Acta histochemica最新文献_第8页

Histological changes in skeletal muscle induced by heart failure in human patients and animal models: A scoping review 人类患者和动物模型心力衰竭引起的骨骼肌组织学变化：范围综述。

IF 2.3 4区生物学 Q4 CELL BIOLOGY

Acta histochemica

Pub Date : 2024-10-23 DOI: 10.1016/j.acthis.2024.152210

Akinori Kaneguchi , Naoyoshi Sakitani , Takuya Umehara

Objective

This scoping review aimed to characterize the histological changes in skeletal muscle after heart failure (HF) and to identify gaps in knowledge.

Methods

On April 03, 2024, systematic searches were performed for papers in which histological analyses were conducted on skeletal muscle sampled from patients with HF or animal models of HF. Screening and data extraction were conducted by two independent authors.

Results and conclusion

A total of 118 papers were selected, including 33 human and 85 animal studies. Despite some disagreements among studies, some trends were observed. These trends included a slow-to-fast transition, a decrease in muscle fiber size, capillary to muscle fiber ratio, and mitochondrial activity and content, and an increase in apoptosis. These changes may contribute to the fatigability and decrease in muscle strength observed after HF. Although there were some disagreements between the results of human and animal studies, the results were generally similar. Animal models of HF will therefore be useful in elucidating the histological changes in skeletal muscle that occur in human patients with HF. Because the muscles subjected to histological analysis were mostly thigh muscles in humans and mostly lower leg muscles in animals, it remains uncertain whether changes similar to those seen in lower limb (hindlimb) muscles after HF also occur in upper limb (forelimb) muscles. The results of this review will consolidate the current knowledge on HF-induced histological changes in skeletal muscle and consequently aid in the rehabilitation of patients with HF and future studies.

目的本综述旨在描述心力衰竭（HF）后骨骼肌组织学变化的特征，并找出知识空白：2024年4月3日，系统检索了对心力衰竭患者或心力衰竭动物模型骨骼肌进行组织学分析的论文。筛选和数据提取由两位独立作者完成：共筛选出 118 篇论文，包括 33 项人体研究和 85 项动物研究。尽管各研究之间存在一些分歧，但还是观察到了一些趋势。这些趋势包括从慢到快的转变，肌肉纤维尺寸、毛细血管与肌肉纤维比率、线粒体活性和含量的减少，以及细胞凋亡的增加。这些变化可能是导致高频后易疲劳和肌力下降的原因。尽管人类和动物研究结果之间存在一些分歧，但总体上结果相似。因此，心房颤动动物模型将有助于阐明人类心房颤动患者骨骼肌组织学上的变化。由于接受组织学分析的肌肉在人类中大多是大腿肌肉，而在动物中大多是小腿肌肉，因此目前仍不确定高血脂后下肢（后肢）肌肉是否也会发生类似于上肢（前肢）肌肉的变化。本综述的结果将巩固目前关于高频诱导的骨骼肌组织学变化的知识，从而有助于高频患者的康复和未来的研究。

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引用次数: 0

The elastic system: A review of elastin-related techniques and hematoxylin-eosin/phloxine applicability for normal and pathological tissue description 弹性系统：弹性蛋白相关技术及苏木精-伊红/荧光素在正常和病理组织描述中的适用性综述。

IF 2.3 4区生物学 Q4 CELL BIOLOGY

Acta histochemica

Pub Date : 2024-10-22 DOI: 10.1016/j.acthis.2024.152209

Thalles Fernando Rocha Ruiz , Luara Jesus Ferrato , Lorena Gabriela de Souza , Gervásio Evangelista Brito-Filho , Ellen Cristina Rivas Leonel , Sebastião Roberto Taboga

