D. V. Krieger, G. V. Vasilyeva, E. V. Lomert, D. G. Tentler
{"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}
E. V. Utkina, V. V. Novakovskaya, M. V. Egorova, N. V. Fomina, L. D. Chesnokova
{"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}
{"title":"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","authors":"V. A. Kutsenko, D. A. Dashkova, T. G. Ruksha","doi":"10.1134/s1990519x2470024x","DOIUrl":"https://doi.org/10.1134/s1990519x2470024x","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Abstract</h3><p>The <i>NFE2L2</i> 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 <i>NFE2L2</i> 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.</p>","PeriodicalId":9705,"journal":{"name":"Cell and Tissue Biology","volume":"309 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141254534","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}
{"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}
{"title":"The Biological Activity and Therapeutic Potential of Curcuma longa: Literature Review","authors":"A. A. Zaporozhchenko, M. A. Subotyalov","doi":"10.1134/s1990519x24700202","DOIUrl":"https://doi.org/10.1134/s1990519x24700202","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Abstract</h3><p>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 <i>Curcuma longa</i> plant. In preparing this publication, we mainly used articles from the PubMed, Scopus, and Web of Science databases. The analysis showed that <i>Curcuma longa</i> 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, <i>Curcuma longa</i> has high therapeutic potential and can be a promising raw material for drug development effective for various diseases.</p>","PeriodicalId":9705,"journal":{"name":"Cell and Tissue Biology","volume":"11 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141254533","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}
Mozafar Khazaei, Mohammad Rasool Khazaei, Elham Ghanbari, Leila Rezakhania
{"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}
{"title":"Short Tandem Repeat Profile for Authentication of Immortal Murine Cancer Cell Line MH-22A","authors":"Ralf Weiskirchen, Stefanie Kankel, Thomas Liehr","doi":"10.1134/s1990519x24700214","DOIUrl":"https://doi.org/10.1134/s1990519x24700214","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Abstract</h3><p>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.</p>","PeriodicalId":9705,"journal":{"name":"Cell and Tissue Biology","volume":"20 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141254541","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}
{"title":"Vimentin in Kolmer Cells of Spontaneously Hypertensive Rats","authors":"D. E. Korzhevskii, V. A. Razenkova, O. V. Kirik","doi":"10.1134/s1990519x24700275","DOIUrl":"https://doi.org/10.1134/s1990519x24700275","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Abstract</h3><p>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.</p>","PeriodicalId":9705,"journal":{"name":"Cell and Tissue Biology","volume":"21 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141254631","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}
D. E. Bobkov, A. V. Lukacheva, A. I. Gorb, G. G. Poljanskaya
{"title":"Role of Rho Family Small GTPases in the Regulation of Normal and Pathological Processes","authors":"D. E. Bobkov, A. V. Lukacheva, A. I. Gorb, G. G. Poljanskaya","doi":"10.1134/s1990519x24700159","DOIUrl":"https://doi.org/10.1134/s1990519x24700159","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Abstract</h3><p>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.</p>","PeriodicalId":9705,"journal":{"name":"Cell and Tissue Biology","volume":"31 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141259579","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}
{"title":"Immunofluorescent Identification of Dystrophin, Actin, and Light and Heavy Myosin Chains in Somatic Cells of Earthworm Lumbricus terrestris","authors":"L. F. Nurullin, E. M. Volkov","doi":"10.1134/s1990519x24700287","DOIUrl":"https://doi.org/10.1134/s1990519x24700287","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Abstract</h3><p>In muscle cells of the motor muscle of earthworm <i>Lumbricus terrestris</i>, 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.</p>","PeriodicalId":9705,"journal":{"name":"Cell and Tissue Biology","volume":"7 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141254538","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}