Experimental cell research最新文献

{"title":"The cystogenic effects of ouabain in autosomal dominant polycystic kidney disease require cell caveolae","authors":"Jordan Trant,&nbsp;Gladis Sanchez,&nbsp;Jeffery P. McDermott,&nbsp;Gustavo Blanco","doi":"10.1016/j.yexcr.2024.114356","DOIUrl":"10.1016/j.yexcr.2024.114356","url":null,"abstract":"<div><div>We have previously shown that the hormone ouabain is a circulating factor which can accelerate the progression of autosomal dominant polycystic kidney disease (ADPKD). At physiologic concentrations, ouabain increases cyst area and fibrosis in kidneys from ADPKD but not wildtype mice. These effects are due to an increased affinity for ouabain by its receptor, Na,K-ATPase (NKA), in the kidneys of ADPKD mice which leads to over-activation of NKA signaling function. Previous studies suggested that ouabain's stimulation of NKA signal transduction is mediated by NKA located within cell caveolae. Here, we determined whether caveolae are involved in the ouabain-induced progression of ADPKD cysts. We generated an ADPKD mouse with a global knockout of the main structural component of caveolae, caveolin-1 (CAV1), which we confirmed lacks caveolae in the kidney. When given physiological amounts of ouabain for 5 months, <em>Pkd1</em>^{<em>RC/RC</em>}<em>Cav1</em>^{<em>−/−</em>} mice did not exhibit any changes in cyst progression, contrasting with the <em>Pkd1</em>^{<em>RC/RC</em>} mice which showed a significant increase in cystic area and kidney fibrosis. Also, measures of ouabain-induced cell proliferation, including the number of Ki67-positive nuclei and phosphorylation of the extracellular regulated kinase (ERK) and protein kinase B (Akt), did not increase in the <em>Pkd1</em>^{<em>RC/RC</em>}<em>Cav1</em>^{<em>−/−</em>} mice compared with the <em>Pkd1</em>^{<em>RC/RC</em>} mice. Moreover, the abnormally increased affinity for ouabain of NKA in <em>Pkd1</em>^{<em>RC/RC</em>} mice was restored to wildtype levels in the <em>Pkd1</em>^{<em>RC/RC</em>}<em>Cav1</em>^{<em>−/−</em>} mice. This work highlights the role of caveolae in ouabain-induced NKA signaling and ADPKD cyst progression.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"444 1","pages":"Article 114356"},"PeriodicalIF":3.3,"publicationDate":"2024-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142715879","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":"Fbxo11 maintains mitochondrial function and prevents podocyte injury in adriamycin-induced nephropathy by mediating the ubiquitin degradation of Fosl2","authors":"Yanhua Jin,&nbsp;Huan Wang,&nbsp;Yu Xin,&nbsp;Yanning Zhang","doi":"10.1016/j.yexcr.2024.114345","DOIUrl":"10.1016/j.yexcr.2024.114345","url":null,"abstract":"<div><div>Mitochondrial dysfunction is a pivotal factor in the onset of podocyte damage, which is a central component in the pathogenesis of nephrotic syndrome (NS). However, the precise mechanisms underlying the changes in podocyte mitochondria remain elusive. Our study aims to clarify the potential mechanisms involved in the role of F-box protein 11 (Fbxo11) in NS, specifically concentrating on its impact on mitochondrial function. A mouse model was established by tail vein injection of adriamycin (ADR, 10 mg/kg) and was infected with lentivirus overexpressing Fbxo11 (lenti-Fbxo11-OE). Mouse podocytes (MPC-5) were infected with lenti-Fbxo11-OE, followed by treatment with 0.4 μg/mL of ADR. We identified the decreased expression of Fbxo11 in mouse renal tissues and MPC-5 cells induced by ADR. Lenti-Fbxo11-OE intervention relieved ADR-induced glomerular lesion, podocyte injury, and mitochondrial dysfunction. In vitro, overexpression of Fbxo11 in mouse podocytes improved mitochondrial function and reduced podocyte damage, thereby inhibiting podocyte apoptosis. Mechanistically, Fbxo11 decreased the protein expression of Fosl2 through ubiquitin-dependent proteasomal degradation. Rescue experiments revealed that overexpression of Fosl2 abolished the protective effects of Fbxo11 overexpression on mitochondrial damage and podocyte injury. Importantly, the regulatory effects of the Fbxo11/Fosl2 axis were reversed when treated with the mitochondrial fission inhibitor mdivi-1. Taken together, our results demonstrated that Fbxo11-mediated protein degradation of Fosl2 is critical for maintaining mitochondrial function and preventing podocyte injury during NS.