The elastic system is one of the most developed interstitial elements in connective tissue. With diverse functions, pre-elastic and elastic fibers contribute to the distensibility and malleability of several organs. Also, microanalyses of the elastic system were obtained by different histological techniques that were employed over years to describe normal and pathological conditions. Compared to conventional stains, hematoxylin-eosin/phloxine (HE/P) under fluorescence and confocal microscopy presented a highly detailed observation of the elastic system in different organs and scenarios. This technique provides a better demarcation of the elastic fibers, favoring their description in relation to their deposition and aggregation in different organs. Also, fibrils with low aggregation or loss of this characteristic are observed in an optimal view in the skin, heart valves, and large-caliber blood vessels. Degradation, fragmentation, and rupture were also well described by the HE/P technique. Several organs, such as the mammary gland, prostate, skin, aorta, and lung, could be described with precision under this technique. In association with non-linear microscopy, the results of the research presented in this paper improved and detailed characteristics of precise pathogenesis. Thus, the HE/P technique presented an interesting efficiency to demonstrate alterations and structures in which the elastic system showed a relevant role, and when compared to other techniques it demonstrated a similar or better result. In addition, it is expected that future studies can reveal more information about the elastin and interactions with specific dyes, thus allowing a greater understanding of the great efficiency of this technique.

弹性系统是结缔组织中最发达的间隙元素之一。前弹力纤维和弹力纤维具有多种功能，对多个器官的伸缩性和延展性做出了贡献。多年来，人们采用不同的组织学技术对弹性系统进行微观分析，以描述正常和病理状态。与传统染色法相比，荧光显微镜和共聚焦显微镜下的苏木精-伊红/荧光素（HE/P）可对不同器官和情况下的弹性系统进行非常详细的观察。这种技术能更好地划分弹性纤维，有利于描述它们在不同器官中的沉积和聚集情况。此外，在皮肤、心脏瓣膜和大口径血管中，还能以最佳视角观察到低聚集或失去这种特性的纤维。HE/P 技术对降解、碎裂和断裂也有很好的描述。乳腺、前列腺、皮肤、主动脉和肺等多个器官都能通过该技术精确描述。结合非线性显微镜，本文介绍的研究结果改进了精确发病机制的详细特征。因此，HE/P 技术在展示弹性系统在其中发挥相关作用的改变和结构方面具有令人感兴趣的效率，与其他技术相比，它显示出类似或更好的结果。此外，未来的研究有望揭示更多有关弹性蛋白以及与特定染料相互作用的信息，从而让人们更深入地了解这种技术的巨大功效。

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引用次数: 0

Neuronal splicing regulator RBFOX3 (NeuN) distribution and organization are modified in response to monosodium glutamate in rat brain at postnatal day 14 出生后第14天大鼠脑内神经元剪接调节因子RBFOX3（NeuN）的分布和组织在谷氨酸钠的作用下发生改变。

IF 2.3 4区生物学 Q4 CELL BIOLOGY

Acta histochemica

Pub Date : 2024-10-19 DOI: 10.1016/j.acthis.2024.152207

Anaís Monzerrat García Juárez, Nidia Jannette Carrillo González, Tania Campos-Ordoñez, Yadira Gasca Martínez, Graciela Gudiño-Cabrera

Neuronal splicing regulator RNA binding protein, fox-1 homolog 3 (NeuN/RbFox3), is expressed in postmitotic neurons and distributed heterogeneously in the cell. During excitotoxicity events caused by the excess glutamate, several alterations that culminate in neuronal death have been described. However, NeuN/RbFox3 organization and distribution are still unknown. Therefore, our objective was to analyze the nucleocytoplasmic distribution and organization of NeuN/RbFox3 in hippocampal and cortical neurons using an excitotoxicity model with monosodium glutamate salt (MSG). We used neonatal Wistar rats administered subcutaneously with 4 MSG mg/kg during the postnatal day (PND) 1, 3, 5, and 7. The control group was rats without MSG administration. On 14 PND, the brain was removed, and coronal sections were used for immunodetection with the antibody NeuN, DAPI, and the propidium iodide staining for histological evaluation. The results indicate that in the control group, NeuN/RbFox3 was organized into macromolecular condensates inside and outside the nucleus, forming defined nuclear compartments. Additionally, NeuN/RbFox3 was distributed proximal to the nucleus in the cytoplasm. In contrast, in the group treated with MSG, the distribution was diffuse and dispersed in the nucleus and cytoplasm without the formation of compartments in the nucleus. Our findings, which highlight the significant impact of MSG administration in the neonatal period on the distribution and organization of NeuN/RbFox3 of neurons in the hippocampus and cerebral cortex, offer a new perspective to investigate MSG alterations in the developmental brain.

