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CHMP4B contributes to maintaining the follicular cells integrity in the panoistic ovary of the cockroach Blattella germanica CHMP4B有助于维持德国蜚蠊泛型卵巢中卵泡细胞的完整性。
IF 2.4 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2024-06-19 DOI: 10.1111/boc.202400010
Nuria Farrus, José Luis Maestro, Maria-Dolors Piulachs

Background

The Endosomal Sorting Complex Required for Transport (ESCRT) is a highly conserved cellular machinery essential for many cellular functions, including transmembrane protein sorting, endosomal trafficking, and membrane scission. CHMP4B is a key component of ESCRT-III subcomplex and has been thoroughly studied in the meroistic ovaries of Drosophila melanogaster showing its relevance in maintaining this reproductive organ during the life of the fly. However, the role of the CHMP4B in the most basal panoistic ovaries remains elusive.

Results

Using RNAi, we examined the function of CHMP4B in the ovary of Blattella germanica in two different physiological stages: in last instar nymphs, with proliferative follicular cells, and in vitellogenic adults when follicular cells enter in polyploidy and endoreplication. In Chmp4b-depleted specimens, the actin fibers change their distribution, appearing accumulated in the basal pole of the follicular cells, resulting in an excess of actin bundles that surround the basal ovarian follicle and modifying their shape. Depletion of Chmp4b also determines an actin accumulation in follicular cell membranes, resulting in different cell morphologies and sizes. In the end, these changes disrupt the opening of intercellular spaces between the follicular cells (patency) impeding the incorporation of yolk proteins to the growing oocyte and resulting in female sterility. In addition, the nuclei of follicular cells appeared unusually elongated, suggesting an incomplete karyokinesis.

Conclusions

These results proved CHMP4B essential in preserving the proper expression of cytoskeleton proteins vital for basal ovarian follicle growth and maturation and for yolk protein incorporation. Moreover, the correct distribution of actin fibers in the basal ovarian follicle emerged as a critical factor for the successful completion of ovulation and oviposition.

Significance

The overall results, obtained in two different proliferative stages, suggest that the requirement of CHMP4B in B. germanica follicular epithelium is not related to the proliferative stage of the tissue.

背景:运输所需的内体分选复合体(ESCRT)是一种高度保守的细胞机制,对许多细胞功能至关重要,包括跨膜蛋白分选、内体运输和膜裂解。CHMP4B是ESCRT-III亚复合物的一个关键成分,在黑腹果蝇的子代卵巢中对它进行了深入研究,显示了它在维持果蝇一生的生殖器官中的重要性。然而,CHMP4B在最基底的泛能卵巢中的作用仍然难以捉摸:结果:我们利用 RNAi 技术研究了 CHMP4B 在德国扁虱卵巢中两个不同生理阶段的功能:末龄若虫卵泡细胞增殖阶段和卵黄形成成虫卵泡细胞进入多倍体和内复制阶段。在缺失 Chmp4b 的标本中,肌动蛋白纤维的分布发生了变化,出现在卵泡细胞的基极,导致过多的肌动蛋白束包围基底卵泡并改变其形状。Chmp4b 的耗竭也决定了卵泡细胞膜上肌动蛋白的积聚,导致细胞形态和大小的不同。最终,这些变化会破坏卵泡细胞间的细胞间隙(通畅性),阻碍卵黄蛋白与生长中的卵母细胞结合,导致女性不育。此外,卵泡细胞的细胞核出现异常拉长,表明核运动不完全:这些结果证明,CHMP4B 对维持细胞骨架蛋白的正常表达至关重要,这些蛋白对基础卵泡的生长和成熟以及卵黄蛋白的结合至关重要。此外,卵巢基底卵泡中肌动蛋白纤维的正确分布也是成功完成排卵和产卵的关键因素:在两个不同增殖阶段获得的总体结果表明,B. germanica卵泡上皮细胞对CHMP4B的需求与组织的增殖阶段无关。
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引用次数: 0
Using carbohydrate-based polymers to facilitate testicular regeneration 利用基于碳水化合物的聚合物促进睾丸再生
IF 2.4 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2024-06-16 DOI: 10.1111/boc.202400013
Aneeqa Majeed, Hanan Afzal, Kaleem Maqsood, Amara Noureen, Zaman Gul, Muhammad Imran, Ali Afzal, Muhammad Babar Khawar

