Experimental cell research最新文献

{"title":"A semi-permeable insert culture model for the distal part of the nephron with human and mouse tubuloid epithelial cells.","authors":"E Dilmen, C J A Olde Hanhof, F A Yousef Yengej, C M E Ammerlaan, M B Rookmaaker, I Orhon, J Jansen, M C Verhaar, J G Hoenderop","doi":"10.1016/j.yexcr.2024.114342","DOIUrl":"10.1016/j.yexcr.2024.114342","url":null,"abstract":"<p><p>Tubuloids are advanced in vitro 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.</p>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"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":"","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":"https://doi.org/10.1016/j.yexcr.2024.114343","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"114343"},"PeriodicalIF":3.3,"publicationDate":"2024-11-18","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":"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, Cheng Qiu, Lexi Zhang","doi":"10.1016/j.yexcr.2024.114341","DOIUrl":"https://doi.org/10.1016/j.yexcr.2024.114341","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"114341"},"PeriodicalIF":3.3,"publicationDate":"2024-11-18","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, Zhengqi Qiu","doi":"10.1016/j.yexcr.2024.114318","DOIUrl":"https://doi.org/10.1016/j.yexcr.2024.114318","url":null,"abstract":"<p><p>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 2008-2023 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.</p>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"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, Bo-Wen Bao, Xue-Hua He, Wen-Qing Lu, Yang Liu, Jin Wang, Xiu-Juan Qu, Dong-Yang Li, Xiao-Fang Che","doi":"10.1016/j.yexcr.2024.114331","DOIUrl":"10.1016/j.yexcr.2024.114331","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"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}

{"title":"SP1-mediated transcriptional repression of SFRP5 is correlated with cardiac fibroblast activation and atrial myocyte apoptosis in the development of atrial fibrillation","authors":"Yanyan Sun,&nbsp;Zhenzhen Hu,&nbsp;Jie Han,&nbsp;Gang Li","doi":"10.1016/j.yexcr.2024.114326","DOIUrl":"10.1016/j.yexcr.2024.114326","url":null,"abstract":"<div><div>Secreted frizzled related protein 5 (SFRP5) is a recognized cardioprotective protein with diminished expression in atrial fibrillation (AF). This study investigates SFRP5's function in AF-related cardiac fibrosis and cardiomyocyte apoptosis, exploring the underlying dysregulation causes. Utilizing C57BL/6 mice, mouse cardiac fibroblasts (CFs), and HC-1 mouse atrial myocyte cell line, AF models were induced by angiotensin Ⅱ (Ang Ⅱ). SFRP5 levels were consistently decreased in plasma samples from clinical patients, modeled mice, and CF culture supernatants. Treatment with recombinant SFRP5 restored its levels, mitigating Ang Ⅱ-induced AF in mice and ameliorating atrial tissue fibrosis and oxidative stress. <em>In vitro</em>, SFRP5 recombinant protein suppressed CF activation and fibrosis-related markers. The study identified Sp1 transcription factor (SP1) binding to the SFRP5 promoter, causing transcriptional repression. SP1 knockdown reinstated SFRP5 levels in mice and CFs, thus suppressing fibrosis. Additionally, SP1 knockdown attenuated Ang Ⅱ-induced apoptosis in HC-1 cells, but this effect was counteracted by concurrent SFRP5 knockdown. In conclusion, this investigation underscores that SP1 mediates SFRP5 loss during AF by transcriptional repression, contributing to fibrosis and myocyte apoptosis. These findings illuminate potential therapeutic interventions targeting the SFRP5-SP1 axis in AF-related cardiac complications.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"443 2","pages":"Article 114326"},"PeriodicalIF":3.3,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142617529","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":"METTL3/YTHDF1 stabilizes CORO6 expression promoting osteosarcoma progression through glycolysis","authors":"Xuzhou Liu ,&nbsp;Wenchong Yu ,&nbsp;Wei Song ,&nbsp;Zhengqian Zhang ,&nbsp;Benqiang Chen ,&nbsp;Hongsheng Lin","doi":"10.1016/j.yexcr.2024.114328","DOIUrl":"10.1016/j.yexcr.2024.114328","url":null,"abstract":"<div><div>This study investigates the role of CORO6 (Coronin 6) in the development of osteosarcoma. Osteosarcoma is a common malignant bone tumor in children and adolescents, characterized by rapid and irregular bone growth and a high risk of distant lung metastasis. CORO6 is a member of the Coronin family, known for its conserved WD40 repeat domain. This structure allows CORO6 to inhibit actin dynamics through interactions with F-actin and Arp2/3, thereby affecting the organization of the cytoskeleton. Our research found that in osteosarcoma patients, the levels of CORO6 are significantly elevated. Experimental observations showed that reducing the expression of CORO6 significantly inhibits the growth, migration, and invasion abilities of osteosarcoma cells. Moreover, in vivo experiments demonstrated that the absence of CORO6 effectively inhibits the growth of osteosarcoma in animal models. We also discovered that CORO6 promotes the proliferation, migration and invasion capabilities of osteosarcoma cells by activating the Wnt/β-catenin signaling pathway. Moreover, CORO6 plays a critical important role in glycolysis of osteosarcoma cells. Mechanically, we found that METTL3/YTHDF1 induced m6A modification of CORO6 mRNA promoted the expression of CORO6 by enhancing its stability. These findings offer new directions for the treatment of osteosarcoma, suggesting that CORO6 could be a novel prognostic biomarker and an effective therapeutic target for patients.