Maria L Perepechaeva, Lyubov S Klyushova, Alevtina Y Grishanova
{"title":"AhR and HIF-1<i>α</i> Signaling Pathways in Benign Meningioma under Hypoxia.","authors":"Maria L Perepechaeva, Lyubov S Klyushova, Alevtina Y Grishanova","doi":"10.1155/2023/6840271","DOIUrl":"https://doi.org/10.1155/2023/6840271","url":null,"abstract":"<p><p>The role of hypoxia in benign meningiomas is less clear than that in the malignant meningiomas. Hypoxia-induced transcription factor 1 subunit alpha (HIF-1<i>α</i>) and its downstream signaling pathways play a central role in the mechanism of hypoxia. HIF-1<i>α</i> forms a complex with the aryl hydrocarbon receptor nuclear translocator (ARNT) protein and can compete for ARNT with aryl hydrocarbon receptor (AhR). In this work, the status of HIF-1<i>α</i>- and AhR-dependent signaling pathways was investigated in World Health Organization (WHO) grade 1 meningioma and patient-derived tumor primary cell culture under hypoxic conditions. mRNA levels of <i>HIF-1α</i>, <i>AhR</i>, and of their target genes as well as of <i>ARNT</i> and nuclear receptor coactivator <i>NCOA2</i> were determined in tumor tissues from patients in whom the tumor was promptly removed either with or without prior endovascular embolization. Using the patient-derived nonembolized tumor primary cell culture, the effects of a hypoxia mimetic cobalt chloride (CoCl<sub>2</sub>) and an activator of the AhR signaling pathway benzo(<i>α</i>)pyrene (B[a]P) on mRNA levels of <i>HIF-1α</i>, <i>AhR</i>, and their target genes were investigated. Our findings show active functioning of AhR signaling in meningioma tissue of patients with tumor embolization and crosstalk between HIF-1<i>α</i> and AhR signaling in meningeal cells under hypoxia.</p>","PeriodicalId":39084,"journal":{"name":"International Journal of Cell Biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10257548/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9612310","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"miRNAs: The Key Regulator of COVID-19 Disease.","authors":"Leyla Tahrani Hardin, Nan Xiao","doi":"10.1155/2022/1645366","DOIUrl":"https://doi.org/10.1155/2022/1645366","url":null,"abstract":"<p><p>As many parts of the world continue to fight the innumerable waves of COVID-19 infection, SARS-CoV-2 continues to sculpt its antigenic determinants to enhance its virulence and evolvability. Several vaccines were developed and used around the world, and oral antiviral medications are being developed against SARS-CoV-2. However, studies showed that the virus is mutating in line with the antibody's neutralization escape; thus, new therapeutic alternatives are solicited. We hereby review the key role that miRNAs can play as epigenetic mediators of the cross-talk between SARS-CoV-2 and the host cells. The limitations resulting from the \"virus intelligence\" to escape and antagonize the host miRNAs as well as the possible mechanisms that could be used in the viral evasion strategies are discussed. Lastly, we suggest new therapeutic approaches based on viral miRNAs.</p>","PeriodicalId":39084,"journal":{"name":"International Journal of Cell Biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9637033/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40672106","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Isolation of Female Germline Stem Cells from Mouse and Human Ovaries by Differential Adhesion.","authors":"Maryam Saber, Pouya Tavakol, Fereshteh Esfandiari","doi":"10.1155/2022/5224659","DOIUrl":"https://doi.org/10.1155/2022/5224659","url":null,"abstract":"<p><p>Spermatogonial stem cell (SSC) counterparts known as female germline stem cells (fGSCs) were found in the mammalian ovary in 2004. Although the existence of fGSCs in the mammalian postnatal ovary is still under controversy, fGSC discovery encourages investigators to better understand the various aspects of these cells. However, their existence is not accepted by all scientists in the field because isolation of fGSCs by fluorescent activated cell sorting (FACS) has not been reproducible. In this study, we used differential adhesion to isolate and enrich fGSCs from