Male infertility is a significant global issue affecting 60–80 million people, with 40%–50% of cases linked to male issues. Exposure to radiation, drugs, sickness, the environment, and oxidative stress may result in testicular degeneration. Carbohydrate-based polymers (CBPs) restore testis differentiation and downregulate apoptosis genes. CBP has biodegradability, low cost, and wide availability, but is at risk of contamination and variations. CBP shows promise in wound healing, but more research is required before implementation in healthcare. Herein, we discuss the recent advances in engineering applications of CBP employed as scaffolds, drug delivery systems, immunomodulation, and stem cell therapy for testicular regeneration. Moreover, we emphasize the promising challenges warranted for future perspectives.

男性不育是一个严重的全球性问题,影响着 6000 万至 8000 万人,其中 40%-50% 的病例与男性问题有关。暴露于辐射、药物、疾病、环境和氧化应激可能导致睾丸退化。基于碳水化合物的聚合物(CBPs)可恢复睾丸分化,并下调凋亡基因。CBP 具有生物可降解性、低成本和广泛的可用性,但存在污染和变异的风险。CBP 在伤口愈合方面大有可为,但在应用于医疗保健之前还需要更多的研究。在此,我们将讨论 CBP 作为支架、给药系统、免疫调节和干细胞疗法用于睾丸再生的工程应用方面的最新进展。此外,我们还强调了未来前景值得期待的挑战。
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引用次数: 0
Association of 3'UTR variations of EGFR and KRAS oncogenes with clinical parameters in lung cancer tumours 表皮生长因子受体和 KRAS 致癌基因的 3'UTR 变异与肺癌肿瘤临床参数的关系。
IF 2.4 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2024-06-16 DOI: 10.1111/boc.202400017
Ozkan Bagci

Bacground Information

Lung cancer is one of the leading types of cancer deaths worldwide, with approximately 2 million people diagnosed with lung cancer each year. In this study, we aimed to determine the exonic and 3′UTR sequences of EGFR, PIK3CA and KRAS genes in 39 sporadic lung cancer tumors and to reveal the changes in the miRNA binding profile of tumors with somatic variation in the 3'UTR region and to examine the relationship of these changes with clinical parameters.

Results

A statistically significant correlation was found between the presence of miRNA that could not bind to the 3′UTR region due to variation in at least one of the EGFR or KRAS genes and the presence of metastasis in the tumor. At the same time, Kaplan-Meier analysis between those with and without alterations in the miRNA profile due to somatic variation in the 3′UTR region showed that survival was lower in those with miRNA alterations and this was statistically significant.

Conclusions

In our study, it was shown that variations in the 3′UTR regions of EGFR and KRAS oncogenes may cause increased expression of these oncogenes by preventing the binding of miRNAs, and it was suggested that this may be related to metastasis, survival and drug resistance mechanism.

Significance

In this study, we show that hsa-miR-124-3p, hsa-miR-506-3p, hsa-miR-1290 and hsa-miR-6514-3p are particularly prominent in lung carcinoma in relation to these biological pathways and the roles that variations in the 3′UTR regions of oncogenes may play in the carcinogenesis process.

