Experimental cell research最新文献

{"title":"Investigating the effects of TRPV4 and Cav1.2 channels in 3D culture for promoting the differentiation of BMSCs at various stages","authors":"Yuanqing Xu ,&nbsp;Yuhang Chen ,&nbsp;Kun Zhang ,&nbsp;Minmin Chen ,&nbsp;Rongquan Duan ,&nbsp;Ying Ren","doi":"10.1016/j.yexcr.2025.114515","DOIUrl":"10.1016/j.yexcr.2025.114515","url":null,"abstract":"<div><div>Hydrogel, as the most suitable bio-scaffold material for simulating extracellular matrix, can be used to study the influence of material mechanical properties on cell behavior under 3D conditions. Mechanical stimulation plays an important role in cartilage differentiation, especially for the mechanosensitive cell-bone marrow mesenchymal stem cells (BMSCs). Currently, TRPV4 and Cav1.2 calcium ion channels have been reported to play significant roles in the cartilage differentiation of BMSCs. However, there is no study on whether the effects of these two ion channels vary in different periods of BMSC differentiation, especially in 3D culture. In this article, we clarified the role of TRPV4 and Cav1.2 signaling pathways in the early and late stages of BMSCs cartilage differentiation during 3D culture in hyaluronic acid hydrogel with specific mechanical properties. This research can provide new ideas for further accelerating the stimulation of BMSCs cartilage differentiation and formulating cartilage repair strategies in vivo.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"447 1","pages":"Article 114515"},"PeriodicalIF":3.3,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143614094","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":"KIFC1 in cancer: Understanding its expression, regulation, and therapeutic potential","authors":"Gaurav Sanghvi ,&nbsp;R. Roopashree ,&nbsp;Aditya Kashyap ,&nbsp;A. Sabarivani ,&nbsp;Subhashree Ray ,&nbsp;Pushpa Negi Bhakuni","doi":"10.1016/j.yexcr.2025.114510","DOIUrl":"10.1016/j.yexcr.2025.114510","url":null,"abstract":"<div><div>Kinesins are a family of motor proteins essential for intracellular transport and cellular dynamics, with kinesin family member C1 (KIFC1) emerging as a key regulator of cancer progression. Recent studies highlight KIFC1's crucial role in mitotic spindle assembly, chromosome segregation, and cell migration—processes frequently dysregulated in cancer. Its involvement in promoting malignant cell proliferation and metastasis underscores its significance in tumor biology. In various cancer types, aberrant KIFC1 expression correlates with poor prognosis and aggressive phenotypes, suggesting its potential as a biomarker for disease severity. Mechanistically, KIFC1 influences signaling pathways linked to cell cycle regulation and programmed cell death, reinforcing its role in oncogenesis. Given its pivotal function in cancer cell dynamics, KIFC1 represents a promising therapeutic target. Strategies aimed at modulating its activity, including small molecules or RNA interference, could disrupt cancer cell viability and proliferation. The current review article highlights KIFC1's importance in cancer biology, advocating for further investigation into its mechanisms and the development of KIFC1-targeted therapies to enhance treatment efficacy and improve patient outcomes across various malignancies.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"447 1","pages":"Article 114510"},"PeriodicalIF":3.3,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143578625","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":"Comparing the therapeutic influence of bone marrow Mesenchymal stem cells versus its derived exosomes against diabetic hepatopathy in rats","authors":"Rehab Mahmoud Khereldin ,&nbsp;Yara Sayed Abouelela ,&nbsp;Noha Ali Elsayed Yasin ,&nbsp;Fady Sayed Youssef ,&nbsp;Marwa Ibrahim Abdelhameed ,&nbsp;Adel Fathy Tohamy ,&nbsp;Hamdy Rizk ,&nbsp;Samer Mohamed Daghash","doi":"10.1016/j.yexcr.2025.114436","DOIUrl":"10.1016/j.yexcr.2025.114436","url":null,"abstract":"<div><div>Diabetes mellitus (DM) is a chronic widespread metabolic disorder, involving a high blood glucose level which causes multiple serious complications including liver, kidney, brain and peripheral nerves damage. Due to the undesirable side effects of the anti-diabetic drugs, the current studies directed to use stem cells and exosomes to overcome the limitations of traditional therapy. We aimed to compare the antidiabetic effect of Bone marrow mesenchymal stem cells (BMMSCs) and its derived exosomes against diabetic hepatopathy induced by streptozotocin (STZ) in albino rats. Our study was conducted on 28 male albino rats divided into 4 groups {control negative non diabetic group, control positive diabetic group, exosomes treated group received (5 × 10⁹ particle/rat) through tail vein twice per week for one month} and Stem cell treated group received (10⁷) BMMSCs through tail vein twice per week for one month. Hepatic structure together with blood glucose level, liver function enzymes were assayed in addition to a lipid profile tests, oxidative stress, and gene expression. Both treated groups by exosomes and stem cells expressed significantly low levels of fasting blood glucose, liver function parameters (ALT, AST, ALP), lipid profile tests (cholesterol and triglycerides), lipid peroxidation index (MDA), with substantial reduction in IL-1β expression compared to diabetic group. Significantly downregulating the VEGF and elevation of eNOS genes and GSH which suggest the effective role provided by BMMSCs and its derived exosomes for treatment of diabetic hepatopathy. Although, the results of both groups showed near average outcomes, the exosome treated group significantly enhanced liver function enzymes and triglyceride, cholesterol level compared to stem cells treated group. These findings were reinforced by the histopathological and immunohistochemistry examination. The latter showed slight but non-significant improvements in VEGF, eNOS, and IL-1β expression. These minor differences together with practical advantages of exosomes make it preferable over BMMSCs in treatment of diabetic hepatopathy.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"447 1","pages":"Article 114436"},"PeriodicalIF":3.3,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143585362","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":"KRM2 promotes renal cell carcinoma progression and inhibits ferroptosis by interacting with ATF2","authors":"Fang Liu ,&nbsp;Mengtong Wang ,&nbsp;Gao Li ,&nbsp;Sha Cheng ,&nbsp;Jia Yu ,&nbsp;Heng Luo ,&nbsp;Xuhui Zhu","doi":"10.1016/j.yexcr.2025.114497","DOIUrl":"10.1016/j.yexcr.2025.114497","url":null,"abstract":"<div><div>The role of kringle-containing transmembrane protein 2 (KRM2) in renal cell carcinoma (RCC) remains unknown. This study aimed to explore KRM2's mechanistic role in regulating RCC progression. Tissue microarrays were used to map KRM2 expression in tumor tissues and analyze its relationship with RCC clinical features. Cell models were constructed by transfecting RCC cell lines with <em>KRM2</em> knockdown, <em>KRM2</em> overexpression, or <em>ATF2</em> knockdown lentiviral vectors. Tumor xenografts were generated in nude mice to observe the effects of KRM2 on tumor formation. A gene expression microarray was used to identify the regulatory genes downstream of KRM2 and their binding relationships were verified by co-immunoprecipitation and cycloheximide pulse-chase assay. Through a series of <em>in vitro</em> experiments, effects of altering KRM2 and ATF2 expression on cell function and ferroptosis indicators were observed. Following these, we found that KRM2 expression significantly increased in RCC tumor tissues and was associated with tumor size, grade, stage, infiltration, and patient age. <em>In vivo</em> experiments confirmed that inhibition of KRM2 expression slowed the tumor growth. Silencing of <em>KRM2</em> in RCC cells also significantly inhibited cell proliferation and migration and facilitated apoptosis and ferroptosis. <em>ATF2</em> is predicted to be downstream of KRM2. Its expression is positively regulated by KRM2 and there was targeted binding between proteins. <em>In vitro</em> experiments further suggested that ATF2 knockdown reversed the cancer-promoting and ferroptosis-inhibiting effects of KRM2 in RCC. In conclusion, KRM2 plays an oncogenic role in RCC by promoting tumor progression and ferroptosis via regulation of its downstream target, <em>ATF2</em>.