</div><div>In summary, CORO6, as an oncogene, plays a key role in the development of osteosarcoma, providing a crucial theoretical basis for the development of new osteosarcoma treatment strategies.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"443 2","pages":"Article 114328"},"PeriodicalIF":3.3,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142617522","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":"Matrix Gla protein suppresses osteoblast senescence and promotes osteogenic differentiation by the PI3K-AKT signaling pathway.","authors":"Min Zhang, Sha Liu, Yulin Chen, Yifa Chen, Jiaojiao He, Yuting Xia, Ya Yang","doi":"10.1016/j.yexcr.2024.114329","DOIUrl":"https://doi.org/10.1016/j.yexcr.2024.114329","url":null,"abstract":"<p><p>Age-related bone loss in mice is associated with senescent cell accumulation and reduced bone formation by osteoblasts. Matrix Gla protein (MGP), secreted by osteoblasts, is pivotal in regulating the bone extracellular matrix mineralization. Previous research has demonstrated that Mgp null mice exhibit osteopenia and fractures, and ultimately die prematurely. To elucidate the mechanisms underlying MGP's role of MGP in bone metabolism, we generated osteoblast-specific Mgp knockout (Mgp cKO) mice by crossing Mgp^fl/fl mice with Bglap-Cre mice. The study revealed that in 3-month-old Mgp cKO male mice, trabecular bone volume decreased, and the senescence marker protein p21 increased. Primary osteoblasts from Mgp cKO mice exhibited markers of DNA damage and senescence, such as increased γH2AX foci, p21, and senescence-associated β-galactosidase staining, as well as attenuated cellular proliferation and osteogenic differentiation abilities. In addition, bone marrow stromal cells' colony formation and spontaneous osteogenic ability were impaired in Mgp cKO mice, whereas osteoclastogenesis was enhanced. In vitro treatment with recombinant human MGP promotes osteogenesis in osteoblasts derived from Mgp cKO mice via the PI3K-AKT signaling pathway. Thus, our results suggest that MGP is protective by suppressing osteoblast senescence, offering new insights into potential therapeutic strategies for age-related osteoporosis.</p>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":" ","pages":"114329"},"PeriodicalIF":3.3,"publicationDate":"2024-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142617493","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":"Exosomes derived from diabetic microenvironment-preconditioned mesenchymal stem cells ameliorate nonalcoholic fatty liver disease and inhibit pyroptosis of hepatocytes","authors":"Anning Wang ,&nbsp;Bing Li ,&nbsp;Wanlu Su ,&nbsp;HaiXia Zhang ,&nbsp;Ruofan Hu ,&nbsp;Yue Zhang ,&nbsp;Jian Zhao ,&nbsp;Rui Ren ,&nbsp;Yiming Mu ,&nbsp;Yu Cheng ,&nbsp;Zhaohui Lyu","doi":"10.1016/j.yexcr.2024.114325","DOIUrl":"10.1016/j.yexcr.2024.114325","url":null,"abstract":"<div><h3>Aim</h3><div>Pyroptosis, a type of programmed cell death, is a key mechanism underlying non-alcoholic fatty liver disease (NAFLD). Mesenchymal stem cell (MSC)-derived exosomes (MSC-Exos) have the potential to ameliorate NAFLD, an effect that is enhanced by curcumin preconditioning. We previously reported that diabetic microenvironment preconditioning enhances the secretion capacity and anti-inflammatory activity of MSCs. Therefore, we hypothesized that MSC-Exos would inhibit hepatocyte pyroptosis and thereby ameliorate NAFLD, and that diabetic microenvironment preconditioning would enhance these effects.</div></div><div><h3>Methods</h3><div>MSCs were preconditioned in a diabetic microenvironment (pMSCs). MSC-Exos and pMSC-Exos collected from MSCs or pMSCs were applied to methionine- and choline-deficient (MCD)-induced NAFLD mice and <em>in vitro</em> models involving induction with lipopolysaccharide or palmitic acid to mimic hepatic steatosis and injury. MCC950 treatment was used as a positive control. We analyzed the characteristics of NAFLD and pyroptosis markers. Protein profiles of MSC-Exos and pMSC-Exos were evaluated by label-free quantitative proteomics.</div></div><div><h3>Results</h3><div><em>In vivo</em>, MSC-Exos partially attenuated inflammation and fibrosis, but not lipid deposition and NAFLD progression in the livers of NAFLD mice. pMSC-Exos significantly improved lipid metabolism, hepatic steatosis, inflammation, and fibrosis but also retarded the progression of NAFLD. Pyroptosis was upregulated in the liver of NAFLD mice. MSC-Exos and pMSC-Exos inhibited pyroptosis, and the effect of the latter was greater than that of the former. <em>In vitro</em>, MSC-Exos and pMSC-Exos ameliorated hepatocyte steatosis, lipid metabolism disorder, and inflammation, and pMSC-Exos exerted a greater inhibitory effect on hepatocyte pyroptosis than MSC-Exos did, which were remitted after inhibition of peroxiredoxin-1 (PRDX-1).</div></div><div><h3>Conclusion</h3><div>MSC-Exos ameliorated NAFLD and inhibited hepatocyte pyroptosis by downregulating the NLRP3/Caspase-1/GSDMD pathway, effects enhanced by pMSC-Exos, partly due to PRDX-1 upregulation.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"443 2","pages":"Article 114325"},"PeriodicalIF":3.3,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142617390","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}