mouse and human ovaries and subsequently cultured them <i>in vitro</i>. fGSCs were able to proliferate <i>in vitro</i> and expressed germ cell-specific markers Vasa, Dazl, Blimp1, Fragilis, Stella, and Oct4, at the protein level. Moreover, mouse and human fGSCs were, respectively, cultured for more than four months and one month in culture. Both mouse and human fGSCs maintained the expression of germ cell-specific markers over these times. <i>In vitro</i> cultured fGSCs spontaneously produced oocyte-like cells (OLCs) which expressed oocyte-relevant markers. Our results demonstrated that differential adhesion allows reproducible isolation of fGSCs that are able to proliferate <i>in vitro</i> over time. This source of fGSCs can serve as a suitable material for studying mechanisms underlying female germ cell development and function.</p>","PeriodicalId":39084,"journal":{"name":"International Journal of Cell Biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9473869/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40369395","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Waynner O. Sousa, Mahmi Fujimori, T. C. Morais, Milena B Santos, Gabriel F. S. Rodrigues, K. P. G. Silva, A. H. F. Torres, A. Honório-França, E. L. França
{"title":"Effects of Modified Melatonin Release on Human Colostrum Neutrophils to Induce Death in the MCF-7 Cell Line","authors":"Waynner O. Sousa, Mahmi Fujimori, T. C. Morais, Milena B Santos, Gabriel F. S. Rodrigues, K. P. G. Silva, A. H. F. Torres, A. Honório-França, E. L. França","doi":"10.1155/2022/8069188","DOIUrl":"https://doi.org/10.1155/2022/8069188","url":null,"abstract":"Cancer is one of the diseases with the highest mortality rate today, with breast cancer being the second most common type among the Brazilian population. Due to its etiological complexity and inefficiency of treatments, studies have focused on new forms of treatment. Among these forms of treatment, hormonal therapy seems to be an excellent auxiliary mechanism in tumoricidal activity, and melatonin has great potential as a modulator of the immune system. Thus, the present study is aimed at evaluating the effect of the hormone melatonin on the coculture of colostrum polymorphonuclear cells and MCF-7 cancer cells and evaluates the effect of this hormone using a modified transport system. A feasibility analysis was performed by fluorescence microscopy at three cell incubation times, 2 hours, 24 hours, and 72 hours. The measurement of cytokines in the cell supernatant occurred in 24 hours, and the apoptosis assay was performed in 72 hours using flow cytometry. The results showed higher levels of cell viability in groups treated with melatonin and less viability in groups containing a coculture of polymorphonuclear cells and MCF-7 after 72 hours of incubation. Furthermore, the apoptosis and necrosis rates were higher in coculture polymorphonuclear and MCF-7 cells, especially in groups containing microemulsion as a modified release agent. These data suggest that melatonin, especially if associated with a modified release system, has immunomodulatory effects on human colostrum polymorphonuclear cells. These cells can play a crucial role in the resolution of the tumor through their mediation and inflammatory action.","PeriodicalId":39084,"journal":{"name":"International Journal of Cell Biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43512078","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}
Camila Bernal, Andrea Otalora, Alejandra Cañas, Alfonso Barreto, Karol Prieto, Martin Montecino, Adriana Rojas