神经元剪接调节器 RNA 结合蛋白 fox-1 同源物 3（NeuN/RbFox3）在有丝分裂后的神经元中表达，并在细胞中异质性分布。在由过量谷氨酸引起的兴奋性中毒事件中，已描述了几种最终导致神经元死亡的改变。然而，NeuN/RbFox3 的组织和分布仍不为人知。因此，我们的目的是利用谷氨酸一钠（MSG）兴奋毒性模型，分析 NeuN/RbFox3 在海马和皮层神经元中的核细胞质分布和组织。我们使用新生 Wistar 大鼠，在出生后第 1、3、5 和 7 天皮下注射 4 毫克/千克 MSG。对照组为未注射味精的大鼠。出生后第 14 天，取出大鼠大脑，用 NeuN 抗体、DAPI 和碘化丙啶染色对冠状切片进行免疫检测，并进行组织学评估。结果表明，在对照组中，NeuN/RbFox3在细胞核内外组织成大分子凝聚体，形成明确的核区。此外，NeuN/RbFox3 还分布在细胞质中核的近端。相比之下，在用味精处理的组中，NeuN/RbFox3呈弥漫性分布，分散在细胞核和细胞质中，没有在细胞核中形成小室。我们的研究结果突显了新生儿期服用味精对海马和大脑皮层神经元NeuN/RbFox3的分布和组织的重要影响，为研究味精在大脑发育过程中的改变提供了一个新的视角。

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引用次数: 0

Metabolic shift as a compensatory response to impaired hippocampal neurogenesis after developmental exposure to sodium fluoride in rats 大鼠发育过程中接触氟化钠后，代谢转变是海马神经发生受损的一种补偿反应

IF 2.3 4区生物学 Q4 CELL BIOLOGY

Acta histochemica

Pub Date : 2024-10-16 DOI: 10.1016/j.acthis.2024.152204

Momoka Shobudani , Yuri Sakamaki , Ayumi Karasawa , Ryota Ojiro , Xinyu Zou , Qian Tang , Shunsuke Ozawa , Meilan Jin , Toshinori Yoshida , Makoto Shibutani

Fluoride affects neurodevelopment in children. In this study, we examined the effects of developmental exposure to sodium fluoride (NaF) on hippocampal neurogenesis in rats. Dams were given drinking water containing NaF at 0 (untreated controls), 30 or 100 ppm from gestational day 6 to day 21 post-delivery upon weaning, and offspring were reared until postnatal day (PND) 77. On PND 21, NaF at 100 ppm altered the numbers in subpopulations of granule cell lineages, including a decrease in type-3 neural progenitor cells (NPCs), as well as a compensatory increase in type-1 neural stem cells (NSCs) and type-2a NPCs. NaF exposure tended to increase GluR2⁺ mossy cells in the hilus of the dentate gyrus (DG) in a dose-dependent manner, suggesting that NaF exposure induces a compensatory neurogenic response. NaF also caused a dose-dependent increase in ARC⁺ granule cells, and it upregulated Ptgs2 in the DG at 100 ppm, suggesting that NaF exposure increases synaptic plasticity in granule cells. NaF at 100 ppm upregulated granule cell lineage marker genes (Nes, Eomes and Rbfox3) and an anti-apoptotic gene (Bcl2), suggesting ameliorating responses against the impaired neurogenesis during NaF exposure. Moreover, NaF at 100 ppm downregulated oxidative phosphorylation-related genes (Atp5f1b and Sdhd) and upregulated a glycolysis-related gene (Hk3), suggesting a metabolic shift in cells undergoing neurogenesis. By PND 77, the changes in granule cell lineages were no longer detected, and GABAergic interneuron marker genes (Calb2 and Reln) were upregulated, suggesting a persistent protective response in granule cell lineages. Together, these findings suggest that developmental NaF exposure causes transient disruption of hippocampal neurogenesis, which in turn induces a metabolic shift as a compensatory response.

