European journal of cell biology最新文献

{"title":"Ropivacaine and lidocaine inhibit SaOS-2 osteosarcoma cell proliferation and invasion via mitochondrial dysfunction and apoptosis","authors":"Inna Zumberg,&nbsp;Amir Hashemi,&nbsp;Masoumeh Ezati,&nbsp;Larisa Chmelikova,&nbsp;Katerina Ingrova,&nbsp;Vratislav Cmiel","doi":"10.1016/j.ejcb.2025.151501","DOIUrl":"10.1016/j.ejcb.2025.151501","url":null,"abstract":"<div><div>Local anesthetics are routinely used for pain management, yet their broader effects on cancer cells remain incompletely understood. Here, we investigate the impact of ropivacaine hydrochloride and lidocaine hydrochloride monohydrate on SaOS-2 human osteosarcoma cells using a series of <em>in vitro</em> assays. Our findings indicate that both anesthetics markedly reduce cell viability and proliferation, as measured by XTT and Colony formation assays, respectively. Mechanistic studies reveal significant disruption of mitochondrial function, evidenced by decreased membrane potential, enhanced mitochondrial superoxide production, and pronounced mitochondrial fragmentation. Concurrently, the expression of matrix metalloproteinases (MMP-2 and MMP-9) is downregulated, while pro-apoptotic markers (Caspase-3, Caspase-9, and BAX) are upregulated. Neither agent alters Vimentin or E-cadherin expression, suggesting a limited effect on epithelial-mesenchymal transition pathways. Notably, lidocaine and ropivacaine also inhibit SaOS-2 cell migration and invasion, as demonstrated by Scratch, single-cell migration, and Transwell invasion assays. Furthermore, both agents suppress alkaline phosphatase activity, a hallmark associated with osteosarcoma differentiation and metastatic potential. Taken together, these results support the conclusion that ropivacaine and lidocaine exert broad anti-tumor effects by impairing both mitochondrial homeostasis and the invasive phenotype in osteosarcoma cells. Their capacity to mitigate core hallmarks of malignancy underscores the need for further investigation into local anesthetics as potential adjuvant therapies for osteosarcoma.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"104 3","pages":"Article 151501"},"PeriodicalIF":4.5,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144501110","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":"Genetic compensation highlights the importance of neural cell adhesion molecule Ncam1 paralogs in balancing signaling pathways during zebrafish lateral line development","authors":"Annemarie Lange,&nbsp;Martin Bastmeyer,&nbsp;Joachim Bentrop","doi":"10.1016/j.ejcb.2025.151500","DOIUrl":"10.1016/j.ejcb.2025.151500","url":null,"abstract":"<div><div>The neural cell adhesion molecule NCAM1 is essential for neuronal development and enables organized cell migration, axon growth, and fasciculation. As a result of genome duplication in zebrafish, the paralogs Ncam1a and Ncam1b arose. Our previously published findings using morpholino knockdown experiments demonstrated the essential role of Ncam1b in the development of the zebrafish lateral line system, a mechanosensory organ critical for detecting water movements. <em>ncam1b</em> morphants exhibited severe defects, including impaired primordium migration, disrupted proneuromast deposition, and reduced cell proliferation within the primordium. These defects were linked to a disrupted interaction between Ncam1b and Fgfr1a, which led to compromised proliferation and abnormal lateral line development. The current study reveals that <em>ncam1b</em> mutants, however, unlike morphants, do not show this severe phenotype. Instead, we observed subtle alterations, including altered FGF and Wnt signaling and a redistribution of proliferating cells within the primordium. Notably, <em>ncam1b</em> mutants displayed elevated levels of the paralog <em>ncam1a</em> mRNA. The knockdown of either <em>ncam1a</em> or <em>upf3a</em> in <em>ncam1b</em> mutants resulted in a phenotype resembling that of <em>ncam1b</em> morphants. Upf3a is a key regulator of genetic compensation, a well-known phenomenon in zebrafish research. This supports the hypothesis that upregulated <em>ncam1a</em> compensates for the loss of <em>ncam1b</em>, facilitating normal lateral line development. These findings emphasize the essential role of Ncam1 in zebrafish lateral line development and suggest that the retention of both paralogs, <em>ncam1a</em> and <em>ncam1b</em>, acts as a protective mechanism to ensure the preservation of critical Ncam1 functions after gene duplication.