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"444 1","pages":"Article 114345"},"PeriodicalIF":3.3,"publicationDate":"2024-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142709147","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":"MOTS-c relieves hepatocellular carcinoma resistance to TRAIL-induced apoptosis under hypoxic conditions by activating MEF2A","authors":"Haiying Shen ,&nbsp;Junjie Nie ,&nbsp;Xiaojun Wang ,&nbsp;Guangqing Li ,&nbsp;Liwei Zhao ,&nbsp;Yuji Jin ,&nbsp;Lianhai Jin","doi":"10.1016/j.yexcr.2024.114354","DOIUrl":"10.1016/j.yexcr.2024.114354","url":null,"abstract":"<div><h3>Background</h3><div>Mitochondrial ORF of the 12S rRNA type-c (MOTS-c) as an AMPK agonist can regulate the expression of adaptive nuclear genes to promote cell homeostasis. However, the investigation of MOTS-c in hepatocellular carcinoma (HCC) is insufficient. This study aims to reveal the role of MOTS-c on HCC cell apoptosis.</div></div><div><h3>Methods</h3><div>Huh7 and HCCLM3 cells were incubated with MOTS-c under a hypoxic condition. MOTS-c levels were quantified by enzyme-linked immunosorbent assay in the peripheral blood of HCC patients and healthy controls. Cell viability was detected by 3-(4,5-Dimethylthazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Cell apoptosis was investigated by flow cytometry and Tunel assay. Protein expression was detected by western blotting or immunohistochemistry assay. Dual-luciferase reporter assay and chromatin immunoprecipitation assay were performed to identify the association among myocyte enhancer factor 2A (MEF2A), death receptor 4 (DR4) and DR5. A tumor-bearing nude mouse model was conducted to assess the effect of MOTS-c on HCC tumor formation <em>in vivo</em>.</div></div><div><h3>Results</h3><div>MOTS-c levels in the peripheral blood of HCC patients were significantly lower compared to healthy individuals. MOTS-c promoted HCC cell apoptosis under hypoxia conditions. Hypoxia stimulation decreased the protein expression of MEF2A, DR4, DR5, fas-associating via death domain (FADD) and caspase-8, while these effects were attenuated after MOTS-c treatment. MOTS-c induced TRAIL-induced apoptosis of HCC cells by activating MEF2A through the phosphorylation of AMPK under hypoxia treatment. In addition, MEF2A transcriptionally up-regulated DR4 and DR5. MOTS-c activated MEF2A to regulate DR4 and DR5 expression, further mediating TRAIL-induced apoptosis. Further, MOTS-c treatment relieved hypoxia-induced tumor growth <em>in vivo</em>.</div></div><div><h3>Conclusion</h3><div>MOTS-c relieved hypoxia-induced HCC cell resistance to TRAIL-caused apoptosis by activating MEF2A.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"444 1","pages":"Article 114354"},"PeriodicalIF":3.3,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142709197","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":"DDX18 influences chemotherapy sensitivity in colorectal cancer by regulating genomic stability","authors":"Wenchao Zhao ,&nbsp;Qingqing Luo ,&nbsp;Han Zhan ,&nbsp;Zhen Du ,&nbsp;Tan Deng ,&nbsp;Huaxin Duan","doi":"10.1016/j.yexcr.2024.114344","DOIUrl":"10.1016/j.yexcr.2024.114344","url":null,"abstract":"<div><div>Chromosomal Instability (CIN) encompasses approximately 65 %–70 % of colorectal cancer (CRC) patients, playing a pivotal role in tumor progression. However, controversies persist regarding the molecular characteristics and treatment strategies associated with these patients. Integrative colorectal cancer proteogenomic analysis identified DDX18 in colorectal cancer. We investigated