氟会影响儿童的神经发育。在这项研究中，我们研究了大鼠在发育过程中接触氟化钠（NaF）对海马神经发生的影响。从妊娠第 6 天到分娩后断奶的第 21 天，给母鼠饮用含 0（未处理对照组）、30 或 100 ppm NaF 的饮用水，并将后代饲养到产后第 77 天。在出生后第21天，百万分之100的NaF改变了颗粒细胞系亚群的数量，包括3型神经祖细胞（NPC）的减少，以及1型神经干细胞（NSC）和2a型NPC的补偿性增加。暴露于 NaF 会以剂量依赖的方式增加齿状回（DG）脊髓的 GluR2+ 苔藓细胞，这表明暴露于 NaF 会诱导代偿性神经源反应。NaF 还会导致 ARC+ 粒细胞的剂量依赖性增加，并且在 100 ppm 浓度下会上调 DG 中的 Ptgs2，这表明 NaF 暴露会增加粒细胞的突触可塑性。ppm浓度为100的NaF能上调颗粒细胞系标记基因（Nes、Eomes和Rbfox3）和抗凋亡基因（Bcl2），这表明NaF暴露可改善神经发生受损的反应。此外，百万分之 100 的 NaF 会下调氧化磷酸化相关基因（Atp5f1b 和 Sdhd），上调糖酵解相关基因（Hk3），这表明神经发生过程中细胞的代谢发生了变化。到 PND 77 时，不再检测到颗粒细胞系的变化，GABA 能中间神经元标记基因（Calb2 和 Reln）上调，表明颗粒细胞系存在持续的保护性反应。这些发现共同表明，发育过程中暴露于 NaF 会导致海马神经发生的短暂中断，进而诱发代谢转变作为补偿反应。

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引用次数: 0

Renal expression of autophagy markers in diabetic kidney of PUFA-supplemented rats 补充 PUFA 的糖尿病大鼠肾脏中自噬标记物的表达

IF 2.3 4区生物学 Q4 CELL BIOLOGY

Acta histochemica

Pub Date : 2024-10-15 DOI: 10.1016/j.acthis.2024.152206

Ivan Brdar , Tomislav Mašek , Anita Racetin , Marija Jurić , Katarina Vukojević , Ivana Bočina , Natalija Filipović

Diabetic nephropathy is the leading cause of end-stage kidney disease, and the association between impaired autophagy and kidney structure damage in diabetes is well known. Diets enriched with polyunsaturated fatty acids (PUFAs) have been the subject of numerous studies on preventing and treating various metabolic disorders. The results of these studies suggest that n-3 PUFA may have a renoprotective effect, reducing the structural damage to the kidneys associated with DM. We hypothesized that the activation of autophagy partly mediates the potential protective effect of n-3 PUFA on diabetic kidneys. Wistar rats were randomly divided into four groups according to the type of diet: control (C) and diabetic (STZ) groups received food including 0.5 % linseed oil and 2 % sunflower oil with an n-6/n-3 ratio of 7; the STZ+N6 group received a diet with 2.5 % sunflower oil with an n-6/n-3 ratio of 60; and the STZ+N3 group received a diet containing 2.5 % fish oil with an n-6/n-3 ratio of 1, with the addition of eicosapentaenoic acid (EPA) and 19 % docosahexaenoic acid (DHA). All rats, except for those in the C group, had diabetes induced by an intraperitoneal injection of streptozotocin. We conducted histological and immunohistochemical assessments to determine the effects of different n-6/n-3 PUFA dietary ratios on the expression levels of different autophagy markers in the kidney of the rats. The results indicate significant effects of n-3 and n-6 PUFA supplementation on the expression of different autophagy markers in the renal cortex of the diabetic rats. In particular, n-6 PUFA supplementation increased LC3B expression while simultaneously decreasing Rab7 expression; meanwhile, n-3 PUFA supplementation resulted in a decreased expression of LAMP2A and Rab7. Moreover, n-3 PUFA supplementation prevented an increase in BECL1 and p62, that was observed in kidneys from diabetic and diabetic n-3 supplemented animals. These results point to the complex interactions of fatty acids and autophagy during the development of diabetic kidney disease, which should be taken into account in future therapeutic approaches.