背景信息:肺癌是全球癌症死亡的主要类型之一,每年约有 200 万人被诊断为肺癌。在这项研究中,我们旨在确定 39 例散发性肺癌肿瘤中 EGFR、PIK3CA 和 KRAS 基因的外显子和 3'UTR 序列,揭示 3'UTR 区域体细胞变异的肿瘤 miRNA 结合谱的变化,并研究这些变化与临床参数的关系:结果发现,因表皮生长因子受体或 KRAS 基因中至少一个基因发生变异而无法与 3'UTR 区结合的 miRNA 的存在与肿瘤是否发生转移之间存在统计学意义上的相关性。同时,对因3'UTR区体细胞变异而导致miRNA谱发生变化的患者和未发生变化的患者进行卡普兰-米尔分析表明,miRNA发生变化的患者生存率较低,且具有统计学意义:我们的研究表明,表皮生长因子受体(EGFR)和克癌基因(KRAS)3'UTR区的变异可能会阻止miRNA的结合,从而导致这些癌基因的表达增加,并认为这可能与转移、生存和耐药机制有关:本研究表明,hsa-miR-124-3p、hsa-miR-506-3p、hsa-miR-1290和hsa-miR-6514-3p在肺癌中的表达尤为突出,这与这些生物通路有关,也与癌基因3'UTR区的变异在致癌过程中可能发挥的作用有关。
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引用次数: 0
The French Society for Cell Biology celebrates its 40th anniversary this year! 今年是法国细胞生物学学会成立 40 周年!
IF 2.4 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2024-06-14 DOI: 10.1111/boc.202400045
Florence Niedergang, Isabelle Tardieux

The French Society for Cell Biology (SBCF) is actively involved in communicating the latest advances and organizing scientific events, as well as supporting young researchers, in this field. The SBCF also supports and organizes outreaching activities designed to raise public awareness of science in general and cell biology in particular. The Society, in its present form, was founded in 1984. To mark this milestone, we are organizing a memorable symposium hosted by the Académie des Sciences (https://sbcf.fr/en/event/symposium-des-40-ans-de-la-sbcf/) on September 10, 2024.

法国细胞生物学学会(SBCF)积极传播该领域的最新进展,组织科学活动,并为年轻研究人员提供支持。SBCF 还支持和组织旨在提高公众对科学,特别是细胞生物学认识的外联活动。目前的学会成立于 1984 年。为了纪念这一里程碑,我们将于 2024 年 9 月 10 日在科学院(https://sbcf.fr/en/event/symposium-des-40-ans-de-la-sbcf/)举办一次值得纪念的研讨会。
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引用次数: 0
Plakins are involved in the regulation of centrosome position in polarized epithelial cells Plakins 参与了极化上皮细胞中心体位置的调节。
IF 2.4 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2024-06-08 DOI: 10.1111/boc.202400048
Juliana Geay, Yoran Margaron, David Gentien, Fabien Reyal, Alain Puisieux, Laurent Blanchoin, Laurent Guyon, Manuel Théry

Background Information

The control of epithelial cell polarity is key to their function. Its dysregulation is a major cause of tissue transformation. In polarized epithelial cells,the centrosome is off-centred toward the apical pole. This asymmetry determines the main orientation of the microtubule network and intra-cellular traffic. However, the mechanism regulating centrosome positioning at the apical pole of polarized epithelial cells is still poorly undertood.

Results

In this study we used transcriptomic data from breast cancer cells to identify molecular changes associated with the different stages of tumour transformation. We correlated these changes with variations in centrosome position or with cell progression along the epithelial-to-mesenchymal transition (EMT), a process that involves centrosome repositioning. We found that low levels of epiplakin, desmoplakin and periplakin correlated with centrosome mispositioning in cells that had progressed through EMT or tissue transformation. We further tested the causal role of these plakins in the regulation of centrosome position by knocking down their expression in a non-tumorigenic breast epithelial cell line (MCF10A). The downregulation of periplakin reduced the length of intercellular junction, which was not affected by the downregulation of epiplakin or desmoplakin. However, down-regulating any of them disrupted centrosome polarisation towards the junction without affecting microtubule stability.

Conclusions

Altogether, these results demonstrated that epiplakin, desmoplakin and periplakin are involved in the maintenance of the peripheral position of the centrosome close to inter-cellular junctions. They also revealed that these plakins are downregulated during EMT and breast cancer progression, which are both associated with centrosome mispositioning.

Significance

These results revealed that the down-regulation of plakins and the consequential centrosome mispositioning are key signatures of disorganised cytoskeleton networks, inter-cellular junction weakening, shape deregulation and the loss of polarity in breast cancer cells. These metrics could further be used as a new readouts for early phases of tumoral development.