the molecular mechanisms underlying the regulation of colorectal cancer by the R-loop binding protein DDX18 using colon cancer tissues, cell lines and patient-derived organoids. Our findings revealed that DDX18 expression positively correlates with the expression of genomic instability marker R-loops. Moreover, heightened DDX18 expression delays the completion of DNA damage repair, leading to an increase in double-strand DNA breaks, thereby promoting genomic instability. Notably, the upregulation of DDX18 enhances sensitivity to DNA-damaging. This study elucidated DDX18 beyond participating in fundamental physiological functions, may play a crucial role in the regulation of genomic stability, and also provides a powerful resource for further functional exploration of DDX18 in cancer progression and therapeutic application.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"444 1","pages":"Article 114344"},"PeriodicalIF":3.3,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142692853","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":"Seven Theorems of Joseph G. Gall","authors":"Ji-Long Liu","doi":"10.1016/j.yexcr.2024.114343","DOIUrl":"10.1016/j.yexcr.2024.114343","url":null,"abstract":"<div><div>On June 30, 2020, Professor Joseph Grafton Gall announced his retirement at 92. On August 13, 2020, Joe's former trainees and colleagues held a retirement celebration online to celebrate Joe's “Remarkable Career with Astonishing Discoveries”, covering Joe's nearly 70 years of education and research. As a representative of Joe's trainees in the 2000s, I gave a speech titled “Seven Theorems of Joe”. On September 12, 2024, Joe passed away peacefully, at 96. In memoriam, here I expand and update my previous speech and explain the “Seven Theorems of Joseph G. Gall”, a scientists' scientist.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"444 1","pages":"Article 114343"},"PeriodicalIF":3.3,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142681152","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":"A semi-permeable insert culture model for the distal part of the nephron with human and mouse tubuloid epithelial cells","authors":"E. Dilmen ,&nbsp;C.J.A. Olde Hanhof ,&nbsp;F.A. Yousef Yengej ,&nbsp;C.M.E. Ammerlaan ,&nbsp;M.B. Rookmaaker ,&nbsp;I. Orhon ,&nbsp;J. Jansen ,&nbsp;M.C. Verhaar ,&nbsp;J.G. Hoenderop","doi":"10.1016/j.yexcr.2024.114342","DOIUrl":"10.1016/j.yexcr.2024.114342","url":null,"abstract":"<div><div>Tubuloids are advanced <em>in vitro</em> models obtained from adult human or mouse kidney cells with great potential for modelling kidney function in health and disease. Here, we developed a polarized human and mouse tubuloid epithelium on cell culture inserts, namely Transwell™ filters, as a model of the distal nephron with an accessible apical and basolateral side that allow for characterization of epithelial properties such as leak-tightness and epithelial resistance. Tubuloids formed a leak-tight and confluent epithelium on Transwells™ and the human tubuloids were differentiated towards the distal part of the nephron. Differentiation induced a significant upregulation of mRNA and protein expression of crucial segment transporters/channels NKCC2 (thick ascending limb of the loop of Henle), NCC (distal convoluted tubule), AQP2 (connecting tubule and collecting duct) and Na⁺/K⁺-ATPase (all segments) in a polarized fashion. In conclusion, this study illustrates the potential of human and mouse tubuloid epithelium on Transwells™ for studies of tubuloid epithelium formation and tubuloid differentiation towards the distal nephron. This approach holds great promise for assisting future research towards kidney (patho)physiology and transport function.