糖尿病肾病是终末期肾病的主要病因，众所周知，糖尿病患者自噬功能受损与肾脏结构损伤之间存在关联。富含多不饱和脂肪酸（PUFA）的饮食已成为预防和治疗各种代谢紊乱的众多研究的主题。这些研究结果表明，n-3 多不饱和脂肪酸可能具有肾脏保护作用，可减少与糖尿病相关的肾脏结构损伤。我们假设自噬的激活在一定程度上介导了 n-3 PUFA 对糖尿病肾脏的潜在保护作用。根据饮食类型将 Wistar 大鼠随机分为四组：对照组（C）和糖尿病组（STZ）接受的食物包括 0.5 % 亚麻籽油和 2 % 葵花籽油，n-6/n-3 比率为 7；STZ+N6 组接受的食物包括 2.5%的葵花籽油，n-6/n-3比例为60；STZ+N3组的食物中含有2.5%的鱼油，n-6/n-3比例为1，并添加了二十碳五烯酸（EPA）和19%的二十二碳六烯酸（DHA）。除 C 组大鼠外，所有大鼠均腹腔注射链脲佐菌素诱发糖尿病。我们进行了组织学和免疫组织化学评估，以确定不同 n-6/n-3 PUFA 膳食比例对大鼠肾脏中不同自噬标记物表达水平的影响。结果表明，补充 n-3 和 n-6 PUFA 对糖尿病大鼠肾皮质中不同自噬标记物的表达有明显影响。其中，补充 n-6 PUFA 会增加 LC3B 的表达，同时降低 Rab7 的表达；而补充 n-3 PUFA 则会降低 LAMP2A 和 Rab7 的表达。此外，补充 n-3 PUFA 还能防止糖尿病动物和补充 n-3 PUFA 的糖尿病动物肾脏中观察到的 BECL1 和 p62 的增加。这些结果表明，在糖尿病肾病的发展过程中，脂肪酸和自噬之间存在复杂的相互作用，未来的治疗方法应考虑到这一点。

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引用次数: 0

Immunohistochemical distribution of cannabinoid receptor type 1 (CB1) and type 2 (CB2) in the rat carotid body 大鼠颈动脉体中大麻素受体 1 型（CB1）和 2 型（CB2）的免疫组化分布

IF 2.3 4区生物学 Q4 CELL BIOLOGY

Acta histochemica

Pub Date : 2024-10-13 DOI: 10.1016/j.acthis.2024.152205

Hiroki Saito, Takuya Yokoyama , Nobuaki Nakamuta, Yoshio Yamamoto

The carotid body is a hypoxia-sensitive chemoreceptor that induces sensory long-term facilitation after exposure to chronic intermittent hypoxia. However, the mechanisms underlying synaptic plasticity in the carotid body remain unknown. In the present study, we examined the immunohistochemical distribution of cannabinoid receptor type 1 (CB1) and type 2 (CB2), which are candidate molecules involved in the modulation of synaptic transmission. Dot-like CB1 immunoreactivity was distributed in the perinuclear cytoplasm of chemoreceptor cells immunoreactive for the catecholamine-synthesizing enzymes, tyrosine hydroxylase and dopamine beta-hydroxylase. Furthermore, CB1 immunoreactivity was observed in sensory nerve endings immunoreactive for P2X₃ purinoceptors that colocalized with vesicular glutamate transporter 2. On the other hand, immunoreactivity for CB2 was mainly distributed in chemoreceptor cells, and was weakly observed in sensory nerve endings immunoreactive for P2X₂ purinoceptors. The present results suggest that CB1 and CB2 regulate the release of catecholamines and glutamate from chemoreceptor cells and sensory nerve endings, respectively. Therefore, CB1 and CB2 may be involved in synaptic plasticity in the carotid body.

