Cell and Tissue Biology最新文献

英文中文

α-Actinin-4-Dependent Regulation of DNA Break Repair Is Not Dependent on NF-kB Activity α-Actinin-4对DNA断裂修复的调控不依赖于NF-kB的活性

Q4 Biochemistry, Genetics and Molecular Biology

Cell and Tissue Biology

Pub Date : 2024-06-03 DOI: 10.1134/s1990519x24700251

D. V. Krieger, G. V. Vasilyeva, E. V. Lomert, D. G. Tentler

Abstract

α-Actinin-4 is an actin-binding protein involved in a wide range of cellular processes. Along with actin and other proteins of the actin cytoskeleton, α-actinin-4 is found not only in the cytoplasm, but also in the nucleus of various types of cells. As a nuclear protein, it takes part in regulating the activity of some transcription factors. In particular, it can regulate the activity of the NF-kB factor, which largely determines the resistance of cancer cells to apoptosis and anticancer therapy. Our previous studies revealed that α-actinin-4 can influence the resistance of cancer cells to topoisomerase II inhibitors and determine the efficiency of DNA double-strand break repair by regulating the assembly of HRR and NHEJ protein complexes. In this work, we tried to answer the question of how α-actinin-4 is involved in the regulation of the double-stranded DNA breaks repair under genotoxic stress. Our results indicate that the effect of α-actinin-4 on the repair process in H1299 non-small-cell lung-cancer cells does not depend on the activity of the transcription factor NF-kB. We found that, in the nucleus of H1299 cells, α-actinin-4 is localized not only in the nucleoplasm, but also shows close association with chromatin.

摘要 α-肌动蛋白-4是一种肌动蛋白结合蛋白，参与多种细胞过程。α-Actinin-4与肌动蛋白和其他肌动蛋白细胞骨架蛋白一起，不仅存在于细胞质中，还存在于各种细胞的细胞核中。作为一种核蛋白，它参与调节一些转录因子的活性。特别是，它可以调节 NF-kB 因子的活性，而 NF-kB 因子在很大程度上决定了癌细胞对凋亡和抗癌治疗的抵抗力。我们之前的研究发现，α-actinin-4 可以影响癌细胞对拓扑异构酶 II 抑制剂的耐受性，并通过调节 HRR 和 NHEJ 蛋白复合物的组装来决定 DNA 双链断裂修复的效率。在这项工作中，我们试图回答α-actinin-4如何参与调控基因毒性应激下的DNA双链断裂修复这一问题。我们的研究结果表明，α-actinin-4 对 H1299 非小细胞肺癌细胞修复过程的影响并不依赖于转录因子 NF-kB 的活性。我们发现，在 H1299 细胞的细胞核中，α-actinin-4 不仅定位于核质，而且还与染色质密切相关。

{"title":"α-Actinin-4-Dependent Regulation of DNA Break Repair Is Not Dependent on NF-kB Activity","authors":"D. V. Krieger, G. V. Vasilyeva, E. V. Lomert, D. G. Tentler","doi":"10.1134/s1990519x24700251","DOIUrl":"https://doi.org/10.1134/s1990519x24700251","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Abstract</h3><p>α-Actinin-4 is an actin-binding protein involved in a wide range of cellular processes. Along with actin and other proteins of the actin cytoskeleton, α-actinin-4 is found not only in the cytoplasm, but also in the nucleus of various types of cells. As a nuclear protein, it takes part in regulating the activity of some transcription factors. In particular, it can regulate the activity of the NF-kB factor, which largely determines the resistance of cancer cells to apoptosis and anticancer therapy. Our previous studies revealed that α-actinin-4 can influence the resistance of cancer cells to topoisomerase II inhibitors and determine the efficiency of DNA double-strand break repair by regulating the assembly of HRR and NHEJ protein complexes. In this work, we tried to answer the question of how α-actinin-4 is involved in the regulation of the double-stranded DNA breaks repair under genotoxic stress. Our results indicate that the effect of α-actinin-4 on the repair process in H1299 non-small-cell lung-cancer cells does not depend on the activity of the transcription factor NF-kB. We found that, in the nucleus of H1299 cells, α-actinin-4 is localized not only in the nucleoplasm, but also shows close association with chromatin.</p>","PeriodicalId":9705,"journal":{"name":"Cell and Tissue Biology","volume":"108 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141254532","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Mechanisms of Kidney Damage Development in Patients with New Coronavirus Infection: Literature Review 新型冠状病毒感染患者肾损伤的发生机制：文献综述