{"title":"Regulatory Role of the RUNX2 Transcription Factor in Lung Cancer Apoptosis.","authors":"Camila Bernal, Andrea Otalora, Alejandra Cañas, Alfonso Barreto, Karol Prieto, Martin Montecino, Adriana Rojas","doi":"10.1155/2022/5198203","DOIUrl":"https://doi.org/10.1155/2022/5198203","url":null,"abstract":"<p><p>Lung cancer is the leading cause of cancer death globally. Numerous factors intervene in the onset and progression of lung tumors, among which the participation of lineage-specific transcription factors stands out. Several transcription factors important in embryonic development are abnormally expressed in adult tissues and thus participate in the activation of signaling pathways related to the acquisition of the tumor phenotype. RUNX2 is the transcription factor responsible for osteogenic differentiation in mammals. Current studies have confirmed that RUNX2 is closely related to the proliferation, invasion, and bone metastasis of multiple cancer types, such as osteosarcoma, breast cancer (BC), prostate cancer, gastric cancer, colorectal cancer, and lung cancer. Thus, the present study is aimed at evaluating the role of the RUNX2 transcription factor in inhibiting the apoptosis process. Loss-of-function assays using sh-RNA from lentiviral particles and coupled with Annexin/propidium iodide (PI) assays (flow cytometry), immunofluorescence, and quantitative PCR analysis of genes related to cell apoptosis (<i>BAD</i>, <i>BAX</i>, <i>BCL2</i>, <i>BCL-XL</i>, and <i>MCL1</i>) were performed. Silencing assays and Annexin/PI assays demonstrated that when RUNX2 was absent, the percentage of dead cells increased, and the expression levels of the <i>BCL2</i>, <i>BCL-XL</i>, and <i>MCL1</i> genes were downregulated. Furthermore, to confirm whether the regulatory role of RUNX2 in the expression of these genes is related to its binding to the promoter region, we performed chromatin immunoprecipitation (ChIP) assays. Here, we report that overexpression of the <i>RUNX2</i> gene in lung cancer may be related to the inhibition of the intrinsic apoptosis pathway, specifically, through direct transcriptional regulation of the antiapoptotic gene <i>BCL2</i> and indirect regulation of <i>BCL-XL</i> and <i>MCL1.</i></p>","PeriodicalId":39084,"journal":{"name":"International Journal of Cell Biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9741537/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10338478","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Tsung-Chang Tsai, Wen-Tung Wu, Jen-Jie Lin, Jui-Hsin Su, Yu-Jen Wu
{"title":"Stellettin B Isolated from <i>Stelletta</i> Sp. Reduces Migration and Invasion of Hepatocellular Carcinoma Cells through Reducing Activation of the MAPKs and FAK/PI3K/AKT/mTOR Signaling Pathways.","authors":"Tsung-Chang Tsai, Wen-Tung Wu, Jen-Jie Lin, Jui-Hsin Su, Yu-Jen Wu","doi":"10.1155/2022/4416611","DOIUrl":"https://doi.org/10.1155/2022/4416611","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is one of the most common malignant tumors, and there is currently a lack of effective treatment options to control the metastasis. This study was performed to examine the mechanisms of the migration and invasion characteristics of HCC, with the aim of reducing metastasis by inhibiting cancer cell migration and invasion. In this study, we used Stellettin B, an active compound isolated from Stelletta sponges, as the experimental drug and evaluated its inhibition effects on cell migration and invasion in human hepatoma cells (HA22T and HepG2). MTT assay, gelatin zymography, and western blotting were employed. The results showed that Stellettin B significantly inhibited the protein expressions of MMP-2, MMP-9, and uPA, while upregulating the protein expressions of TIMP-1 and TIMP-2. The expressions of p-FAK, p-PI3K, p-AKT, p-mTOR, and MAPKs (p-JNK, p-JUN, p-MAPKp38, and p-ERK) were decreased with increasing concentrations of Stellettin B. Our results suggest that Stellettin B-dependent downregulation of MMP-2 and MMP-9 activities could be mediated by FAK/PI3K/AKT/mTOR and MAPKs signaling pathways in HA22T and HepG2 cells, preventing HCC invasion and migration.</p>","PeriodicalId":39084,"journal":{"name":"International Journal of Cell Biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9726252/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10379774","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Manoj J Mammen, Jamil Ali, Amita Aurora, Umesh C Sharma, Ravikumar Aalinkeel, Supriya D Mahajan, Mark Sands, Stanley A Schwartz
