Journal of Cellular Physiology最新文献

{"title":"The Potential Role of Bone Morphogenetic Protein-2/-4 in Excessive Mechanical Overloading-Initiated Joint Degeneration","authors":"Rong-Ze Hsieh,&nbsp;Kuo-Chin Huang,&nbsp;Yu-Ping Su,&nbsp;Chung-Sheng Shi,&nbsp;Shun-Fu Chang","doi":"10.1002/jcp.31509","DOIUrl":"10.1002/jcp.31509","url":null,"abstract":"<div>\u0000 \u0000 <p>Excessive mechanical overloading of articular cartilage caused by excessive exercise or severe trauma is considered a critical trigger in the development of osteoarthritis (OA). However, the available clinical theranostic molecular targets and underlying mechanisms still require more elucidation. Here, we aimed to examine the possibility that bone morphogenetic proteins (BMPs) serve as molecular targets in rat cartilages and human chondrocytes under conditions of excessive mechanical overloading. Two rat models involving high-intensity running training and surgery for destabilization of medial meniscus, along with a cell model subjected to cyclic tensile strain, were established to simulate and investigate excessive mechanical overloading effects on cartilages/chondrocytes. We employed various methods, including immunohistochemistry, real-time polymerase chain reaction, western blot analysis, and enzyme-linked immunosorbent assay, to evaluate the expression, secretion, phosphorylation, and nuclear translocation of mRNA/proteins in cartilages and chondrocytes. Our findings revealed a simultaneous upregulation of BMP-2 and downregulation of BMP-4 in degenerated and inflamed cartilages and chondrocytes under excessive mechanical overloading. Furthermore, toll-like receptor 2 and nuclear factor kappa B-p50/p65 subunits signaling were identified as regulators governing this distinct expression pattern. Treatment with recombinant BMP-2 and/or BMP-4 proteins significantly ameliorated cartilage degeneration and chondrocyte inflammation induced by excessive mechanical overloading. These results strongly suggest that BMP-2 upregulation and BMP-4 downregulation might represent mechanisms for self-rescue and degeneration in damaged cartilage/chondrocytes, respectively. Our findings advance new insights that BMP-2/-4 might be potential molecular targets for excessive mechanical overloading-caused OA development and should be taken into account in future clinical applications.</p>\u0000 </div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 2","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142877276","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum: MiR-136-5p/FZD4 Axis Is Critical for Wnt Signaling-Mediated Myogenesis and Skeletal Muscle Regeneration","authors":"","doi":"10.1002/jcp.31508","DOIUrl":"10.1002/jcp.31508","url":null,"abstract":"<p><b>This article corrects the following:</b></p><p>miR-136-5p/FZD4 axis is critical for Wnt signaling-mediated myogenesis and skeletal muscle regeneration</p><p>Zhang, Donghao, Lingqian Yin, Zhongzhen Lin, Chunlin Yu, Jingjing Li, Peng Ren, Chaowu Yang, Mohan Qiu, and Yiping Liu</p><p>Journal of Cellular Physiology</p><p>https://doi.org/10.1002/jcp.31046</p><p>First published online: 23 May 2023</p><p><b>Correction text</b>:</p><p>A reviewer alerted the publisher that an earlier version of the revised manuscript had mistakenly been published in place of the accepted version of the article. This error occurred accidentally during the production process. We apologize for the error and any inconvenience that may have arisen as a result. The following changes align with the final accepted version of the article.</p><p>Figure 1F has been updated to include MyHC and Hoechst immunofluorescence staining of C2C12 at different stages. The corrected Figure 1 and associated legend are as follows:</p><p>The layout of Figure 4 has been changed to improve the visibility of the images of the cells in panels A and G. In addition, the MyoG Western blot image in panel E has been changed. The corrected Figure 4 and associated legend are as follows:</p><p>The Bcl+antagomir ZsGreen panel in Figure 5F has been replaced, and the title of the figure has been updated to accurately reflect that FZD4 expression attenuates antagomiR-136-5p-mediated muscle regeneration after injury. The corrected Figure 5 and associated legend are as follows:</p><p>Finally, the missing Supplemental Figure 1 has been added as follows:</p><p><b>Figure S1.