颈动脉体是一种对缺氧敏感的化学感受器，在暴露于慢性间歇性缺氧后会诱发感觉的长期促进。然而，颈动脉体突触可塑性的机制仍然未知。在本研究中，我们检测了大麻素受体 1 型（CB1）和 2 型（CB2）的免疫组化分布，它们是参与调节突触传递的候选分子。点状 CB1 免疫活性分布在对儿茶酚胺合成酶、酪氨酸羟化酶和多巴胺 beta-羟化酶有免疫活性的化学感受器细胞的核周细胞质中。此外，在对 P2X3 嘌呤受体有免疫反应的感觉神经末梢也观察到了 CB1 免疫反应，这些受体与囊泡谷氨酸转运体 2 共同定位。另一方面，CB2 的免疫反应主要分布在化学感受器细胞中，在对 P2X2 嘌呤受体免疫反应的感觉神经末梢中观察到微弱的 CB2 免疫反应。本研究结果表明，CB1 和 CB2 分别调节化学感受器细胞和感觉神经末梢儿茶酚胺和谷氨酸的释放。因此，CB1 和 CB2 可能参与了颈动脉体的突触可塑性。

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引用次数: 0

Corrigendum to “Protective effect of FXN overexpression on ferroptosis in L-Glu-induced SH-SY5Y cells” [Acta Histochem. 126 (2024) 152135] 更正："FXN 过表达对 L-Glu 诱导的 SH-SY5Y 细胞铁突变的保护作用" [Acta Histochem.

IF 2.3 4区生物学 Q4 CELL BIOLOGY

Acta histochemica

Pub Date : 2024-09-28 DOI: 10.1016/j.acthis.2024.152192

Mengran Wang , Tingting Xuan , Haining Li , Jing An , Tianhui He , Jiang Cheng

引用次数: 0

Nrf2: A critical participant in regulation of apoptosis, ferroptosis, and autophagy in gastric cancer Nrf2：调控胃癌细胞凋亡、铁变态反应和自噬的关键参与者

IF 2.3 4区生物学 Q4 CELL BIOLOGY

Acta histochemica

Pub Date : 2024-09-28 DOI: 10.1016/j.acthis.2024.152203

LiJie Tang, DongXiu He, Bo Su

Nuclear factor erythroid 2-related factor-2 (Nrf2) is a specific transcription factor that maintains redox homeostasis by regulating the expression of anti-oxidative stress-related genes. Hyperactivation of Nrf2 is involved in tumor progression and is associated with chemoresistance in a large number of solid tumors. Programmatic cell death (PCD), such as apoptosis, ferroptosis, and autophagy, plays a crucial role in tumor development and chemotherapy sensitivity. Accumulating evidence suggests that some anti-tumor compounds and genes can induce massive production of reactive oxygen species (ROS) via inhibiting Nrf2 expression, which exacerbates oxidative stress and promotes Gastric cancer (GC) cell death, thereby enhancing the sensitivity of GC cells to chemotherapy-induced PCD. In this review, we summarize the role of antitumor drugs in interfering in three different types of PCD (apoptosis, ferroptosis, and autophagy) in GC cells by modulating Nrf2 expression, as well as the molecular mechanisms through which targeting Nrf2 brings about PCD and chemosensitivity. It is reasonable to believe that Nrf2 serves as a potential therapeutic target, and targeting Nrf2 by drug or gene regulation could provide a new strategy for the treatment of GC.