Q4 Biochemistry, Genetics and Molecular Biology

Cell and Tissue Biology

Pub Date : 2024-06-03 DOI: 10.1134/s1990519x24700196

E. V. Utkina, V. V. Novakovskaya, M. V. Egorova, N. V. Fomina, L. D. Chesnokova

Abstract

Every fourth person in the world currently has kidney problems to one or another degree. It is known that the novel coronavirus infection (COVID-19) is primarily a respiratory disease, but the kidney is a target organ. The coronavirus is tropic to kidney tissue due to the presence in the organ of RNA of angiotensin-converting enzyme type 2 and transmembrane serine protease 2, which is considered to be a target of this virus. The presence of renal failure in any stage is an independent unfavorable risk factor for contracting coronavirus and leads to a high frequency of hospitalization and mortality rate. Kidney failure is caused by various pathogenetic mechanisms: the direct cytopathic effect of the virus on their structures (podocytes, mesangial cells in the renal corpuscle, capillary endothelium in the glomerulus, epithelial cells in the proximal tubules), cytokine storm, damage to the renin–angiotensin–aldosterone system, and immunothrombosis. In many patients with confirmed coronavirus infection, from the first days of the disease, laboratory tests show significant changes in urine analysis (hematuria, proteinuria) and increased level of creatinine in the blood serum. The development of acute kidney injury is a main mortality risk factor. More research is needed into the exact effects of SARS-CoV-2 on the kidneys. Understanding the main pathogenetic pathways of their damage in COVID-19 is necessary to develop strategies and effective treatments.

摘要目前世界上每四个人中就有一个人或多或少存在肾脏问题。众所周知，新型冠状病毒感染（COVID-19）主要是一种呼吸道疾病，但肾脏也是一个靶器官。由于肾脏组织中存在血管紧张素转换酶 2 型和跨膜丝氨酸蛋白酶 2 的 RNA，冠状病毒对肾脏组织具有趋性，而肾脏组织被认为是该病毒的靶器官。任何阶段的肾功能衰竭都是感染冠状病毒的一个独立的不利风险因素，并导致高住院率和高死亡率。肾衰竭由多种致病机制引起：病毒对肾脏结构（荚膜细胞、肾小球系膜细胞、肾小球毛细血管内皮细胞、近端肾小管上皮细胞）的直接细胞病理效应、细胞因子风暴、肾素-血管紧张素-醛固酮系统损伤和免疫血栓形成。在许多确诊感染冠状病毒的患者中，从发病的最初几天起，实验室检查就会显示尿液分析的显著变化（血尿、蛋白尿）和血清中肌酐水平的升高。急性肾损伤是主要的死亡风险因素。需要对 SARS-CoV-2 对肾脏的确切影响进行更多的研究。有必要了解 COVID-19 对肾脏造成损害的主要致病途径，以便制定策略和有效的治疗方法。