</b> FZD4 promotes differentiation of C2C12 cells in vitro.</p><p>(A) Expression levels of PCNA, CDK2, MyoD and MyoG mRNA in C2C12 cells after overexpression of FZD4 (n = 9 cultures; mean ± SEM). (B) Western blot analysis analysis of the PCNA and MyoG protein levels in C2C12 cells. β-Tubulin was used as an internal reference. (C) EdU and Hoechst (nuclei) staining analysis. The scale bar represents 100 μm. (D) Fold change of proliferation rate of C2C12 cells in each group (n = 6 cultures; mean ± SEM). EdU (red), Hoechst (blue). *<i>p</i> &lt; 0.05, **<i>p</i> &lt; 0.01, ***<i>p</i> &lt; 0.001.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 2","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.31508","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142877275","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tissue Engineering 3D-Printed Scaffold Using Allograft/Alginate/Gelatin Hydrogels Coated With Platelet-Rich Fibrin or Adipose Stromal Vascular Fraction Induces Osteogenesis In Vitro","authors":"Sahar Baniameri,&nbsp;Hossein Aminianfar,&nbsp;Niusha Gharehdaghi,&nbsp;Amir-Ali Yousefi-Koma,&nbsp;Sadra Mohaghegh,&nbsp;Hanieh Nokhbatolfoghahaei,&nbsp;Arash Khojasteh","doi":"10.1002/jcp.31497","DOIUrl":"10.1002/jcp.31497","url":null,"abstract":"<div>\u0000 \u0000 <p>Incorporating autologous patient-derived products has become imperative to enhance the continually improving outcomes in bone tissue engineering. With this objective in mind, this study aimed to evaluate the osteogenic potential of 3D-printed allograft-alginate-gelatin scaffolds coated with stromal vascular fraction (SVF) and platelet-rich fibrin (PRF). The primary goal was to develop a tissue-engineered construct capable of facilitating efficient bone regeneration through the utilization of biomaterials with advantageous properties and patient-derived products. To achieve this goal, 3D-printed gelatin, allograft, and alginate scaffolds were utilized, along with stem cells derived from the buccal fat pad and human-derived components (PRF, SVF). Cells were seeded onto scaffolds, both with and without SVF/PRF, and subjected to comprehensive assessments including adhesion, proliferation, differentiation (gene expression and protein secretion levels), penetration, and gene expression analysis over 14 days. The data was reported as mean ± standard deviation (SD). Two-way or one-way analysis of variance (ANOVA) was performed, followed by a Tukey post hoc test for multiple comparisons. Statistical significance was determined as a <i>p</i> value below 0.05. The scaffolds demonstrated structural integrity, and the addition of PRF coatings significantly enhanced cellular adhesion, proliferation, and differentiation compared to other groups. Gene expression analysis showed increased expression of osteogenic and angiogenic markers in the PRF-coated scaffolds. These findings highlight the promising role of PRF-coated scaffolds in promoting osteogenesis and facilitating bone tissue regeneration. This study emphasizes the development of patient-specific tissue-engineered constructs as a valuable approach for effective bone regeneration.</p>\u0000 </div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142864225","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CBFβ Regulates RUNX3 ADP-Ribosylation to Mediate Homologous Recombination Repair","authors":"William E. Samsa,&nbsp;Zhen Zhang,&nbsp;Zihua Gong","doi":"10.1002/jcp.31503","DOIUrl":"10.1002/jcp.31503","url":null,"abstract":"<div>\u0000 \u0000 <p>RUNX3 is a master developmental transcriptional factor that has been implicated as a tumor suppressor in many cancers. However, the exact role of RUNX3 in cancer pathogenesis remains to be completely elucidated. Recently, it has emerged that RUNX3 is involved in the DNA damage response. Here, we demonstrate that heterodimerization of RUNX3 with CBFβ is necessary for its stability by protecting RUNX3 from RUNX3 ADP-ribosylation-dependent ubiquitination and degradation. We further identify new amino acid residues that are targets for PARylation and demonstrate that RUNX3 PARylation at these residues is necessary for localization of RUNX3 to DNA double strand break sites (DBSs). We also demonstrate that both RUNX3 PARylation and CBFβ heterodimerization with RUNX3 positively regulates homologous recombination (HR) repair, in part by promoting the recruitment of CtIP and phospho-RPA2 to the DBSs to mediate HR repair. In summary, we provide evidence that RUNX3 regulates HR repair activity in a PARylation-dependent manner.