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"447 1","pages":"Article 114497"},"PeriodicalIF":3.3,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143585365","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":"Crosstalk between microRNA and inflammation; critical regulator of diabetes","authors":"Amr Ali Mohamed Abdelgawwad El-Sehrawy ,&nbsp;Mohammed Hashim Mohammed ,&nbsp;Omar dheyauldeen salahldin ,&nbsp;Subasini Uthirapathy ,&nbsp;Suhas Ballal ,&nbsp;Rishiv Kalia ,&nbsp;Renu Arya ,&nbsp;Kamal Kant Joshi ,&nbsp;Arshed Shakir Kadim ,&nbsp;Abed J. Kadhim","doi":"10.1016/j.yexcr.2025.114507","DOIUrl":"10.1016/j.yexcr.2025.114507","url":null,"abstract":"<div><div>A growing body of evidence indicates that microRNAs (miRNAs may be used as biomarkers for the diagnosis, prognosis, and treatment of diabetes, given their changed expression profile as the disease progresses. There is growing interest in using individual miRNAs or whole miRNA clusters linked to diabetes as therapeutic targets because of their abnormal expression and functioning. In diabetes, miRNAs are also involved in inflammatory and immunological responses. Additionally, the inflammatory response controls the generation, processing, and stability of pre- or mature miRNAs and miRNA biogenesis. With a comprehensive grasp of molecular biological activities and the signaling axis, this review emphasizes the critical functions of miRNAs in inflammatory and immunological processes in diabetes. We further emphasized the potential role of these miRNAs in controlling inflammation associated with diabetes. This assessment will direct the shift from many studies to practical applications for tailored diabetes treatment and assist in identifying new therapeutic targets and approaches.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"447 1","pages":"Article 114507"},"PeriodicalIF":3.3,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143578628","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":"Farnesoid X receptor induction decreases invasion and tumor progression by JAK2/occludin signaling in human glioblastoma cells","authors":"TzuMin Chen ,&nbsp;JenFu Yang ,&nbsp;YiHsuan Lin ,&nbsp;YuLing Tsai ,&nbsp;ChienRui Lai ,&nbsp;WenChiuan Tsai ,&nbsp;Ying Chen","doi":"10.1016/j.yexcr.2025.114500","DOIUrl":"10.1016/j.yexcr.2025.114500","url":null,"abstract":"<div><div>Glioblastoma multiforme (GBM) is a brain cancer characterized by low survival and high recurrence rates. Farnesoid X receptor (FXR), a nuclear receptor for bile acids, is expressed at low levels in GBM. This study explores the impact of FXR regulation on GBM cell migration and invasion. Higher FXR expression correlated with increased survival in GBM patients, based on TCGA data. FXR overexpression inhibited cell viability, migration and invasion as well as matrix metalloproteinase 2 (MMP2) activity, while knockdown of FXR exerted the opposite effects. The expression of the tight junction proteins occludin and ZO-1 was enhanced after FXR overexpression. Moreover, a JAK2 activator reversed the migration and invasion of FXR-overexpressing GBM cells. In an animal study, FXR overexpression combined with temozolomide treatment decreased tumor mass, and MMP2 expression and elevated occludin expression in mice. In conclusion, FXR overexpression inhibits the progression of GBM, which may be mediated by inhibiting JAK2 and enhancing tight junction protein expression.