{"title":"Mechanisms of Kidney Damage Development in Patients with New Coronavirus Infection: Literature Review","authors":"E. V. Utkina, V. V. Novakovskaya, M. V. Egorova, N. V. Fomina, L. D. Chesnokova","doi":"10.1134/s1990519x24700196","DOIUrl":"https://doi.org/10.1134/s1990519x24700196","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Abstract</h3><p>Every fourth person in the world currently has kidney problems to one or another degree. It is known that the novel coronavirus infection (COVID-19) is primarily a respiratory disease, but the kidney is a target organ. The coronavirus is tropic to kidney tissue due to the presence in the organ of RNA of angiotensin-converting enzyme type 2 and transmembrane serine protease 2, which is considered to be a target of this virus. The presence of renal failure in any stage is an independent unfavorable risk factor for contracting coronavirus and leads to a high frequency of hospitalization and mortality rate. Kidney failure is caused by various pathogenetic mechanisms: the direct cytopathic effect of the virus on their structures (podocytes, mesangial cells in the renal corpuscle, capillary endothelium in the glomerulus, epithelial cells in the proximal tubules), cytokine storm, damage to the renin–angiotensin–aldosterone system, and immunothrombosis. In many patients with confirmed coronavirus infection, from the first days of the disease, laboratory tests show significant changes in urine analysis (hematuria, proteinuria) and increased level of creatinine in the blood serum. The development of acute kidney injury is a main mortality risk factor. More research is needed into the exact effects of SARS-CoV-2 on the kidneys. Understanding the main pathogenetic pathways of their damage in COVID-19 is necessary to develop strategies and effective treatments.</p>","PeriodicalId":9705,"journal":{"name":"Cell and Tissue Biology","volume":"37 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141254539","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Inhibition of the Expression of NRF2 Transcription Factor Mediated by miR-155 Causes a Decrease in the Viability of Melanoma Cells Regardless of Redox Status miR-155 介导的 NRF2 转录因子的表达抑制会降低黑色素瘤细胞的活力，与氧化还原状态无关

Q4 Biochemistry, Genetics and Molecular Biology

Cell and Tissue Biology

Pub Date : 2024-06-03 DOI: 10.1134/s1990519x2470024x

V. A. Kutsenko, D. A. Dashkova, T. G. Ruksha

Abstract

The NFE2L2 gene of the redox-sensitive transcription factor NRF2 is a target of miR-155 microRNA. In the present work, a transfection of miR-155 imitator (mimic) was performed into dacarbazine-resistant B16 melanoma cells. It was determined that, under the influence of miR-155 microRNA mimic, the expression level of NRF2 encoded by the NFE2L2 decreases in melanoma cells both in conditions of oxidative stress and without it. A decrease in the level of NRF2 was accompanied by a decrease in the viability of dacarbazine-resistant melanoma cells. Thus, miR-155-mediated activation of NRF2, which regulates the intensity of antioxidant processes in the cell, can be associated with the preservation of viability and development of drug resistance of tumor cells. The latter can be used to overcome chemoresistance in the treatment of oncological diseases.

摘要氧化还原敏感转录因子 NRF2 的 NFE2L2 基因是 miR-155 microRNA 的靶标。本研究将 miR-155 模仿物（mimic）转染到抗达卡巴嗪的 B16 黑色素瘤细胞中。结果表明，在 miR-155 microRNA 模拟物的影响下，黑色素瘤细胞中 NFE2L2 编码的 NRF2 的表达水平在氧化应激条件下和无氧化应激条件下都会下降。NRF2 水平的降低伴随着抗达卡巴嗪黑色素瘤细胞活力的降低。因此，miR-155 介导的 NRF2 激活可调节细胞内抗氧化过程的强度，这可能与肿瘤细胞存活率的保持和耐药性的产生有关。后者可用于克服肿瘤疾病治疗中的化疗耐药性。

引用次数: 0

The Role of Autophagy and Macrophage Polarization in the Process of Chronic Inflammation and Regeneration 自噬和巨噬细胞极化在慢性炎症和再生过程中的作用