背景信息:上皮细胞极性的控制是其功能的关键。极性失调是组织变革的主要原因。在极化的上皮细胞中,中心体偏离中心,朝向顶极。这种不对称性决定了微管网络和细胞内交通的主要方向。然而,对极化上皮细胞顶端中心体定位的调控机制还知之甚少:在这项研究中,我们利用乳腺癌细胞的转录组数据确定了与肿瘤转化的不同阶段相关的分子变化。我们将这些变化与中心体位置的变化或细胞在上皮细胞向间质细胞转变(EMT)过程中的进展联系起来,EMT 是一个涉及中心体重新定位的过程。我们发现,在经历了 EMT 或组织转化的细胞中,低水平的 epiplakin、desmoplakin 和 periplakin 与中心体错位有关。我们通过在非致瘤性乳腺上皮细胞系(MCF10A)中敲除这些蛋白的表达,进一步检测了这些蛋白在中心体位置调控中的因果作用。下调periplakin会减少细胞间接合点的长度,而下调epiplakin或desmoplakin则不会影响细胞间接合点的长度。然而,下调其中任何一种都会破坏中心体向交界处的极化,而不会影响微管的稳定性:总之,这些结果表明,外端粒蛋白、去端粒蛋白和周端粒蛋白参与维持靠近细胞间连接的中心体的外周位置。他们还发现,在EMT和乳腺癌进展过程中,这些plakin被下调,而EMT和乳腺癌进展都与中心体位置错误有关:这些结果表明,plakins 的下调和随之而来的中心体错位是乳腺癌细胞中细胞骨架网络混乱、细胞间连接减弱、形状失调和极性丧失的关键标志。这些指标可进一步用作肿瘤发展早期阶段的新读数。
{"title":"Plakins are involved in the regulation of centrosome position in polarized epithelial cells","authors":"Juliana Geay,&nbsp;Yoran Margaron,&nbsp;David Gentien,&nbsp;Fabien Reyal,&nbsp;Alain Puisieux,&nbsp;Laurent Blanchoin,&nbsp;Laurent Guyon,&nbsp;Manuel Théry","doi":"10.1111/boc.202400048","DOIUrl":"10.1111/boc.202400048","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background Information</h3>\u0000 \u0000 <p>The control of epithelial cell polarity is key to their function. Its dysregulation is a major cause of tissue transformation. In polarized epithelial cells,the centrosome is off-centred toward the apical pole. This asymmetry determines the main orientation of the microtubule network and intra-cellular traffic. However, the mechanism regulating centrosome positioning at the apical pole of polarized epithelial cells is still poorly undertood.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>In this study we used transcriptomic data from breast cancer cells to identify molecular changes associated with the different stages of tumour transformation. We correlated these changes with variations in centrosome position or with cell progression along the epithelial-to-mesenchymal transition (EMT), a process that involves centrosome repositioning. We found that low levels of epiplakin, desmoplakin and periplakin correlated with centrosome mispositioning in cells that had progressed through EMT or tissue transformation. We further tested the causal role of these plakins in the regulation of centrosome position by knocking down their expression in a non-tumorigenic breast epithelial cell line (MCF10A). The downregulation of periplakin reduced the length of intercellular junction, which was not affected by the downregulation of epiplakin or desmoplakin. However, down-regulating any of them disrupted centrosome polarisation towards the junction without affecting microtubule stability.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Altogether, these results demonstrated that epiplakin, desmoplakin and periplakin are involved in the maintenance of the peripheral position of the centrosome close to inter-cellular junctions. They also revealed that these plakins are downregulated during EMT and breast cancer progression, which are both associated with centrosome mispositioning.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Significance</h3>\u0000 \u0000 <p>These results revealed that the down-regulation of plakins and the consequential centrosome mispositioning are key signatures of disorganised cytoskeleton networks, inter-cellular junction weakening, shape deregulation and the loss of polarity in breast cancer cells. These metrics could further be used as a new readouts for early phases of tumoral development.</p>\u0000 </section>\u0000 </div>","PeriodicalId":8859,"journal":{"name":"Biology of the Cell","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2024-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/boc.202400048","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141293101","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Reconsidering red blood cells as the diagnostic potential for neurodegenerative disorders 重新考虑红细胞作为神经退行性疾病的诊断潜力。
IF 2.4 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2024-05-31 DOI: 10.1111/boc.202400019
Somu Yadav,  Deepika, Kareena Moar, Akshay Kumar, Nikhila Khola, Anuja Pant, Ganseh S. Kakde, Pawan Kumar Maurya