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"444 1","pages":"Article 114342"},"PeriodicalIF":3.3,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142681103","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":"Knockdown of Leucine-rich alpha-2-glycoprotein 1 alleviates renal ischemia-reperfusion injury by inhibiting NOX4-mediated apoptosis, inflammation, and oxidative stress","authors":"Jianfeng Ye,&nbsp;Cheng Qiu,&nbsp;Lexi Zhang","doi":"10.1016/j.yexcr.2024.114341","DOIUrl":"10.1016/j.yexcr.2024.114341","url":null,"abstract":"<div><div>Renal ischemia-reperfusion (I/R) injury leads mainly to acute kidney injury. Leucine-rich alpha-2-glycoprotein 1 (LRG) is upregulated in kidney tissues of mice after renal I/R injury. However, its role in renal I/R injury has not been fully elucidated. A mouse model of renal I/R injury was constructed by unilateral renal pedicle clamping and reperfusion. Mice undergoing I/R procedures exhibited renal function impairment and increased LRG protein expression compared with mice receiving sham operations. Tail vein injection with lentivirus carrying shLRG decreased renal I/R injury-induced increase in caspase-3 activity, IL-1β and IL-18 concentrations, and ROS production. Furthermore, shRNA-mediated LRG knockdown in HK-2 cells protected against H/R-induced cell damage. LRG could upregulate the expression of NADPH oxidase 4 (NOX4). We also determined the increased NOX4 expression in kidney tissues of renal I/R-operated mice and H/R-treated HK-2 cells. NOX4 overexpression reversed the inhibitory role of LRG knockdown in HK-2 cell damage caused by H/R. Collectively, our findings demonstrate that LRG knockdown decreases the NOX4 expression, thereby alleviating renal I/R injury by inhibiting cell apoptosis, inflammation, and oxidative stress.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"444 1","pages":"Article 114341"},"PeriodicalIF":3.3,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142681148","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":"Hyaluronic acid-modified extracellular vesicles for targeted doxorubicin delivery in hepatocellular carcinoma","authors":"Yue Liu ,&nbsp;Benjamin Hinnant ,&nbsp;Shang Chen ,&nbsp;Hongyan Tao ,&nbsp;Ziyu Huang ,&nbsp;Meng Qian ,&nbsp;Manqian Zhou ,&nbsp;Zhibo Han ,&nbsp;Zhong-Chao Han ,&nbsp;Jun Zhang ,&nbsp;Zongjin Li","doi":"10.1016/j.yexcr.2024.114332","DOIUrl":"10.1016/j.yexcr.2024.114332","url":null,"abstract":"<div><div>Hepatocellular carcinoma (HCC), a prevalent and deadly cancer, poses a significant challenge with current treatments due to limitations such as poor stability, off-target effects, and severe side effects. Extracellular vesicles (EVs), derived from tumor cells, have the remarkable ability to home back to their cells of origin and can serve as Trojan horses for drug delivery. CD44, a cell surface glycoprotein, promotes cancer stem cell-like properties and is linked to poor prognosis and resistance to chemotherapy in HCC. Therefore, targeting CD44-expressing HCC cells is of interest in the development of novel therapeutic strategies for the treatment of HCC. In this study, we developed tumor cell-derived EVs (TEVs) functionalized with hyaluronic acid (HA) to serve as natural carriers for the precise delivery of doxorubicin (Dox), which specifically targets HCC cells expressing CD44. Our results demonstrated that HA-engineered EVs (HA-EVs) significantly enhanced Dox accumulation within HCC cells. In a mouse model, HA-EVs effectively delivered Dox to tumors, suppressing their growth and progression while minimizing systemic toxicity. This study demonstrates the potential of HA-functionalized EVs as a novel and targeted therapeutic platform for HCC, offering a valuable strategy for improving drug delivery and patient outcomes. This study presents a promising strategy to advance targeted chemotherapy for HCC and address the challenges associated with conventional treatments. Engineered HA-functionalized EVs offer a tailored and efficient approach to increase drug delivery precision, underscoring their potential as a novel therapeutic platform in the realm of HCC treatment.