Q4 Biochemistry, Genetics and Molecular Biology

Cell and Tissue Biology

Pub Date : 2024-06-03 DOI: 10.1134/s1990519x24700184

S. G. Zubova, A. V. Morshneva

Abstract

Many serious illnesses, including diabetes, obesity, osteoporosis, and neurodegenerative diseases, are caused by chronic inflammation that develops in fat tissue, bones, or the brain. This inflammation occurs due to a shift in macrophage (microglia) polarization toward a proinflammatory M1 phenotype. It has now been proven that macrophage polarization is determined by the intracellular level of autophagy in the macrophage. By modulating autophagy, it is possible to cause a switch in macrophage activity towards M1 or M2. Summarizing the material accumulated in the literature, we believe that activation of autophagy reprograms the macrophage towards M2, replacing its protein content and receptor apparatus, and activate a another type of metabolism. The term “reprogramming” is most appropriate for this process, since it is followed by a change in the functional activity of the macrophage, namely a switch from cytotoxic proinflammatory activity to anti-inflammatory (regenerative) activity. Modulation of autophagy may be an approach to the treatment of cancer, neurodegenerative disorders, osteoporosis, diabetes and other serious diseases.

摘要许多严重疾病，包括糖尿病、肥胖症、骨质疏松症和神经退行性疾病，都是由脂肪组织、骨骼或大脑中的慢性炎症引起的。发生这种炎症的原因是巨噬细胞（小胶质细胞）的极化转向了促炎的 M1 表型。现已证实，巨噬细胞的极化是由巨噬细胞内的自噬水平决定的。通过调节自噬，有可能使巨噬细胞的活动转向 M1 或 M2。总结文献中积累的材料，我们认为，激活自噬可使巨噬细胞向 M2 重编程，更换其蛋白质含量和受体装置，并激活另一种类型的新陈代谢。用 "重编程 "一词来形容这一过程最为恰当，因为在这一过程之后，巨噬细胞的功能活动发生了变化，即从细胞毒性促炎活动转变为抗炎（再生）活动。调节自噬可能是治疗癌症、神经退行性疾病、骨质疏松症、糖尿病和其他严重疾病的一种方法。

{"title":"The Role of Autophagy and Macrophage Polarization in the Process of Chronic Inflammation and Regeneration","authors":"S. G. Zubova, A. V. Morshneva","doi":"10.1134/s1990519x24700184","DOIUrl":"https://doi.org/10.1134/s1990519x24700184","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Abstract</h3><p>Many serious illnesses, including diabetes, obesity, osteoporosis, and neurodegenerative diseases, are caused by chronic inflammation that develops in fat tissue, bones, or the brain. This inflammation occurs due to a shift in macrophage (microglia) polarization toward a proinflammatory M1 phenotype. It has now been proven that macrophage polarization is determined by the intracellular level of autophagy in the macrophage. By modulating autophagy, it is possible to cause a switch in macrophage activity towards M1 or M2. Summarizing the material accumulated in the literature, we believe that activation of autophagy reprograms the macrophage towards M2, replacing its protein content and receptor apparatus, and activate a another type of metabolism. The term “reprogramming” is most appropriate for this process, since it is followed by a change in the functional activity of the macrophage, namely a switch from cytotoxic proinflammatory activity to anti-inflammatory (regenerative) activity. Modulation of autophagy may be an approach to the treatment of cancer, neurodegenerative disorders, osteoporosis, diabetes and other serious diseases.</p>","PeriodicalId":9705,"journal":{"name":"Cell and Tissue Biology","volume":"22 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141254432","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The Biological Activity and Therapeutic Potential of Curcuma longa: Literature Review 姜黄的生物活性和治疗潜力：文献综述

Q4 Biochemistry, Genetics and Molecular Biology

Cell and Tissue Biology

Pub Date : 2024-06-03 DOI: 10.1134/s1990519x24700202

A. A. Zaporozhchenko, M. A. Subotyalov

Abstract

The review presents an analysis of publications devoted to identifying the biological activity, component composition, pharmacological properties, and therapeutic potential of various components of the Curcuma longa plant. In preparing this publication, we mainly used articles from the PubMed, Scopus, and Web of Science databases. The analysis showed that Curcuma longa contains a wide range of biologically active substances, including curcuminoids, volatile oils, resins, and alkaloids. Numerous in vivo and in vitro studies have demonstrated its anti-inflammatory, antioxidant, antibacterial, antitumor, neuroprotective, antiproliferative, and a number of other effects. Thus, Curcuma longa has high therapeutic potential and can be a promising raw material for drug development effective for various diseases.

