Human CellPub Date : 2024-09-01Epub Date: 2024-06-15DOI: 10.1007/s13577-024-01093-8
Raymond Dalgleish
{"title":"Re: Identification of a family with van der Hoeve's syndrome harboring a novel COL1A1 mutation and generation of patient-derived iPSC lines and CRISPR/Cas9-corrected isogenic iPSCs.","authors":"Raymond Dalgleish","doi":"10.1007/s13577-024-01093-8","DOIUrl":"10.1007/s13577-024-01093-8","url":null,"abstract":"","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":" ","pages":"1610-1611"},"PeriodicalIF":3.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141327941","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Human CellPub Date : 2024-09-01Epub Date: 2024-07-05DOI: 10.1007/s13577-024-01098-3
José-Luis Carrasco-Juan, Miriam González-Gómez, Olga Tapia, Sonia García-Hernández, Abian Vega-Falcón, Rafael Méndez-Medina, Hugo Álvarez-Argüelles Cabrera, Lucio Díaz-Flores
{"title":"The origin of ovarian Leydig cells: a possibly solved enigma?","authors":"José-Luis Carrasco-Juan, Miriam González-Gómez, Olga Tapia, Sonia García-Hernández, Abian Vega-Falcón, Rafael Méndez-Medina, Hugo Álvarez-Argüelles Cabrera, Lucio Díaz-Flores","doi":"10.1007/s13577-024-01098-3","DOIUrl":"10.1007/s13577-024-01098-3","url":null,"abstract":"<p><p>Over the years, the origin of ovarian Leydig cells has been, and still is, a topic subject to deep debate. Seven years ago, we proposed that this origin resided in intraneural elements that came from a possible reservoir of neural crest cells, a reservoir that may be located in the ganglia of the celiac plexus. We believe we have found the evidence necessary to prove this hypothesis.</p>","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":" ","pages":"1544-1552"},"PeriodicalIF":3.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141535737","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Human CellPub Date : 2024-09-01Epub Date: 2024-07-10DOI: 10.1007/s13577-024-01099-2
Ran You, Zhanjun Jia
{"title":"Pathophysiological role of Na-Cl cotransporter in kidneys, blood pressure, and metabolism.","authors":"Ran You, Zhanjun Jia","doi":"10.1007/s13577-024-01099-2","DOIUrl":"10.1007/s13577-024-01099-2","url":null,"abstract":"<p><p>The Na-Cl cotransporter (NCC) is a well-recognized regulator of ion transportation in the kidneys that facilitates Na<sup>+</sup> reabsorption in the distal convoluted tubule. It is also the pharmacologic inhibitory target of thiazide diuretics, a class of front-line antihypertensive agents that have been widely used for decades. NCC is a potent regulator of Na<sup>+</sup> reabsorption and homeostasis. Hence, its overactivation and suppression lead to hypertension and hypotension, respectively. Genetic mutations that affect NCC function contribute to several diseases such as Gordon and Gitelman syndromes. We summarized the role of NCC in various physiologic processes and pathological conditions, such as maintaining ion and water homeostasis, controlling blood pressure, and influencing renal physiology and injury. In addition, we discussed the recent advancements in understanding cryo-EM structure of NCC, the regulatory mechanisms and binding mode of thiazides with NCC, and novel physiologic implications of NCC in regulating the cross-talk between the immune system and adipose tissue or the kidneys. This review contributes to a comprehensive understanding of the pivotal role of NCC in maintaining ion homeostasis, regulating blood pressure, and facilitating kidney function and NCC's novel role in immune and metabolic regulation.</p>","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":" ","pages":"1306-1315"},"PeriodicalIF":3.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141564935","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Human CellPub Date : 2024-09-01Epub Date: 2024-07-12DOI: 10.1007/s13577-024-01102-w
Yalin Yuan, Mi Zou, Shuqin Wu, Congcong Liu, Liang Hao