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"104 3","pages":"Article 151500"},"PeriodicalIF":4.5,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144471038","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":"Editorial – Advances in cell, tissue, organ engineering, and organoid technology","authors":"Shoen Kume,&nbsp;Yoichi Tagawa,&nbsp;Ryuichi Okamoto,&nbsp;Hiroshi Kawasaki","doi":"10.1016/j.ejcb.2025.151499","DOIUrl":"10.1016/j.ejcb.2025.151499","url":null,"abstract":"","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"104 3","pages":"Article 151499"},"PeriodicalIF":4.3,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144316187","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":"Considerations for developing CYP induction assays in hepatocytes: Insights from a multilaboratory study","authors":"Hiroko Toyoda ,&nbsp;Ayaka Nozue ,&nbsp;Yuki Nishida ,&nbsp;Yasuko Yakabe ,&nbsp;Yasuhiko Aiki ,&nbsp;Yukiko Ueyama-Toba ,&nbsp;Kazuo Takayama ,&nbsp;Hiroyuki Mizuguchi ,&nbsp;Chihiro Mori ,&nbsp;Yu-suke Torisawa ,&nbsp;Yoko Sakai ,&nbsp;Takahiro Iwao ,&nbsp;Tamihide Matsunaga ,&nbsp;Shinichiro Horiuchi ,&nbsp;Daiju Yamazaki ,&nbsp;Seiichi Ishida ,&nbsp;Nobuhiko Kojima ,&nbsp;Kosuke Inamura ,&nbsp;Yasuyuki Sakai ,&nbsp;Masaki Nishikawa ,&nbsp;Yuzuru Ito","doi":"10.1016/j.ejcb.2025.151497","DOIUrl":"10.1016/j.ejcb.2025.151497","url":null,"abstract":"<div><div>Cytochrome P450 (CYP) induction studies using primary human hepatocytes (PHH) were conducted across seven laboratories. Standard operating procedures (SOPs) were developed and distributed, ensuring all laboratories used PHH from the same donor and CYP inducers prepared at a single location. In each laboratory, PHH was seeded, cultured, and tested for CYP induction. Induction levels of CYP1A2, CYP2B6, and CYP3A4 mRNA were analyzed by collecting and processing PHH lysates at one site. A review of laboratory work records revealed differences in PHH seeding density and CYP inducer treatment times, which were suggested as potential sources of variability in RNA yield and CYP induction patterns. Follow-up tests confirmed that both seeding density and induction duration significantly influenced CYP mRNA expression levels, beyond lot-to-lot differences in PHH. Despite adhering to shared SOPs, these inconsistencies contributed to variability in study results. To address these challenges, we discuss key considerations for SOP development and implementation to improve reproducibility in CYP induction assays.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"104 3","pages":"Article 151497"},"PeriodicalIF":4.5,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144306430","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":"Self-organization and applications of neural organoids","authors":"Hideya Sakaguchi","doi":"10.1016/j.ejcb.2025.151496","DOIUrl":"10.1016/j.ejcb.2025.151496","url":null,"abstract":"<div><div>Organoid technology has become a field that attract many researcher’s attention and involvement. “Organoid” is a coined word which means organ like-tissue (Organ+oid), and organoid is determined as stem cell-derived three-dimensional (3D) tissues that recapitulate developmental processes and tissue specific function in vivo. Generally, they are derived from pluripotent stem cells (PSCs) including induced pluripotent stem cells (iPSCs) and embryonic stem cells (ESCs), or from tissue stem cells. The first report that created human 3D cerebral tissue arose in 2008 which is currently considered as the pioneering work of “neural organoid” (Eiraku et al., 2008, Sasai 2013a, Sasai 2013b). The neural organoids provide living human neural tissues that bring opportunities to study human development, human