核因子红细胞 2 相关因子-2（Nrf2）是一种特异性转录因子，它通过调节抗氧化应激相关基因的表达来维持氧化还原平衡。Nrf2 的过度激活参与了肿瘤的进展，并与大量实体瘤的化疗耐药性有关。程序性细胞死亡（PCD），如细胞凋亡、铁凋亡和自噬，在肿瘤发生和化疗敏感性中起着至关重要的作用。越来越多的证据表明，一些抗肿瘤化合物和基因可通过抑制Nrf2的表达诱导活性氧（ROS）的大量产生，从而加剧氧化应激并促进胃癌（GC）细胞的死亡，从而提高胃癌细胞对化疗诱导的PCD的敏感性。在这篇综述中，我们总结了抗肿瘤药物通过调节 Nrf2 的表达干扰 GC 细胞三种不同类型的 PCD（凋亡、铁突变和自噬）的作用，以及靶向 Nrf2 带来 PCD 和化疗敏感性的分子机制。我们有理由相信，Nrf2 是一个潜在的治疗靶点，通过药物或基因调控靶向 Nrf2 可为治疗 GC 提供一种新策略。

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引用次数: 0

Early PSA-NCAM reduction in the dentate gyrus and impaired plasticity in the Alzheimer´s disease 3xTg-mice model 阿尔茨海默病 3xTg 小鼠模型中齿状回早期 PSA-NCAM 减少和可塑性受损

IF 2.3 4区生物学 Q4 CELL BIOLOGY

Acta histochemica

Pub Date : 2024-09-16 DOI: 10.1016/j.acthis.2024.152194

J.J. Rodríguez , E. Gardenal , F. Zallo , J. Cabot , X. Busquets

Neurodegenerative diseases such as Alzheimer´s (AD) and physiological ageing are characterized by a decline in neurogenesis and in the polysialylated isoforms of neural cell adhesion molecule (PSA-NCAM) expression within the hippocampus and specifically in the dentate gyrus (DG). In the 3xTG-AD mouse model, which mimics the human disease in both pathological and behavioral features, this decline in PSA-NCAM is associated with the presence of Aβ plaques at 9 months and Tau tangles at 12–15 months. In this work we studied the presence of PSA-NCAM at early ages (1–6 months) in the same model. Our results demonstrated that even as early as the first month of age there is a strong decrease in PSA-NCAM dendritic tree mainly altering the molecular layer (MolL) coverage affecting the synaptic plasticity and furthermore confirmed by the reduction of PSA-NCAM area density (Sv) in the 3xTG-AD. Similar and more marked early changes were seen during aging in both NTG and 3xTg-AD animals. Our results demonstrate for the first time a precipitate decrease of PSA-NCAM cells at such very early phases of the disease. This result suggests an early effect of the disease in the progression of immature and pluripotent cells resulting in an ulterior and early diminution of neurogenesis and therefore an impaired hippocampal cellular and synaptic plasticity.

阿尔茨海默病（AD）等神经退行性疾病和生理性衰老的特征是神经发生和神经细胞粘附分子多聚糖化异构体（PSA-NCAM）在海马，特别是在齿状回（DG）中的表达下降。3xTG-AD小鼠模型在病理和行为特征上都模拟了人类疾病，PSA-NCAM的下降与9个月时出现的Aβ斑块和12-15个月时出现的Tau缠结有关。在这项工作中，我们研究了同一模型中早期（1-6 个月）PSA-NCAM 的存在情况。我们的研究结果表明，即使是在第一个月大时，PSA-NCAM树突树就会出现强烈的减少，主要是分子层（MolL）覆盖的改变影响了突触的可塑性，3xTG-AD中PSA-NCAM面积密度（Sv）的减少也进一步证实了这一点。NTG和3xTg-AD动物在衰老过程中也出现了类似且更明显的早期变化。我们的研究结果首次证明，在疾病的早期阶段，PSA-NCAM 细胞会出现骤减。这一结果表明，疾病早期会影响未成熟和多能细胞的发育，导致神经发生的早期衰减，从而损害海马细胞和突触的可塑性。