摘要这篇综述分析了致力于确定莪术植物各种成分的生物活性、成分组成、药理特性和治疗潜力的出版物。在编写本出版物时，我们主要使用了 PubMed、Scopus 和 Web of Science 数据库中的文章。分析表明，莪术含有多种生物活性物质，包括姜黄素、挥发油、树脂和生物碱。大量体内和体外研究表明，莪术具有抗炎、抗氧化、抗菌、抗肿瘤、神经保护、抗增殖等多种功效。因此，莪术具有很高的治疗潜力，是一种很有前途的原料，可用于开发治疗各种疾病的有效药物。

引用次数: 0

Decellularized Prostate for Cancer Studies 用于癌症研究的脱细胞前列腺

Q4 Biochemistry, Genetics and Molecular Biology

Cell and Tissue Biology

Pub Date : 2024-06-03 DOI: 10.1134/s1990519x24700160

Mozafar Khazaei, Mohammad Rasool Khazaei, Elham Ghanbari, Leila Rezakhania

Abstract

Regenerative medicine researchers are interested in extracellular matrix (ECM) investigations around fabricating scaffolds that mimic the biological environment. These structures can be utilized in different disease and drug screenings as three-dimensional (3D) models. This study aimed to decellularization of rat prostate by different methods to reach a suitable scaffold and introduce it in cancer studies. In this experimental study, rat prostates were decellularized by 1% sodium dodecyl sulfate (SDS) and 1% sodium deoxycholate (SD) methods. Decellularized prostate matrix (DPM) was stained using hematoxylin-eosin (H&E) and Masson’s trichrome (MT) techniques to determine the presence of the nucleus and collagen. A scanning electron microscope (SEM) was used to examine the morphology and cell attachment to the DPM. By culturing LNcap cells on the DPM, recellularization was studied. Both decellularization methods (1% SDS and 1% SD) completely removed the cells from the DPM. The tissue structure has been significantly preserved, which is confirmed by the staining methods and SEM images. The preservation of a large amount of collagen content was established through MT staining and using the kit. Cell adhesion in the DPM was reported by SEM. No toxicity or hemolysis was observed in the DPM. Migration of cancer cells into the DPM was seen. Prostate decellularization with SDS and SD, in addition to cell removal, can maintain the ECM structure to a large extent without having cytotoxic and hemolysis effects.

摘要再生医学研究人员对细胞外基质（ECM）的研究很感兴趣，他们围绕着制造模拟生物环境的支架展开研究。这些结构可作为三维（3D）模型用于不同疾病和药物筛选。本研究旨在通过不同方法对大鼠前列腺进行脱细胞处理，以获得合适的支架，并将其引入癌症研究中。本实验研究采用 1%十二烷基硫酸钠（SDS）和 1%脱氧胆酸钠（SD）两种方法对大鼠前列腺进行脱细胞处理。脱细胞前列腺基质（DPM）采用苏木精-伊红（H&E）和马森三色染色（MT）技术染色，以确定细胞核和胶原蛋白的存在。扫描电子显微镜（SEM）用于检查形态和细胞附着在 DPM 上的情况。通过在 DPM 上培养 LNcap 细胞，对再细胞化进行了研究。两种脱细胞方法（1% SDS 和 1%SD）都能完全去除 DPM 上的细胞。染色方法和扫描电镜图像证实，组织结构得到了明显的保留。通过 MT 染色和使用试剂盒，大量胶原蛋白成分得以保留。扫描电镜显示了 DPM 中的细胞粘附情况。在 DPM 中未观察到毒性或溶血现象。癌细胞迁移到 DPM 中。使用 SDS 和 SD 进行前列腺脱细胞处理，除了能去除细胞外，还能在很大程度上保持 ECM 结构，而不会产生细胞毒性和溶血效应。