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"443 2","pages":"Article 114332"},"PeriodicalIF":3.3,"publicationDate":"2024-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142647211","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":"Spotlight on the function and trends on extrachromosomal circular DNA (eccDNA): A bibliometric analysis from 2008 - 2023","authors":"Fan Hu ,&nbsp;Zhengqi Qiu","doi":"10.1016/j.yexcr.2024.114318","DOIUrl":"10.1016/j.yexcr.2024.114318","url":null,"abstract":"<div><div>Extrachromosomal circular DNA (eccDNA),a type of circular DNA that has a nucleosomal structure, is widely distributed in eukaryotic chromosomes and has been found to modulate genome instability and plasticity, playing a role in regulating gene expression and genome evolution. To comprehensively outline the stages of eccDNA research development, including author collaborations, research topics and hotspots, and their temporal evolution trends, we conducted a bibliometric analysis of 242 publications related to eccDNA research published from 2008 to 2023 in the Web of Science Core Collection. The bibliometric analysis was performed using CiteSpace, the R package Bibliometrix, and VOSviewer. The USA, the University of California system, and Turner Km were found to be the most influential nation, organization, and author in this field, respectively. The exploration of Characterization and Diagnosis, Heterochromatin,Circ-Seq and Cancer Drug Resistance on eccDNA are the most concerned hotspots. EccDNA research has become a rapidly growing hotspot, receiving extensive attention from scholars in recent years. This study is the first to investigate the development and current challenges of eccDNA research through bibliometric analysis.The research on eccDNA has advanced from disorder to more intricate molecular functions. At present, the rapid growth of eccDNA studies in cancer has not been accompanied by an intuitive analysis of its evolutionary patterns. This review provides an overview of eccDNA's biological characteristics and functions, with a focus on its role in cancer research.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"444 1","pages":"Article 114318"},"PeriodicalIF":3.3,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142638435","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":"LOXL1 promotes gastric cancer progression by β-catenin-cyclinD mediated proliferation","authors":"Jin-e Liang ,&nbsp;Bo-wen Bao ,&nbsp;Xue-hua He ,&nbsp;Wen-qing Lu ,&nbsp;Yang Liu ,&nbsp;Jin Wang ,&nbsp;Xiu-juan Qu ,&nbsp;Dong-yang Li ,&nbsp;Xiao-fang Che","doi":"10.1016/j.yexcr.2024.114331","DOIUrl":"10.1016/j.yexcr.2024.114331","url":null,"abstract":"<div><div>Although much progress has been made in chemotherapy or target therapy for advanced gastric cancer, the prognosis is still poor. It is necessary to screen biomarkers for early diagnosis and prognosis prediction. However, the prognostic value of LOX family in gastric cancer and the underlying molecular mechanisms for promoting the progression of gastric cancer remains unclear. Among five members of LOX family, LOXL1 was the unique independent prognostic risk factor. The nomogram established based on the expression of LOXL1 and other clinical parameters could predict the overall survival rate of gastric cancer. Knockdown (KD) of LOXL1 decreased cell proliferation and led to G1 phase arrest in gastric cells. According to GSEA analysis that LOXL1 was positively correlated with the WNT signaling pathway, in vitro experiment proved that LOXL1-KD reduced the phosphorylation level of β-catenin and the expression of the downstream G1 phase checkpoint CCND1. In conclusion, LOXL1 has been identified as a potential risk prognostic biomarker for gastric cancer by promoting gastric cancer proliferation via WNT/β-catenin/cyclinD1 pathway.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"443 2","pages":"Article 114331"},"PeriodicalIF":3.3,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142638416","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}