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引用次数: 0

Maternal hyperglycemia affects cell proliferation signalling and stromal organization in the prostate of neonatal and juvenile rat offspring 母体高血糖会影响新生大鼠和幼鼠后代前列腺的细胞增殖信号和基质组织

IF 2.3 4区生物学 Q4 CELL BIOLOGY

Acta histochemica

Pub Date : 2024-09-07 DOI: 10.1016/j.acthis.2024.152193

Luiz Felipe Fernandes Peixoto , Laura Eduarda Dinato Sudário , Marina das Graças Carneiro e Silva , Fernanda Naves Araújo do Prado Mascarenhas , Elusca Helena Muniz , Renata Graciele Zanon , Daniele Lisboa Ribeiro

Gestational diabetes mellitus is a common medical complication during pregnancy. It creates a hyperglycemic environment and impacts offspring development, increasing the risk of long-term complications, including obesity, impaired glucose metabolism and cardiovascular disease. The impact of gestational diabetes on the prostates of adult offspring has already been described; however, it is not known whether these effects are due only to the maternal condition or whether the offspring develop them throughout life. This investigation evaluated the prostates of neonatal and juvenile offspring of hyperglycemic rats due to diabetes. Diabetes was induced with streptozotocin (50 mg/kg, ip) in pregnant Wistar rats and the prostates of 7- or 30-day-old pups from healthy (PC7, PC30) or diabetic (PD7, PD30) mothers were evaluated. We found reduced body weight in pups of PD7 and PD30 and prostate weight in PD30. Prostate branching was not affected, but a reduction in apoptotic levels was associated with impaired acinar bud canalization in neonates. Additionally, PD7 presented reduced ERK1/2 phosphorylation, cell proliferation and collagen, but fibroblasts were increased. In PD30, there was a reduction in the area of the secretory epithelium and stroma, but the luminal area was increased. Moreover, fibroblasts, smooth muscle cells, collagen and metalloproteinase 2 were decreased in these juvenile pups. These data indicate that maternal hyperglycemia inactivates an important cell proliferation signaling pathway in the prostate in the first postnatal days (which is restored in the juvenile period), but it was not sufficient to avoid epithelial and stromal atrophy. This effect on postnatal gland development may impact the reproductive capacity of the prostate in adult life.

妊娠糖尿病是孕期常见的并发症。妊娠糖尿病会造成高血糖环境，影响后代的发育，增加长期并发症的风险，包括肥胖、糖代谢受损和心血管疾病。妊娠糖尿病对成年后代前列腺的影响已有描述，但这些影响是否仅由母体状况引起，还是后代终生都会受到影响，目前尚不清楚。这项研究评估了因糖尿病而患高血糖的大鼠的新生儿和幼年后代的前列腺。用链脲佐菌素（50 毫克/千克，ip）诱导妊娠 Wistar 大鼠患糖尿病，并对健康（PC7、PC30）或糖尿病（PD7、PD30）母鼠的 7 天或 30 天大幼鼠的前列腺进行评估。我们发现，PD7 和 PD30 的幼鼠体重减轻，PD30 的幼鼠前列腺重量减轻。前列腺分支未受影响，但凋亡水平的降低与新生儿尖状体芽管化受损有关。此外，PD7 的 ERK1/2 磷酸化、细胞增殖和胶原减少，但成纤维细胞增加。在 PD30 中，分泌上皮和基质面积减少，但管腔面积增加。此外，这些幼崽的成纤维细胞、平滑肌细胞、胶原蛋白和金属蛋白酶 2 都有所减少。这些数据表明，母体高血糖在出生后最初几天会使前列腺中一个重要的细胞增殖信号通路失活（在幼年期会恢复），但这不足以避免上皮和基质萎缩。这种对出生后腺体发育的影响可能会影响前列腺在成年后的生殖能力。

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