{"title":"Recent advances in nanomaterials for the treatment of femoral head necrosis.","authors":"Yalin Yuan, Mi Zou, Shuqin Wu, Congcong Liu, Liang Hao","doi":"10.1007/s13577-024-01102-w","DOIUrl":"10.1007/s13577-024-01102-w","url":null,"abstract":"<p><p>Osteonecrosis of the femoral head (ONFH) is a condition that causes considerable pain and discomfort for patients, and its pathogenic mechanisms are not yet fully understood. While there have been many studies that suggest multiple factors may contribute to its development, current treatments involve both surgical and nonsurgical options. However, there is still much room for improvement in these treatment methods, particularly when it comes to preventing postoperative complications and optimizing surgical procedures. Nanomaterials, as a type of small molecule material, have shown great promise in treating bone tissue diseases, including ONFH. In fact, several nanocomposite materials have demonstrated specific effects in preventing ONFH, promoting bone tissue repair and growth, and optimizing surgical treatment. This article provides a comprehensive overview of current treatments for ONFH, including their advantages and limitations, and reviews the latest advances in nanomaterials for treating this condition. Additionally, this article explores the therapeutic mechanisms involved in using nanomaterials to treat ONFH and to identify new methods and ideas for improving outcomes for patients.</p>","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":" ","pages":"1290-1305"},"PeriodicalIF":3.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141591867","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The function of long non-coding RNA IFNG-AS1 in autoimmune diseases.","authors":"Jiale Zhao, Yibei Gui, Wei Wu, Xueqing Li, Lijun Wang, Hailin Wang, Yiyang Luo, Gang Zhou, Chengfu Yuan","doi":"10.1007/s13577-024-01103-9","DOIUrl":"10.1007/s13577-024-01103-9","url":null,"abstract":"<p><p>The prevalence of autoimmune diseases ranks as the third most common disease category globally, following cancer and heart disease. Numerous studies indicate that long non-coding RNA (lncRNA) plays a pivotal role in regulating human growth, development, and the pathogenesis of various diseases. It is more than 200 nucleotides in length and is mostly involve in the regulation of gene expression. Furthermore, lncRNAs are crucial in the development and activation of immune cells, with an expanding body of research exploring their association with autoimmune disorders in humans. LncRNA Ifng antisense RNA 1 (IFNG-AS1), a key regulatory factor in the immune system, also named NeST or TMEVPG1, is proximally located to IFNG and participates in the regulation of it. The dysregulation of IFNG-AS1 is implicated in the pathogenesis of several autoimmune diseases. This study examines the role and mechanism of IFNG-AS1 in various autoimmune diseases and considers its potential as a therapeutic target.</p>","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":" ","pages":"1325-1335"},"PeriodicalIF":3.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141617485","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Human CellPub Date : 2024-09-01Epub Date: 2024-07-16DOI: 10.1007/s13577-024-01104-8
Xiaoli Hu, Wan Wang, Teng Ma, Wanqi Zhang, Xiaohui Tang, Yingru Zheng, Xiuhui Zheng
{"title":"Long non-coding RNA SIX1-1 promotes proliferation of cervical cancer cells via negative transcriptional regulation of RASD1.","authors":"Xiaoli Hu, Wan Wang, Teng Ma, Wanqi Zhang, Xiaohui Tang, Yingru Zheng, Xiuhui Zheng","doi":"10.1007/s13577-024-01104-8","DOIUrl":"10.1007/s13577-024-01104-8","url":null,"abstract":"<p><p>Cervical cancer poses a significant health burden for women globally, and the rapid proliferation of cervical cancer cells greatly worsens patient prognosis. Long non-coding RNAs (lncRNAs) play a crucial role in regulating tumor cell proliferation. However, the involvement of lncRNAs in cervical cancer cell proliferation remains unclear. In this study, we investigated the lncRNA SIX1-1, which was found to be upregulated in cervical cancer tissues and cell lines. Functional assays revealed that knockdown of SIX1-1 inhibited cell proliferation in vitro and reduced tumor growth in vivo. Mechanistically, SIX1-1 was predominantly localized in the nucleus and could bind with DNMT1 protein. The expression of SIX1-1 enhanced the interaction of DNMT1 with RASD1 promoter, leading to the methylation of the promoter and decreased mRNA transcription. Then RASD1 downregulation activated the cAMP/PKA/CREB signaling pathway, promoting cell proliferation. Rescue experiments showed that knockdown of RASD1 restored the inhibited cell proliferation caused by decreased expression of SIX1-1, indicating that RASD1 acted as the functional mediator of SIX1-1. In conclusion, SIX1-1 promoted cervical cancer cell proliferation by modulating RASD1 expression. This suggests that targeting the SIX1-1/RASD1 axis could be a potential antitumor strategy for cervical cancer.</p>","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":" ","pages":"1446-1461"},"PeriodicalIF":3.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141628145","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Human CellPub Date : 2024-09-01Epub Date: 2024-08-05DOI: 10.1007/s13577-024-01113-7