{"title":"Decellularized Prostate for Cancer Studies","authors":"Mozafar Khazaei, Mohammad Rasool Khazaei, Elham Ghanbari, Leila Rezakhania","doi":"10.1134/s1990519x24700160","DOIUrl":"https://doi.org/10.1134/s1990519x24700160","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Abstract</h3><p>Regenerative medicine researchers are interested in extracellular matrix (ECM) investigations around fabricating scaffolds that mimic the biological environment. These structures can be utilized in different disease and drug screenings as three-dimensional (3D) models. This study aimed to decellularization of rat prostate by different methods to reach a suitable scaffold and introduce it in cancer studies. In this experimental study, rat prostates were decellularized by 1% sodium dodecyl sulfate (SDS) and 1% sodium deoxycholate (SD) methods. Decellularized prostate matrix (DPM) was stained using hematoxylin-eosin (H&E) and Masson’s trichrome (MT) techniques to determine the presence of the nucleus and collagen. A scanning electron microscope (SEM) was used to examine the morphology and cell attachment to the DPM. By culturing LNcap cells on the DPM, recellularization was studied. Both decellularization methods (1% SDS and 1% SD) completely removed the cells from the DPM. The tissue structure has been significantly preserved, which is confirmed by the staining methods and SEM images. The preservation of a large amount of collagen content was established through MT staining and using the kit. Cell adhesion in the DPM was reported by SEM. No toxicity or hemolysis was observed in the DPM. Migration of cancer cells into the DPM was seen. Prostate decellularization with SDS and SD, in addition to cell removal, can maintain the ECM structure to a large extent without having cytotoxic and hemolysis effects.</p>","PeriodicalId":9705,"journal":{"name":"Cell and Tissue Biology","volume":"51 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141254543","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Short Tandem Repeat Profile for Authentication of Immortal Murine Cancer Cell Line MH-22A 用于鉴定不死小鼠癌症细胞系 MH-22A 的短串联重复序列图

Q4 Biochemistry, Genetics and Molecular Biology

Cell and Tissue Biology

Pub Date : 2024-06-03 DOI: 10.1134/s1990519x24700214

Ralf Weiskirchen, Stefanie Kankel, Thomas Liehr

Abstract

The murine cell line MH-22A was originally established at least 50 years ago from a non-metastasizing tumor induced by 3-methylcholanthrene in C3HA mice and further adapted for in vitro growth. MH-22A cells grow predominantly epithelioid and they lead to the formation of transplantable tumors when injected subcutaneously into mice. In silico translation of genome data of this nearly triploid cell line to the human genome has recently characterized MH-22A as a suitable model for hepatoblastoma or early hepatocellular carcinoma. Here we established a multi-loci short tandem repeat signature for this cell line that allows quick and reliable cell line authentication.

摘要小鼠细胞系 MH-22A 最初是在至少 50 年前从 C3HA 小鼠体内由 3-甲基胆蒽诱发的非转移性肿瘤中建立的，后经进一步改造用于体外生长。MH-22A 细胞主要呈上皮样生长，向小鼠皮下注射后可形成可移植肿瘤。最近，将这一近乎三倍体细胞系的基因组数据转化为人类基因组的硅学研究表明，MH-22A 是肝母细胞瘤或早期肝细胞癌的合适模型。在这里，我们为该细胞系建立了一个多基因短串联重复特征，可以快速可靠地鉴定细胞系。

引用次数: 0

Vimentin in Kolmer Cells of Spontaneously Hypertensive Rats 自发性高血压大鼠 Kolmer 细胞中的波形蛋白