neuroscience, neurological and psychiatric disorders, and evolutions. The neural organoid can be said as “cut &amp; paste” of developmental biological process into a dish. Thus, understanding the background of neural organoid needs developmental knowledge, but current organoid researches looks to use organoid as a tool to study the aim that the researchers want to focus. This leads the organoid research more methodological, and the improvement or sophistication of organoid methods has still been difficult for most of new coming researchers. For this problem, this review provide insights of how to assemble organoid methods from viewpoints of development especially from morphological/structual changes. In this review, I start from the brief history of how neural organoid research emerged from developmental biology. Then I introduce some interesting aspects of neural organoid generation focusing on self-organization of regions and structures. From the viewpoint of a developer of this field, this review also show how to think and adjust the methods to generate novel regional organoids taking hippocampal organoids as an example. Regarding structural self-organization I will introduce cerebral organoid for an example of layer organization in a dish. By showing background knowledge with scientific achievements and interesting aspects, this review will help researchers who want to create novel neural organoids.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"104 2","pages":"Article 151496"},"PeriodicalIF":4.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144185230","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":"Tri-culture model of intestinal epithelial cell, macrophage, and bacteria for the triggering of inflammatory bowel disease on a microfluidic device","authors":"Shiori Tamura ,&nbsp;Clarissa Ellice Talitha Pasang ,&nbsp;Minami Tsuda ,&nbsp;Shilan Ma ,&nbsp;Hiromasa Shindo ,&nbsp;Noriyuki Nagaoka ,&nbsp;Tomoki Ohkubo ,&nbsp;Yoichi Fujiyama ,&nbsp;Miho Tamai ,&nbsp;Yoh-ichi Tagawa","doi":"10.1016/j.ejcb.2025.151495","DOIUrl":"10.1016/j.ejcb.2025.151495","url":null,"abstract":"<div><div>Inflammatory bowel disease (IBD) involves gastrointestinal inflammation, due to intestinal epithelial barrier destruction caused by excessive immune activation. Conventional cell culture systems do not provide a model system that can recapitulate the complex interactions between epithelial cells, immune cells, and intestinal bacteria. To address this, we developed a microfluidic device that mimics the inflammatory response associated with microbial invasion of the intestinal mucosa. The device consisted of two media channels, an upper and a lower channel, and a porous membrane between these channels on which C2BBe1 intestinal epithelial cells were seeded to form a tight junction layer. Each electrode was placed in contact with both channels to continuously monitor the tight junction state. Fresh medium flow allowed bacterial numbers to be controlled and bacterial toxins to be removed, allowing co-culture of mammalian cells and bacteria. In addition, RAW264 macrophage cells were attached to the bottom of the lower channel. By introducing <em>E. coli</em> into the lower channel, the RAW264 cells were activated and produced TNF-α, successfully recapitulating a culture model of inflammation in which the C2BBe1cell tight junction layer was destroyed. The main structure of the device was initially made of polydimethylsiloxane to facilitate its widespread use, but with a view to introducing anaerobic bacteria in the future, a similar phenomenon was successfully reproduced using polystyrene. When TPCA-1, an IκB kinase 2 inhibitor was added into this IBD culture model, the tight junction destruction was significantly suppressed. The results suggest that this IBD culture model also is useful as a screening system for anti-IBD drugs.