Jan Strnadel, Mark A Valasek, Grace Y Lin, Huahui Lin, Ann M Ponsford Tipps, Sang Myung Woo, Ken Fujimura, Huawei Wang, Sunkyu Choi, Jack Bui, Christopher Hermosillo, Kristen Jepsen, Michael R Navarro, Jonathan A Kelber, Richard L Klemke, Michael Bouvet
{"title":"Development of 3D-iNET ORION: a novel, pre-clinical, three-dimensional in vitro cell model for modeling human metastatic neuroendocrine tumor of the pancreas.","authors":"Jan Strnadel, Mark A Valasek, Grace Y Lin, Huahui Lin, Ann M Ponsford Tipps, Sang Myung Woo, Ken Fujimura, Huawei Wang, Sunkyu Choi, Jack Bui, Christopher Hermosillo, Kristen Jepsen, Michael R Navarro, Jonathan A Kelber, Richard L Klemke, Michael Bouvet","doi":"10.1007/s13577-024-01113-7","DOIUrl":"10.1007/s13577-024-01113-7","url":null,"abstract":"<p><p>Neuroendocrine tumors (NETs) of the pancreas are rare neoplasms that present complex challenges to diagnosis and treatment due to their indolent course. The incidence of pancreatic neuroendocrine tumors has increased significantly over the past two decades. A limited number of pancreatic neuroendocrine cell lines are currently available for the research. Here, we present 3D-iNET ORION, a novel 3-dimensional (spheroid) cell line, isolated from human pancreatic neuroendocrine tumor liver metastasis. Three-dimensionally grown (3D) cancer cell lines have gained interest over the past years as 3D cancer cell lines better recapitulate the in vivo structure of tumors, and are more suitable for in vitro and in vivo experiments. 3D-iNET ORION cancer cell line showed high potential to form tumorspheres when embedded in Matrigel matrix and expresses synaptophysin and EpCAM. Electron microscopy analysis of cancer cell line proved the presence of dense neurosecretory granules. When xenografted into athymic mice, 3D-iNET ORION cells produce slow-growing tumors, positive for chromogranin and synaptophysin. Human Core Exome Panel Analysis has shown that 3DiNET ORION cell line retains the genetic aberration profile detected in the original tumor. In conclusion, our newly developed neuroendocrine cancer cell line can be considered as a new research tool for in vitro and in vivo experiments.</p>","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":" ","pages":"1593-1601"},"PeriodicalIF":3.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11341600/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141894748","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Assessing the antitumor effects of metformin on ovarian clear cell carcinoma.","authors":"Satoshi Takemori, Tohru Morisada, Makoto Osaka, Momoe Watanabe, Atsushi Tajima, Shinji Tanigaki, Yoichi Kobayashi","doi":"10.1007/s13577-024-01116-4","DOIUrl":"10.1007/s13577-024-01116-4","url":null,"abstract":"<p><p>Developing novel therapies that outperform the existing chemotherapeutic treatments is required for treatment-resistant ovarian clear cell carcinoma. We investigated the antitumor effect of metformin on ovarian clear cell carcinoma, enhancement of the antitumor effect by its combination with chemotherapy, and its molecular regulatory mechanism. First, we evaluated the viability of ovarian clear cell carcinoma lines using the water-soluble tetrazolium-1 assay and found that metformin suppressed cell viability. Cell viability was significantly suppressed by co-treatment with cisplatin and metformin. In contrast, co-treatment with paclitaxel and metformin showed no significant difference in viability compared with the group without metformin. Western blot analysis showed increased phosphorylation of AMP-activated protein kinase in some cell lines and suppressed phosphorylation of the mammalian target of rapamycin in a particular cell line. Flow cytometry analysis revealed a significant increase in the rate of apoptosis in the metformin-treated group and rate of cell cycle arrest at the G2/M phase in a particular cell line. These results indicated that metformin may be effective against cultured ovarian clear cell carcinoma cells, particularly in combination with cisplatin.</p>","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":" ","pages":"1462-1474"},"PeriodicalIF":3.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141903393","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Human CellPub Date : 2024-09-01Epub Date: 2024-06-11DOI: 10.1007/s13577-024-01086-7