Background

Red blood cells (RBCs) are usually considered simple cells and transporters of gases to tissues.

Hypothesis

However, recent research has suggested that RBCs may have diagnostic potential in major neurodegenerative disorders (NDDs).

Results

This review summarizes the current knowledge on changes in RBC in Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and other NDDs. It discusses the deposition of neuronal proteins like amyloid-β, tau, and α-synuclein, polyamines, changes in the proteins of RBCs like band-3, membrane transporter proteins, heat shock proteins, oxidative stress biomarkers, and altered metabolic pathways in RBCs during neurodegeneration. It also highlights the comparison of RBC diagnostic markers to other in-market diagnoses and discusses the challenges in utilizing RBCs as diagnostic tools, such as the need for standardized protocols and further validation studies.

Significance statement

The evidence suggests that RBCs have diagnostic potential in neurodegenerative disorders, and this study can pave the foundation for further research which may lead to the development of novel diagnostic approaches and treatments.

背景:红细胞(RBC)通常被认为是简单的细胞和向组织输送气体的运输工具。假设:然而,最近的研究表明,红细胞在主要神经退行性疾病(NDD)中可能具有诊断潜力:本综述总结了目前有关阿尔茨海默病、帕金森病、肌萎缩侧索硬化症和其他 NDDs 中 RBC 变化的知识。它讨论了神经变性过程中淀粉样蛋白-β、tau 和 α-突触核蛋白等神经元蛋白的沉积、多胺、带-3 等 RBC 蛋白的变化、膜转运蛋白、热休克蛋白、氧化应激生物标志物以及 RBC 代谢途径的改变。报告还强调了 RBC 诊断标记物与市场上其他诊断方法的比较,并讨论了利用 RBC 作为诊断工具所面临的挑战,如需要标准化方案和进一步的验证研究:证据表明,RBC 具有诊断神经退行性疾病的潜力,这项研究可为进一步研究奠定基础,从而开发出新型诊断方法和治疗手段。
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引用次数: 0
Neutrophil extracellular traps modulate chemotherapy efficacy and its adverse side effects 中性粒细胞胞外捕获物调节化疗疗效及其不良副作用。
IF 2.4 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2024-05-09 DOI: 10.1111/boc.202400031
Alexandra Mousset, Jean Albrengues

Neutrophils, major regulator of innate immunity have recently emerged as key components of the tumor microenvironment. The role of neutrophils in cancer has been linked to their ability to form neutrophil extracellular traps (NETs), structures composed of decondensed DNA decorated with enzymes that are released into the extracellular space. Here, we discuss the pivotal roles of NETs, in influencing responses to chemotherapy and its severe adverse effect. Highlighting recent insights, we discuss the dual nature of NETs in the context of chemotherapy treatment, examining their potential to either counteract or enhance treatment outcomes. Strategic targeting of NETs emerges as a promising avenue for determining combination therapies that could help counteracting resistance or enhancing chemotherapy efficacy as well as limiting complications due to this type of treatment.