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"104 2","pages":"Article 151495"},"PeriodicalIF":4.5,"publicationDate":"2025-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144117049","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":"microRNA-183–5p induces cell density-dependent apoptosis through the regulation of Presenilin 2","authors":"Yuki Yabuuchi ,&nbsp;Yosuke Matsuno ,&nbsp;Kai Yazaki ,&nbsp;Wei Zhen Ting ,&nbsp;Kengo Nishino ,&nbsp;Sosuke Matsumura ,&nbsp;Kenya Kuramoto ,&nbsp;Kazufumi Yoshida ,&nbsp;Masashi Matsuyama ,&nbsp;Takumi Kiwaoto ,&nbsp;Yuko Morishima ,&nbsp;Nobuyuki Hizawa","doi":"10.1016/j.ejcb.2025.151494","DOIUrl":"10.1016/j.ejcb.2025.151494","url":null,"abstract":"<div><div>Cells undergo apoptosis under dense culture condition to maintain homeostasis. Impaired apoptosis may contribute to the excessive accumulation of pathogenetic cells in such diseases as cancer and organ fibrosis. Elucidating the molecular mechanisms regulating cell density-dependent apoptosis may provide novel therapeutic strategy against these diseases. We have reported Notch signaling, activated by γ-secretase under dense culture condition, regulates cell density-dependent apoptosis through the induction of IL-6. Presenilin 2 (PSEN2) is a subunit of γ-secretase and has been shown to modulate apoptosis. The role for PSEN2 in cell density-dependent apoptosis and Notch signaling activation, however, remains unclear. Here, we show a crucial role for PSEN2 in the regulation of cell density-dependent apoptosis in NIH 3T3 cells. PSEN2 protein primarily existed as C-terminal fragment (CTF). PSEN2 CTF expression was upregulated as cell density increased. PSEN2 regulated the development of apoptosis, which is accompanied by increased Bcl-2 expression, decreased Bax expression, and activated PI3K/Akt pathway. PSEN2 is predicted to be targeted by microRNA-183–5p (miR-183–5p) by several algorithms. We verified miR-183–5p directly regulates PSEN2 expression and induces apoptosis. In conclusion, our results demonstrate a crucial role of PSEN2 and its regulation by miR-183–5p in the regulation of cell density-dependent apoptosis.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"104 2","pages":"Article 151494"},"PeriodicalIF":4.5,"publicationDate":"2025-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143941191","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":"Role of the sodium/calcium exchanger type 3 in cancer cells","authors":"Galvankova Kristina ,&nbsp;Rezuchova Ingeborg ,&nbsp;Klena Ladislav ,&nbsp;Grman Marian ,&nbsp;Gazova Simona ,&nbsp;Liskova Veronika ,&nbsp;Kozovska Zuzana ,&nbsp;Roller Ladislav ,&nbsp;Babula Petr ,&nbsp;Krizanova Olga","doi":"10.1016/j.ejcb.2025.151493","DOIUrl":"10.1016/j.ejcb.2025.151493","url":null,"abstract":"<div><div>The sodium/calcium exchanger (NCX) type 1 has been well described in various cancers, but little is known about the other two NCX types (NCX2 and NCX3). In this study, we used the selective blocker of NCX3 – YM-244769 to investigate changes in apoptosis induction, migration, proliferation, intracellular calcium and ATP in four cancer cell lines – DLD1, HeLa, MDA-MB-231 and JIMT1. In all four cell lines we observed a concentration-dependent increase in the number of apoptotic cells, as well as reduced migration and proliferation. Induction of hypoxic conditions did not alter the response of these cells to YM-244769 in any of the above-mentioned parameters. These results indicate the role of NCX3 in cancer cell migration, proliferation and apoptosis, as inhibition of NCX1 by the specific blocker SEA0400 had no significant effect on these parameters. However, we verified the effect of NCX3 inhibition by using CRISPR/Cas9 to generate clones in which the <em>SLC8A3</em> (NCX3) gene was deleted, and we obtained the same results. In addition, mitochondrial respiration was impaired in the clones with NCX3 knocked-out, suggesting that NCX3 also play a role in bioenergetics. In conclusion, we have clearly shown that NCX3 plays an important anti-apoptotic, pro-migratory and proliferative role in the cancer cells by affecting mitochondrial bioenergetics, thus supporting their survival and fate.