{"title":"IL-17 Is a Key Regulator of Mucin-Galectin-3 Interactions in Asthma.","authors":"Manoj J Mammen, Jamil Ali, Amita Aurora, Umesh C Sharma, Ravikumar Aalinkeel, Supriya D Mahajan, Mark Sands, Stanley A Schwartz","doi":"10.1155/2021/9997625","DOIUrl":"10.1155/2021/9997625","url":null,"abstract":"<p><p>Mucus hypersecretion and chronic airway inflammation are standard characteristics of several airway diseases, such as chronic obstructive pulmonary disease and asthma. Increased mucus secretion from increased mucin gene expression in the airway epithelium is associated with poor prognosis and mortality. We previously showed that the absence of tissue inhibitor of metalloproteinase 1 (TIMP-1) enhances lung inflammation, airway hyperreactivity, and lung remodeling in asthma in an ovalbumin (OVA) asthma model of TIMP-1 knockout (TIMPKO) mice as compared to wild-type (WT) controls and mediated by increased galectin-3 (Gal-3) levels. Additionally, we have shown that in the lung epithelial cell line A549, Gal-3 inhibition increases interleukin-17 (IL-17) levels, leading to increased mucin expression in the airway epithelium. Therefore, in the current study, we further examined the relationship between Gal-3 and the production of IL-17-axis cytokines and critical members of the mucin family in the murine TIMPKO asthma model and the lung epithelium cell line A549. While Gal-3 may regulate a Th<sub>1</sub>/Th<sub>2</sub> response, IL-17 could stimulate the mucin genes, MUC5B and MUC5AC. Gal-3 and IL-17 interactions induce mucus expression in OVA-sensitized mice. We conclude that Gal-3 may play an essential role in the pathogenesis of asthma, and modulation of Gal-3 may prove helpful in the treatment of this disease.</p>","PeriodicalId":39084,"journal":{"name":"International Journal of Cell Biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8211528/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39148710","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Asporin Reduces Adult Aortic Valve Interstitial Cell Mineralization Induced by Osteogenic Media and Wnt Signaling Manipulation <i>In Vitro</i>.","authors":"Anisha Polley, Riffat Khanam, Arunima Sengupta, Santanu Chakraborty","doi":"10.1155/2020/2045969","DOIUrl":"https://doi.org/10.1155/2020/2045969","url":null,"abstract":"<p><p>Worldwide, calcific aortic valve disease is one of the leading causes of morbidity and mortality among patients with cardiac abnormalities. Aortic valve mineralization and calcification are the key events of adult calcific aortic valve disease manifestation and functional insufficiency. Due to heavy mineralization and calcification, adult aortic valvular cusps show disorganized and dispersed stratification concomitant with deposition of calcific nodules with severely compromised adult valve function. Interestingly, shared gene regulatory pathways are identified between bone-forming cells and heart valve cells during development. <i>Asporin</i>, a small leucine-rich proteoglycan (43 kDa), acts to inhibit mineralization in periodontal ligament cells and is also detected in normal murine adult aortic valve leaflets with unknown function. Therefore, to understand the Asporin function in aortic cusp mineralization and calcification, adult avian aortic valvular interstitial cell culture system is established and osteogenesis has been induced in these cells successfully. Upon induction of osteogenesis, reduced expression of <i>Asporin</i> mRNA and increased expression of bone and osteogenesis markers are detected compared to cells maintained without osteogenic induction. Importantly, treatment with human recombinant Asporin protein reduces the mineralization level in osteogenic media-induced aortic valvular interstitial cells with the concomitant decreased level of Wnt/<i>β</i>-catenin signaling. Overall, all these data are highly indicative that <i>Asporin</i> might be a novel biomolecular target to treat patients of calcific aortic valve disease over current cusp replacement surgery.</p>","PeriodicalId":39084,"journal":{"name":"International Journal of Cell Biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2020/2045969","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37867028","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Fangfang Bi, Wenbo Liu, Zongtao Wu, Chen Ji, Cuicui Chang