中性粒细胞是先天性免疫的主要调节因子,最近已成为肿瘤微环境的关键组成部分。中性粒细胞在癌症中的作用与它们形成中性粒细胞胞外捕获物(NETs)的能力有关,NETs 是由脱凝 DNA 组成的结构,上面装饰有释放到细胞外空间的酶。在此,我们将讨论 NETs 在影响化疗反应及其严重不良反应方面的关键作用。我们重点介绍了最近的研究成果,讨论了 NETs 在化疗过程中的双重性质,研究了 NETs 抵消或增强治疗效果的潜力。以 NETs 为战略目标是确定联合疗法的一个很有前景的途径,有助于抵消化疗耐药性或提高化疗疗效,并限制此类治疗引起的并发症。
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引用次数: 0
A review on the nexus of autophagy genes from the perspective of polycystic ovary syndrome 从多囊卵巢综合征的角度综述自噬基因的关系
IF 2.4 4区 生物学 Q4 CELL BIOLOGY Pub Date : 2024-04-28 DOI: 10.1111/boc.202300069
Arifa Khatun, Taslima Nasrin, Md Samim Hassan, Mehboob Hoque, Muddasarul Hoda, Safdar Ali

Polycystic ovary syndrome or PCOS is an endocrine disorder in women of reproductive age. It is a diversified multi factorial disorder and diagnosis is very complicated because of its overlapping symptoms some of which are irregular menstrual cycle, acne in face, excess level of androgen (AE), insulin resistance, obesity, cardiovascular disease, mood disorder and type 2 diabetes (T2DM). PCOS may be caused by hormonal imbalance, genetic and epigenetic vulnerability, hypothalamic and ovarian troubles. PCOS is essentially hyperandrogenimia with oligo-anovulation. This review explains the abnormal regulation of autophagy related genes and proteins in different cells at various stages which leads to the genesis of PCOS. During nutrient starvation cells face stress condition, which it tries to overcome by activating its macroautophagy mechanism and by degrading the cytoplasmic material. This provides energy to the cell facilitating its survival. Downregulation of autophagy related genes in endometria has been observed in PCOS women. PCOS can be managed by maintaining proper lifestyle and medical treatment. Healthy meals and regular exercise can prevent the excessive weight and also reduce the PCOS complications. Medicines such as metformin, clomiphene, and the oral contraceptive pill can also balance the hormonal level. The imbalance in regulation of autophagy genes has been discussed with correlation to PCOS. The different management strategies for PCOS have also been summarized.

多囊卵巢综合征(PCOS)是育龄妇女的一种内分泌疾病。多囊卵巢综合征是一种多样化的多因素疾病,由于其症状相互重叠,诊断起来非常复杂,其中一些症状包括月经周期不规律、面部痤疮、雄激素(AE)水平过高、胰岛素抵抗、肥胖、心血管疾病、情绪障碍和 2 型糖尿病(T2DM)。多囊卵巢综合症可能是由内分泌失调、遗传和表观遗传脆弱性、下丘脑和卵巢问题引起的。多囊卵巢综合征本质上是高雄激素血症,伴有少排卵。这篇综述解释了自噬相关基因和蛋白质在不同细胞中不同阶段的异常调控,从而导致多囊卵巢综合症的发生。细胞在缺乏营养时会面临压力,并试图通过激活大自噬机制和降解细胞质来克服这种压力。这为细胞提供了能量,使其得以存活。在多囊卵巢综合症妇女的子宫内膜中观察到自噬相关基因的下调。多囊卵巢综合症可以通过保持正确的生活方式和药物治疗来控制。健康饮食和定期锻炼可以防止体重过重,还能减少多囊卵巢综合症的并发症。二甲双胍、克罗米芬和口服避孕药等药物也可以平衡荷尔蒙水平。自噬基因的调节失衡与多囊卵巢综合症的相关性也得到了讨论。此外,还总结了治疗多囊卵巢综合症的不同策略。
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引用次数: 0
Tobacco aquaporin NtAQP1 and human aquaporin hAQP1 contribute to single cell photosynthesis in Synechococcus 烟草水蒸气素 NtAQP1 和人类水蒸气素 hAQP1 对 Synechococcus 的单细胞光合作用做出了贡献。
IF 2.7 4区 生物学 Q2 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-04-23 DOI: 10.1111/boc.202470003
Franziska M. Joseph, Ralf Kaldenhoff

Background Information

Aquaporins are H2O-permeable membrane protein pores. However, some aquaporins are also permeable to other substances such as CO2. In higher plants, overexpression of such aquaporins has already led to an enhanced photosynthetic performance due to improved CO2 mesophyll conductance. In this work, we investigated the effects of such aquaporins on unicellular photosynthetically active organisms, specifically cyanobacteria.