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"447 1","pages":"Article 114500"},"PeriodicalIF":3.3,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143578627","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":"Carbon monoxide inhibits human bronchial epithelial CCL5 and IL-6 secretion induced by SARS-CoV-2 spike RBD protein","authors":"Xiao-Min Fang,&nbsp;Xing-Jian Liu,&nbsp;Rui-Gang Zhang","doi":"10.1016/j.yexcr.2025.114499","DOIUrl":"10.1016/j.yexcr.2025.114499","url":null,"abstract":"<div><div>Carbon monoxide (CO) is a novel anti-inflammatory molecule, but the effects of CO on SARS-CoV-2 spike RBD (S-RBD)-induced human bronchial epithelial cytokines release remains unclear. CO was delivered using CO-releasing molecule 3 (CORM-3). The effects of S-RBD, ATPγS and CO on cytokines secretion were determined by enzyme-linked immunosorbent assay (ELISA) in 16HBE14o-human bronchial epithelial cell line. The inhibitory effect of CO on S-RBD-induced ERK phosphorylation was assessed by Western blot analysis. The regulatory effect of CO on extracellular nucleotide-induced ion transport was quantified by short-circuit current (<em>I</em>_<em>SC</em>). S-RBD evoked CCL5 and IL-6 release and this effect could be suppressed by CO. However, CO failed to inhibit ATP release induced by S-RBD while decreased ATP-induced CCL5 and IL-6 secretion as well as ion transport. Furthermore, CO significantly inhibited ERK phosphorylation induced by S-RBD. These findings suggest an anti-inflammatory role of CO during inflammation induced by S-RBD and extracellular nucleotide in human bronchiol epithelial cells.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"447 1","pages":"Article 114499"},"PeriodicalIF":3.3,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143585359","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":"TGF-β-induced acetylation of KLF5 drives TNFAIP2 transcription and EMT in nasopharyngeal carcinoma: Unveiling a novel regulatory mechanism","authors":"Yi Qian ,&nbsp;Xuxu Zhao ,&nbsp;Feiyang Wu ,&nbsp;Xiaoqiang Wang ,&nbsp;Tao Chen","doi":"10.1016/j.yexcr.2025.114498","DOIUrl":"10.1016/j.yexcr.2025.114498","url":null,"abstract":"<div><div>Epithelial-mesenchymal transition (EMT) is one of the critical mechanisms underlying migration, invasion, and metastasis of nasopharyngeal carcinoma (NPC) cells. The transcription factor KLF5 plays a pivotal role in various cancers, however, its precise functions in NPC remain incompletely understood. This study aims to explore the detailed mechanisms by which TGF-β enhances TNFAIP2 transcription by acetylating KLF5, thereby inducing EMT in NPC. KLF5 was significantly overexpressed in NPC tissues and closely associated with adverse clinicopathological features of the patients. Further studies revealed that TGF-β markedly increased the expression of KLF5 and its acetylated form, Ac-KLF5, in NPC cells, with the acetylation status of KLF5 being crucial for its function. KLF5 induced EMT in NPC cells by directly binding to the TNFAIP2 promoter and promoting its transcription. The pro-migratory and pro-invasive effects of acetylated KLF5 on NPC cells depended on TNFAIP2. Additionally, in vivo experiments confirmed that TGF-β treatment induced tumors in NPC mouse models to exhibit apparent EMT characteristics. These results collectively support the central role of the TGF-β-KLF5-TNFAIP2 axis in EMT of NPC. This study elucidates the specific mechanisms by which TGF-β promotes TNFAIP2 transcription by acetylating KLF5, thereby inducing EMT in NPC. This discovery not only provides new insights into the pathogenesis of NPC but also identifies potential therapeutic targets for NPC treatment.