Q4 Biochemistry, Genetics and Molecular Biology

Cell and Tissue Biology

Pub Date : 2024-06-03 DOI: 10.1134/s1990519x24700275

D. E. Korzhevskii, V. A. Razenkova, O. V. Kirik

Abstract

Epiplexus (Kolmer) cells are a special population of phagocytic cells of the choroid plexus involved in maintaining the blood–cerebrospinal fluid barrier in the brain. In the present work, the structural organization of these cells was studied in Wistar, Wistar Kyoto, and spontaneously hypertensive (SHR) rats. A comparative immunohistochemical investigation using antibodies against macrophage markers Iba-1 and CD68 and intermediate filament protein vimentin showed that Kolmer cells in three studied groups of animals differ in their functional activity. In Wistar Kyoto and SHR rats, not only signs of activation of Kolmer cells were noted, visible in the disappearance of processes and cells acquiring a rounded shape, but also vimentin presence in activated cells. The obtained result indicates a relationship between vimentin expression and activation of brain phagocytic cells.

摘要Epiplexus（Kolmer）细胞是脉络丛中一种特殊的吞噬细胞群，参与维持大脑中的血-脑脊液屏障。本研究以 Wistar、Wistar Kyoto 和自发性高血压（SHR）大鼠为研究对象，对这些细胞的结构组织进行了研究。使用针对巨噬细胞标记物 Iba-1 和 CD68 以及中间丝蛋白波形蛋白的抗体进行的免疫组化比较研究表明，三组动物的 Kolmer 细胞在功能活性上存在差异。在 Wistar Kyoto 大鼠和 SHR 大鼠中，不仅发现了 Kolmer 细胞活化的迹象（可见于突起消失和细胞形状变圆），而且在活化的细胞中还发现了波形蛋白。研究结果表明，波形蛋白的表达与脑吞噬细胞的活化之间存在关系。

引用次数: 0

Role of Rho Family Small GTPases in the Regulation of Normal and Pathological Processes Rho 家族小 GTP 酶在正常和病理过程调控中的作用

Q4 Biochemistry, Genetics and Molecular Biology

Cell and Tissue Biology

Pub Date : 2024-06-03 DOI: 10.1134/s1990519x24700159

D. E. Bobkov, A. V. Lukacheva, A. I. Gorb, G. G. Poljanskaya

Abstract

Small GTPases are monomeric (approximately 21 kDa) proteins that regulate a number of biological processes, such as vesicle transport, cell division cycle, cell migration, invasion, adhesion, proliferation, and DNA repair. They are also involved in carcinogenesis and neurodegenerative diseases. Some of these proteins, such as the Rho family proteins, are essential regulators of actin cytoskeleton, controlling cell adhesion and motility. This review examines both normal and pathological processes in human cells that are regulated by small GTPases of the Rho family. Particular attention is paid to small GTPase inhibitors and their use in the treatment of various diseases.

摘要小 GTP 酶是一种单体蛋白（约 21 kDa），可调节多种生物过程，如囊泡运输、细胞分裂周期、细胞迁移、侵袭、粘附、增殖和 DNA 修复。它们还与致癌和神经退行性疾病有关。其中一些蛋白，如 Rho 家族蛋白，是肌动蛋白细胞骨架的重要调节因子，控制着细胞的粘附和运动。本综述探讨了人体细胞中受 Rho 家族小 GTP 酶调控的正常和病理过程。其中特别关注小 GTP 酶抑制剂及其在治疗各种疾病中的应用。

引用次数: 0

Immunofluorescent Identification of Dystrophin, Actin, and Light and Heavy Myosin Chains in Somatic Cells of Earthworm Lumbricus terrestris 蚯蚓 Lumbricus terrestris 体细胞中肌萎缩蛋白、肌动蛋白、轻肌球蛋白链和重肌球蛋白链的免疫荧光鉴定

Q4 Biochemistry, Genetics and Molecular Biology

Cell and Tissue Biology

Pub Date : 2024-06-03 DOI: 10.1134/s1990519x24700287

L. F. Nurullin, E. M. Volkov

Abstract

In muscle cells of the motor muscle of earthworm Lumbricus terrestris, the dystrophin and actin proteins and fast and slow isoforms of myosin heavy chains were determined using fluorescence microscopy. It can be thought that the expression of these proteins occurred at the earliest stages of the evolutionary formation of the intracellular contractile apparatus of the motor tissue in both invertebrates and vertebrates. This study will complement the picture of the evolutionary development of motor muscle tissue.

