型中的作用。我们发现,NLRP3参与了IL-1b和IL-6的产生,但在无菌组织损伤过程中,需要另一个依赖于ASC的炎性体产生IL-18。我们的研究表明,在对细胞外基质降解的免疫反应中,可能在不同细胞区表达的不同炎性体能够以不同方式控制体内IL-1b和IL-18的产生。这些结果表明,针对ASC的疗法有可能用于治疗肌腱病。
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引用次数: 0
Axonal neurotransmitter release in the regulation of myelination. 调节髓鞘化的轴突神经递质释放
IF 3.8 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-25 DOI: 10.1042/BSR20231616
Katy L H Marshall-Phelps, Rafael G Almeida

Myelination of axons is a key determinant of fast action potential propagation, axonal health and circuit function. Previously considered a static structure, it is now clear that myelin is dynamically regulated in response to neuronal activity in the central nervous system (CNS). However, how activity-dependent signals are conveyed to oligodendrocytes remains unclear. Here, we review the potential mechanisms by which neurons could communicate changing activity levels to myelin, with a focus on the accumulating body of evidence to support activity-dependent vesicular signalling directly onto myelin sheaths. We discuss recent in vivo findings of activity-dependent fusion of neurotransmitter vesicles from non-synaptic axonal sites, and how modulation of this vesicular fusion regulates the stability and growth of myelin sheaths. We also consider the potential mechanisms by which myelin could sense and respond to axon-derived signals to initiate remodelling, and the relevance of these adaptations for circuit function. We propose that axonal vesicular signalling represents an important and underappreciated mode of communication by which neurons can transmit activity-regulated signals to myelinating oligodendrocytes and, potentially, more broadly to other cell types in the CNS.

轴突的髓鞘化是决定快速动作电位传播、轴突健康和回路功能的关键因素。髓鞘以前被认为是一种静态结构,但现在很清楚,髓鞘是随着中枢神经系统中神经元的活动而动态调节的。然而,依赖于活动的信号是如何传递给少突胶质细胞的仍不清楚。在此,我们回顾了神经元向髓鞘传递不断变化的活动水平的潜在机制,并重点讨论了支持活动依赖性囊泡信号直接传递到髓鞘的不断积累的证据。我们讨论了最近在体内发现的非突触轴突部位神经递质囊泡的活动依赖性融合,以及这种囊泡融合的调控如何调节髓鞘的稳定性和生长。我们还考虑了髓鞘感知和响应轴突信号以启动重塑的潜在机制,以及这些适应对电路功能的相关性。我们认为,轴突囊泡信号是一种重要的、未被充分重视的交流模式,神经元可通过这种模式将活动调节信号传递给髓鞘化少突胶质细胞,并有可能更广泛地传递给中枢神经系统中的其他细胞类型。
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引用次数: 0
Clo-miR-14: a medicinally valued spice-derived miRNA with therapeutic implications in rheumatoid arthritis. Clo-miR-14:一种具有药用价值的香料提取 miRNA,对类风湿性关节炎具有治疗意义。
IF 3.8 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-25 DOI: 10.1042/BSR20240311
Ashish Sarkar, Mohd Saquib, Debolina Chakraborty, Sonia Mann, Swati Malik, Prachi Agnihotri, Lovely Joshi, Rajesh Malhotra, Sagarika Biswas

Plant microRNAs (miRNA) are regularly consumed orally along with diet, gaining attention for their RNA-based drug potential because of their ability to regulate mammalian gene expression specifically at the post-transcriptional level. Medicinally valued plants are well known for their anti-inflammatory property; however, the contribution of their miRNA in managing inflammation has been less studied. We investigated miRNA from four medicinally valued regularly consumed spices, and validated one of the most potential miRNA 'Clo-miR-14' for its thermal stability, and absorption in the plasma samples of RA patient's by RT-PCR. In vitro and in vivo studies were performed to investigate the effect of Clo-miR-14 in ameliorating rheumatoid arthritis (RA) like symptoms. Our results suggest that 'Clo-miR-14,' an exogenous miRNA present in Curcuma longa, absorbed through regular diet, has robust thermal stability at 100°C in humans. It significantly reduced pro-inflammatory cytokines (TNF, IL-1β, IL-6) and RA-like symptoms, suggesting that plant-based miRNA could be a promising candidate as an RNA-based drug for RA pathogenesis.