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"447 1","pages":"Article 114498"},"PeriodicalIF":3.3,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143578626","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":"Ano5 deficiency disturbed bone formation by inducing osteoclast apoptosis in Gnathodiaphyseal dysplasia","authors":"Xiu Liu ,&nbsp;Shengnan Wang ,&nbsp;Chao Liang ,&nbsp;Shuai Zhang ,&nbsp;Sirui Liu ,&nbsp;Ying Hu","doi":"10.1016/j.yexcr.2025.114493","DOIUrl":"10.1016/j.yexcr.2025.114493","url":null,"abstract":"<div><div>Gnathodiaphyseal dysplasia (GDD) is a rare genetic syndrome characterized by cemento-ossifying fibroma lesions in the mandible and sclerosis of tubular bones. Currently, the clinical treatment of GDD is limited to surgical resection; therefore, novel treatment strategies developed through exploration of the related mechanisms are needed. Mutations in the TMEM16E/ANO5 gene are considered the main pathogenic factor of GDD, and the <em>Ano5</em> knockout mouse model (<em>Ano5</em>^{<em>−/−</em>}) established previously, which presented GDD-like characteristics, exhibited decreased osteoclastogenesis. <em>ANO5</em>, a calcium-activated chloride channel (CaCC), plays an important role in the maintenance of intracellular calcium homeostasis, which is crucial for osteoclast differentiation. In this study, our data indicated that the intracellular calcium concentration ([Ca²⁺]_i) and calcium transients were significantly decreased in <em>Ano5</em>^{<em>−/−</em>} osteoclasts accompanied by abnormally altered expression of calcium transporters, resulting in calcium dyshomeostasis. In addition, the endoplasmic reticulum stress (ERS) response was significantly enhanced in <em>Ano5</em>^{<em>−/−</em>} osteoclasts, possibly because of calcium dyshomeostasis, which leading to the increased proportion of apoptotic osteoclasts via the activation of the C/EBP homologous protein (CHOP) signalling pathway, accompanied by abnormal changes in the expression of apoptosis-related factors. In summary, <em>Ano5</em> deficiency impairs the function of osteoclasts by increasing osteoclast apoptosis, which is induced by an overactivated ERS response via calcium dyshomeostasis.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"447 1","pages":"Article 114493"},"PeriodicalIF":3.3,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143550256","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":"Protocadherin 17 weakens the lenvatinib resistance of liver cancer through inducing ferroptosis","authors":"Jun Yang ,&nbsp;Bin Hu ,&nbsp;Guowei Zhang ,&nbsp;Kai Wu ,&nbsp;Xue Zhang ,&nbsp;Mengxuan Ji ,&nbsp;Bin Zhang ,&nbsp;Hengliang Shi ,&nbsp;Dechun Li","doi":"10.1016/j.yexcr.2025.114495","DOIUrl":"10.1016/j.yexcr.2025.114495","url":null,"abstract":"<div><div>Lenvatinib has been employed in the treatment of advanced liver cancer; however, its clinical application is significantly impeded by frequent drug resistance. Recent studies have revealed that lenvatinib treatment triggers ferroptosis in liver cancer cells, providing a novel approach to addressing lenvatinib resistance. In this study, we initially validated the induction of ferroptosis by lenvatinib in liver cancer cells. Remarkably, protocadherin 17 (PCDH17), an adhesion-related protein, was found to be down-regulated in liver cancer, and overexpression of PCDH17 could induce ferroptosis in liver cancer cells. Importantly, silencing PCDH17 inhibited the impact of lenvatinib on liver cancer cell ferroptosis, while overexpression of PCDH17 had the opposite effect. These findings were further confirmed using a xenograft tumor model in BALB/c nude mice. Additionally, lenvatinib-resistant (LR) liver cancer cells were generated for additional validation purposes. It was observed that LR-liver cancer cells lost their susceptibility to ferroptosis induction by lenvatinib; however, overexpression of PCDH17 reactivated their sensitivity to ferroptosis. Corresponding results were also verified in BALB/c nude mice models. In conclusion, these results suggest that as a novel regulator of ferroptosis, PCDH17 can alleviate lenvatinib resistance and potentially enhance the therapeutic efficacy of lenvatinib in treating liver cancer.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"447 1","pages":"Article 114495"},"PeriodicalIF":3.3,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143561765","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}