摘要利用荧光显微镜测定了蚯蚓运动肌的肌肉细胞中肌萎缩蛋白和肌动蛋白以及肌球蛋白重链的快慢异构体。可以认为，这些蛋白质的表达发生在无脊椎动物和脊椎动物运动组织胞内收缩装置进化形成的最早阶段。这项研究将补充运动肌肉组织进化发展的图景。

引用次数: 0

首页上一页

下一页尾页

类型

全部化学•材料生命科学医学物理工程技术环境•农林材料科学地球科学法学管理学化学环境科学与生态学计算机科学教育学经济学农林科学人文科学生物学数学物理与天体物理心理学综合性期刊其他工业工程理学历史学农学文学信息工程

数据库

全部 ACS Publications Elsevier ieeexplore Springer The Royal Society of Chemistry Wiley

期刊

Cell and Tissue Biology

全部 Acc. Chem. Res. ACS Applied Bio Materials ACS Appl. Electron. Mater. ACS Appl. Energy Mater. ACS Appl. Mater. Interfaces ACS Appl. Nano Mater. ACS Appl. Polym. Mater. ACS BIOMATER-SCI ENG ACS Catal. ACS Cent. Sci. ACS Chem. Biol. ACS Chemical Health & Safety ACS Chem. Neurosci. ACS Comb. Sci. ACS Earth Space Chem. ACS Energy Lett. ACS Infect. Dis. ACS Macro Lett. ACS Mater. Lett. ACS Med. Chem. Lett. ACS Nano ACS Omega ACS Photonics ACS Sens. ACS Sustainable Chem. Eng. ACS Synth. Biol. Anal. Chem. BIOCHEMISTRY-US Bioconjugate Chem. BIOMACROMOLECULES Chem. Res. Toxicol. Chem. Rev. Chem. Mater. CRYST GROWTH DES ENERG FUEL Environ. Sci. Technol. Environ. Sci. Technol. Lett. Eur. J. Inorg. Chem. IND ENG CHEM RES Inorg. Chem. J. Agric. Food. Chem. J. Chem. Eng. Data J. Chem. Educ. J. Chem. Inf. Model. J. Chem. Theory Comput. J. Med. Chem. J. Nat. Prod. J PROTEOME RES J. Am. Chem. Soc. LANGMUIR MACROMOLECULES Mol. Pharmaceutics Nano Lett. Org. Lett. ORG PROCESS RES DEV ORGANOMETALLICS J. Org. Chem. J. Phys. Chem. J. Phys. Chem. A J. Phys. Chem. B J. Phys. Chem. C J. Phys. Chem. Lett. Analyst Anal. Methods Biomater. Sci. Catal. Sci. Technol. Chem. Commun. Chem. Soc. Rev. CHEM EDUC RES PRACT CRYSTENGCOMM Dalton Trans. Energy Environ. Sci. ENVIRON SCI-NANO ENVIRON SCI-PROC IMP ENVIRON SCI-WAT RES Faraday Discuss. Food Funct. Green Chem. Inorg. Chem. Front. Integr. Biol. J. Anal. At. Spectrom. J. Mater. Chem. A J. Mater. Chem. B J. Mater. Chem. C Lab Chip Mater. Chem. Front. Mater. Horiz. MEDCHEMCOMM Metallomics Mol. Biosyst. Mol. Syst. Des. Eng. Nanoscale Nanoscale Horiz. Nat. Prod. Rep. New J. Chem. Org. Biomol. Chem. Org. Chem. Front. PHOTOCH PHOTOBIO SCI PCCP Polym. Chem.

﹀