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"104 2","pages":"Article 151493"},"PeriodicalIF":4.5,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143904048","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":"Combining prelamin A accumulation and oxidative stress: A strategy to target glioblastoma","authors":"Maria Vittoria Marvi ,&nbsp;Camilla Evangelisti ,&nbsp;Camilla Bruna Cerchier ,&nbsp;Antonietta Fazio ,&nbsp;Irene Neri ,&nbsp;Foteini-Dionysia Koufi ,&nbsp;William Blalock ,&nbsp;Vittoria Cenni ,&nbsp;Matteo Zoli ,&nbsp;Sofia Asioli ,&nbsp;Luca Morandi ,&nbsp;Enrico Franceschi ,&nbsp;Lucia Manzoli ,&nbsp;Cristina Capanni ,&nbsp;Stefano Ratti","doi":"10.1016/j.ejcb.2025.151491","DOIUrl":"10.1016/j.ejcb.2025.151491","url":null,"abstract":"<div><div>Glioblastoma is the most aggressive and prevalent tumor of the Central Nervous System (CNS) with limited treatment options and poor patient outcomes. Standard therapies, including surgery, radiation, and chemotherapy, provide only modest survival benefits, highlighting the need for innovative therapeutic approaches. This study investigates a novel strategy targeting prelamin A processing in glioblastoma cells. By inhibiting the farnesyltransferase enzyme using SCH66336 (Lonafarnib), we promote the accumulation of lamin A precursor (prelamin A) in glioblastoma cells, thereby increasing their susceptibility to oxidative stress induced by Menadione administration, while sparing normal human astrocytes. Notably, the combined SCH66336-Menadione treatment reduced cell proliferation, modified the expression of stemness markers, and decreased viability in patient-derived glioblastoma stem cells, which represent the population responsible for tumor aggressiveness and recurrence. These findings indicate that inhibiting prelamin A processing could be a potential strategy to reduce glioblastoma aggressiveness and enhance therapeutic outcomes, particularly for treatment-resistant glioblastoma stem cell populations. This approach shows potential for integrating prelamin A processing disruption as a complementary strategy in glioblastoma therapy.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"104 2","pages":"Article 151491"},"PeriodicalIF":4.5,"publicationDate":"2025-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143885938","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":"Holotomographic microscopy reveals label-free quantitative dynamics of endothelial cells during endothelialization","authors":"William D. Leineweber ,&nbsp;Gabriela Acevedo Munares ,&nbsp;Christian Leycam ,&nbsp;Raul Michael ,&nbsp;Juliette Noyer ,&nbsp;Patrick Jurney","doi":"10.1016/j.ejcb.2025.151492","DOIUrl":"10.1016/j.ejcb.2025.151492","url":null,"abstract":"<div><div>Holotomograhic microscopy (HTM) has emerged as a non-invasive imaging technique that offers high-resolution, quantitative 3D imaging of biological samples. This study explores the application of HTM in examining endothelial cells (ECs). HTM overcomes the limitations of traditional microscopy methods in capturing the real-time dynamics of ECs by leveraging the refractive index (RI) to map 3D distributions label-free. This work demonstrates the utility of HTM in visualizing key cellular processes during endothelialization, wherein ECs anchor, adhere, migrate, and proliferate. Leveraging the high resolution and quantitative power of HTM, we show that lipid droplets and mitochondria are readily visualized, enabling more comprehensive studies on their respective roles during endothelialization. The study highlights how HTM on a commercial instrument can uncover novel insights into HUVEC cell behavior, offering potential applications in medical diagnostics and research, particularly in developing treatments for cardiovascular diseases. This advanced imaging technique not only enhances our understanding of EC biology but also presents a significant step forward in the study of cardiovascular diseases, providing a robust platform for future research and therapeutic development.</div></div>","PeriodicalId":12010,"journal":{"name":"European journal of cell biology","volume":"104 2","pages":"Article 151492"},"PeriodicalIF":4.5,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143878935","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}