Results

Overexpression of aquaporins NtAQP1 or hAQP1 that might have a function to improve CO2 membrane permeability lead to increased photosynthesis rates in the cyanobacterium Synechococcus sp. PCC7002 as concluded by the rate of evolved O2. A shift in the Plastoquinone pool state of the cells supports our findings. Water permeable aquaporins without CO2 permeability, such as NtPIP2;1, do not have this effect.

Conclusions and Significance

We conclude that also in single cell organisms like cyanobacteria, membrane CO2 conductivity could be rate limiting and CO2-porins reduce the respective membrane resistance. We could show that besides the tobacco aquaporin NtAQP1 also the human hAQP1 most likely functions as CO2 diffusion facilitator in the photosynthesis assay.

背景资料水汽素是一种透水蒸气的膜蛋白孔。然而,有些水汽素也能渗透其他物质,如二氧化碳。在高等植物中,过量表达这类水汽素已能改善叶绿体对 CO2 的传导,从而提高光合作用的性能。结果在蓝藻 Synechococcus sp. PCC7002 中,过量表达可能具有改善 CO2 膜通透性功能的水汽素 NtAQP1 或 hAQP1 可提高光合作用速率,这一点可通过 O2 的进化速率得出结论。细胞中塑醌池状态的变化支持了我们的发现。我们的结论是,在蓝藻等单细胞生物中,膜的 CO2 传导性也可能限制速率,而 CO2-孔蛋白可降低相应的膜电阻。我们可以证明,除了烟草水孔蛋白 NtAQP1 外,人类 hAQP1 也很有可能在光合作用试验中起到二氧化碳扩散促进剂的作用。
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引用次数: 0
Therapeutic potential of exosomes in spermatogenesis regulation and male infertility 外泌体在精子发生调节和男性不育症中的治疗潜力
IF 2.7 4区 生物学 Q2 Biochemistry, Genetics and Molecular Biology Pub Date : 2024-04-09 DOI: 10.1111/boc.202300127
Amirhossein Mohammadi, Ronak Shabani, Zahra Bashiri, Sara Rafiei, Hamidreza Asgari, Morteza Koruji

Background

Spermatogenesis is a fundamental process crucial for male reproductive health and fertility. Exosomes, small membranous vesicles released by various cell types, have recently garnered attention for their role in intercellular communication.

Objective

This review aims to comprehensively explore the role of exosomes in regulating spermatogenesis, focusing on their involvement in testicular development and cell-to-cell communication.

Methods

A systematic examination of literature was conducted to gather relevant studies elucidating the biogenesis, composition, and functions of exosomes in the context of spermatogenesis.

Results

Exosomes play a pivotal role in orchestrating the complex signaling networks required for proper spermatogenesis. They facilitate the transfer of key regulatory molecules between different cell populations within the testes, including Sertoli cells, Leydig cells, and germ cells.

Conclusion

The emerging understanding of exosome-mediated communication sheds light on novel mechanisms underlying spermatogenesis regulation. Further research in this area holds promise for insights into male reproductive health and potential therapeutic interventions.

背景精子发生是对男性生殖健康和生育能力至关重要的基本过程。本综述旨在全面探讨外泌体在调节精子发生过程中的作用,重点关注外泌体参与睾丸发育和细胞间通讯的情况。结果 外泌体在协调正常精子发生所需的复杂信号网络中发挥着关键作用。结果外泌体在协调正常精子发生所需的复杂信号网络中发挥着关键作用。它们促进了睾丸内不同细胞群(包括Sertoli细胞、Leydig细胞和生殖细胞)之间关键调控分子的传递。该领域的进一步研究有望深入了解男性生殖健康和潜在的治疗干预措施。
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Biology of the Cell
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