Wenting Bi, Xiaodan Mu, Yongfeng Li, Qingyan Sun, Lei Xiang, Min Hu, Huawei Liu
{"title":"Delivery of neurotrophin-3 by RVG-Lamp2b-modified mesenchymal stem cell-derived exosomes alleviates facial nerve injury.","authors":"Wenting Bi, Xiaodan Mu, Yongfeng Li, Qingyan Sun, Lei Xiang, Min Hu, Huawei Liu","doi":"10.1007/s13577-024-01086-7","DOIUrl":"10.1007/s13577-024-01086-7","url":null,"abstract":"<p><p>We aim to investigate the effect of RVG-Lamp2b-modified exosomes (exos) loaded with neurotrophin-3 (NT-3) on facial nerve injury. Exos were collected from control cells (Ctrl Exo) or bone marrow mesenchymal stem cells co-transfected with RVG-Lamp2b and NT-3 plasmids (RVG-NT-3 Exo) by gradient centrifugation and identified by western blotting, transmission electron microscopy, and nanoparticle tracking analysis. Effect of RVG-NT-3 Exo on oxidative stress damage was determined by analysis of the morphology, viability, and ROS production of neurons. Effect of RVG-NT-3 Exo on facial nerve axotomy (FNA) was determined by detecting ROS production, neuroinflammatory reaction, microglia activation, facial motor neuron (FMN) death, and myelin sheath repair. Loading NT-3 and modifying with RVG-Lamp2b did not alter the properties of the exos. Moreover, RVG-NT-3 Exo could effectively target neurons to deliver NT-3. Treatment with RVG-NT-3 Exo lowered H<sub>2</sub>O<sub>2</sub>-induced oxidative stress damage in primary neurons and Nsc-34 cells. RVG-NT-3 Exo treatment significantly decreased ROS production, neuroinflammatory response, FMN death, and elevated microglia activation and myelin sheath repair in FNA rat models. Our findings suggested that RVG-NT-3 Exo-mediated delivery of NT-3 is effective for the treatment of facial nerve injury.</p>","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":" ","pages":"1378-1393"},"PeriodicalIF":3.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141301983","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Human CellPub Date : 2024-09-01Epub Date: 2024-06-16DOI: 10.1007/s13577-024-01091-w
Yan Wang, Yi Zhang, Xiaowei Qi
{"title":"EP300 promotes tumor stemness via epigenetic activation of CRISP3 leading to lobaplatin resistance in triple-negative breast cancer.","authors":"Yan Wang, Yi Zhang, Xiaowei Qi","doi":"10.1007/s13577-024-01091-w","DOIUrl":"10.1007/s13577-024-01091-w","url":null,"abstract":"<p><p>Lobaplatin shows antitumor activity against a wide range of tumors, including triple-negative breast cancer (TNBC), and has been linked to cancer stem cell pool. Here, we investigated the molecular mechanisms behind lobaplatin resistance and stemness in vitro and in vivo. Two chemoresistance-related GEO data sets (GSE70690 and GSE103115) were included to screen out relevant genes. Cysteine-rich secretory protein 3 (CRISP3) was found to be overexpressed in lobaplatin-resistant TNBC and related to poor diagnosis. CRISP3 expression was significantly correlated with tumor stemness markers in lobaplatin-resistant cells. E1A-associated protein p300 (EP300) regulated CRISP3 expression by affecting the H3K27ac modification of the CRISP3 promoter. In addition, knocking down EP300 curbed the malignant biological behavior of lobaplatin-resistant cells, which was antagonized by CRISP3 overexpression. Collectively, our results highlight the EP300/CRISP3 axis as a key driver of lobaplatin resistance in TNBC and suggest that therapeutic targeting of this axis may be an effective strategy for enhancing platinum sensitivity in TNBC.</p>","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":" ","pages":"1475-1488"},"PeriodicalIF":3.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141327940","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}