植物微核糖核酸(miRNA)经常与饮食一起口服,由于它们能够在转录后水平调节哺乳动物基因的表达,因此其基于核糖核酸的药物潜力备受关注。有药用价值的植物以其抗炎特性而闻名,但对其 miRNA 在控制炎症方面的贡献研究较少。我们研究了四种经常食用的药用香料中的 miRNA,并通过 RT-PCR 验证了最有潜力的 miRNA 之一 "Clo-miR-14 "的热稳定性以及在 RA 患者血浆样本中的吸收情况。为了研究 Clo-miR-14 在改善类风湿关节炎(RA)症状方面的作用,我们进行了体外和体内研究。我们的研究结果表明,"Clo-miR-14 "是一种存在于莪术中的外源性 miRNA,可通过正常饮食吸收,在 100℃的温度下对人体具有很强的热稳定性。它能明显降低促炎细胞因子(TNF、IL-1β、IL-6)和类 RA 症状,这表明以植物为基础的 miRNA 有可能成为一种治疗类 RA 发病机制的 RNA 药物。
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引用次数: 0
Integration of clotting and fibrinolysis: central role of platelets and factor XIIIa. 凝血和纤维蛋白溶解的整合:血小板和因子 XIIIa 的核心作用。
IF 3.8 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-25 DOI: 10.1042/BSR20240332
Irina Patalakh, Olga Revka, Agata Gołaszewska, Natalia Bielicka, Tomasz Misztal

Purpose: The aim of the present study was to establish the role of platelets and activated factor XIIIa (FXIIIa) in the structuring of the fibrin network as well as to clarify the effect of network compaction on clot lysis.

Methods: Turbidimetry was used for the one-stage clotting test where platelet-free plasma (PFP) is regarded as single factor-deficient plasma (platelets as lacking factor) and autologous platelet-rich plasma (PRP) as deficiency corrected plasma. Structural features of the developed and subsequently lysed fibrin network, formed under static and flow conditions, were visualized by confocal microscopy.

Results: Thrombin-initiated plasma clotting revealed changes in the shape of the absorption curve, more pronounced in the presence of platelets. These changes correlate with the transformation of the fibrin scaffold during clot maturing. With the combined action of platelets, thrombin and Ca2+, plasma clotting passes through two phases: initial formation of a platelet-fibrin network (first peak in the polymerization curve), and then the compaction of fibrin, driven by FXIIIa (the second peak) which can be further modulate by the contractile action of platelets. These structural changes, mediated by platelets and FXIIIa, have been shown to determine subsequent clot lysis.

Conclusions: Platelet aggregates serve as organizing centers that determine the distribution of fibrin in clot volume. The openwork structure of the platelet-transformed fibrin provides the necessary prerequisites for its timely lysis. The revealed aspects of the interaction of platelets and FXIIIa, which accompanies the maturation of a fibrin clot, may lead to new approaches in the pharmacological correction of disorders associated with both thrombotic episodes and bleeding tendency.

本研究旨在确定血小板和活化因子 XIIIa (FXIIIa) 在纤维蛋白网络结构中的作用,并阐明网络压实对血块溶解的影响。 浊度测定法用于单阶段凝血试验,其中 PFP 被视为单因子缺乏血浆(血小板为缺乏因子),而自体 PRP 被视为缺乏因子校正血浆。共聚焦显微镜观察了在静态和流动条件下形成的纤维蛋白网络的结构特征。凝血酶引发的血浆凝固显示出吸收曲线形状的变化,在血小板存在的情况下更为明显。这些变化与凝块成熟过程中纤维蛋白支架的转变有关。在血小板、凝血酶和 Ca2+ 的共同作用下,血浆凝结会经历两个阶段:最初形成血小板-纤维蛋白网络(聚合曲线的第一个峰值),然后在 FXIIIa 的驱动下压实纤维蛋白(第二个峰值),血小板的收缩作用可进一步调节纤维蛋白的压实。这些由血小板和 FXIIIa 介导的结构变化已被证明能决定随后的血块溶解。 血小板聚集体是决定纤维蛋白在血块体积中分布的组织中心。血小板转化的纤维蛋白的镂空结构为其及时裂解提供了必要的先决条件。血小板和 FXIIIa 的相互作用伴随着纤维蛋白凝块的成熟,揭示了这一相互作用的方方面面,可能会为药物治疗与血栓发作和出血倾向相关的疾病提供新的方法。
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