{"title":"Antiaging Factor Klotho Retards the Progress of Intervertebral Disc Degeneration through the Toll-Like Receptor 4-NF-<i>κ</i>B Pathway.","authors":"Fangfang Bi, Wenbo Liu, Zongtao Wu, Chen Ji, Cuicui Chang","doi":"10.1155/2020/8319516","DOIUrl":"https://doi.org/10.1155/2020/8319516","url":null,"abstract":"<p><p>Antiaging protein Klotho exhibits impressive properties of anti-inflammation, however is declined early after intervertebral disc injury, making Klotho restoration an attractive strategy of treating intervertebral disc inflammatory disorders. Here, we have found that Klotho is enriched in nucleus pulposus (NP) cells and Klotho overexpression attenuates H<sub>2</sub>O<sub>2</sub>-induced acute inflammation essentially via suppressing Toll-like receptor 4 (TLR4). The proinflammatory NF-<i>κ</i>B signaling and cytokine expressions paralleled with Klotho repression and TLR4 elevation in both NP cells (H<sub>2</sub>O<sub>2</sub> treatment) and rat intervertebral disc (needle puncture treatment). Overexpression of TLR4 downregulated expression of Klotho, whereas interfering TLR4 expression diminished the inhibitory effects of H<sub>2</sub>O<sub>2</sub> on Klotho in NP cells. Consistently, Klotho knockdown by RNA interferences largely diminished the anti-inflammatory and intervertebral disc protective effects in an Intervertebral Disc Degeneration (IDD) model. Thus, our study indicates that TLR4-NF-<i>κ</i>B signaling and Klotho form a negative-feedback loop in NP cells. Also, we demonstrate that the expression of Klotho is regulated by the balance between upregulation and downregulation of TLR4-NF-<i>κ</i>B signaling.</p>","PeriodicalId":39084,"journal":{"name":"International Journal of Cell Biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2020/8319516","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37809389","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Rui D Alvites, Mariana V Branquinho, Ana R Caseiro, Irina Amorim, Sílvia Santos Pedrosa, Alexandra Rêma, Fátima Faria, Beatriz Porto, Cláudia Oliveira, Paula Teixeira, Rui Magalhães, Stefano Geuna, Artur S P Varejão, Ana C Maurício
{"title":"Rat Olfactory Mucosa Mesenchymal Stem/Stromal Cells (OM-MSCs): A Characterization Study.","authors":"Rui D Alvites, Mariana V Branquinho, Ana R Caseiro, Irina Amorim, Sílvia Santos Pedrosa, Alexandra Rêma, Fátima Faria, Beatriz Porto, Cláudia Oliveira, Paula Teixeira, Rui Magalhães, Stefano Geuna, Artur S P Varejão, Ana C Maurício","doi":"10.1155/2020/2938258","DOIUrl":"10.1155/2020/2938258","url":null,"abstract":"<p><p>Stem/stromal cell-based therapies are a branch of regenerative medicine and stand as an attractive option to promote the repair of damaged or dysfunctional tissues and organs. Olfactory mucosa mesenchymal stem/stromal cells have been regarded as a promising tool in regenerative therapies because of their several favorable properties such as multipotency, high proliferation rate, helpful location, and few associated ethical issues. These cells are easily accessible in the nasal cavity of most mammals, including the rat, can be easily applied in autologous treatments, and do not cope with most of the obstacles associated with the use of other stem cells. Despite this, its application in preclinical trials and in both human and animal patients is still limited because of the small number of studies performed so far and to the nonexistence of a standard and unambiguous protocol for collection, isolation, and therapeutic application. In the present work a validation of a protocol for isolation, culture, expansion, freezing, and thawing of olfactory mucosa mesenchymal stem/stromal cells was performed, applied to the rat model, as well as a biological characterization of these cells. To investigate the therapeutic potential of OM-MSCs and their eventual safe application in preclinical trials, the main characteristics of OMSC stemness were addressed.</p>","PeriodicalId":39084,"journal":{"name":"International Journal of Cell Biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7212324/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37937504","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}