</p>\u0000 </div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142854241","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Novel Therapeutic Strategies Targeting Fibroblasts to Improve Heart Disease","authors":"Yujuan Li","doi":"10.1002/jcp.31504","DOIUrl":"10.1002/jcp.31504","url":null,"abstract":"<div>\u0000 \u0000 <p>Cardiac fibrosis represents the terminal pathological manifestation of various heart diseases, with the formation of fibroblasts playing a pivotal role in this process. Consequently, targeting the formation and function of fibroblasts holds significant potential for improving outcomes in heart disease. Recent research reveals the considerable potential of fibroblasts in ameliorating cardiac conditions, demonstrating different functional characteristics at various time points and spatial locations. Therefore, precise modulation of fibroblast activity may offer an effective approach for treating cardiac fibrosis and achieving targeted therapeutic outcomes. In this review, we focus on the fate and inhibition of fibroblasts, analyze their dynamic changes in cardiac diseases, and propose a framework for identifying markers of fibroblast activation mechanisms and selecting optimal time windows for therapeutic intervention. By synthesizing research findings in these areas, we aim to provide new strategies and directions for the precise treatment of fibroblasts in cardiac diseases.</p>\u0000 </div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142846675","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RRM2 Is a Putative Biomarker and Promotes Bladder Cancer Progression via PI3K/AKT/mTOR Pathway","authors":"Linfa Guo,&nbsp;Yiqiao Zhao,&nbsp;Xiaojie Bai,&nbsp;Xiaolong Wang,&nbsp;Kuerban Tuoheti,&nbsp;Yuanfei Cao,&nbsp;Yingtong Zuo,&nbsp;Xinhua Zhang,&nbsp;Tongzu Liu","doi":"10.1002/jcp.31501","DOIUrl":"10.1002/jcp.31501","url":null,"abstract":"<div>\u0000 \u0000 <p>Bladder cancer (BLCA) is the tenth most common cancer worldwide, characterized by its high recurrence and progression rates. Thus, identifying prognostic biomarkers and understanding its underlying mechanisms are imperative to enhance patient outcomes. In this study, we aimed to investigate the prognostic significance, expression, functional activity, and underlying mechanisms of RRM2 in BLCA. RRM2 expression and its association with pathological grading and survival were investigated in samples from TCGA dataset and BLCA tissue microarray. CCK8 assays, colony formation assays, wound healing, and transwell assays were performed to assess the role of RRM2 in BLCA cell proliferation and migration. Western blot was employed to investigate alterations in markers associated with epithelial-to-mesenchymal transition (EMT), apoptosis, and cell cycle regulation. Gene set enrichment analysis was performed to investigate the biological processes associated with RRM2, which were subsequently validated. The expression of RRM2 was significantly elevated in both BLCA tissues and cells. Our results also indicated a positive correlation between RRM2 expression and high tumor stage, high tumor grade, and poor survival. Knockdown of RRM2 inhibited cell proliferation and migration of BLCA. RRM2 knockdown significantly induced apoptosis and arrested the cell cycle at the G0/G1 phase. Opposite results were observed in the RRM2 overexpression cells. Additionally, our study demonstrates that RRM2 promotes BLCA progression by activating the PI3K/AKT/mTOR pathway. RRM2 is remarkably correlated with poor prognosis in BLCA and facilitate its progression via PI3K/AKT/mTOR pathway. It is suggested that RRM2 might become an effective prognostic biomarker and potential therapeutic target for BLCA.</p></div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142828602","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cover Image, Volume 239, Number 12, December 2024","authors":"Yongya Zhang,&nbsp;Fei Wu,&nbsp;Sibei Guo,&nbsp;Ruijie Yin,&nbsp;Min Yuan,&nbsp;Xue Li,&nbsp;Xueru Zhao,&nbsp;Xiaohua Li","doi":"10.1002/jcp.31514","DOIUrl":"https://doi.org/10.1002/jcp.31514","url":null,"abstract":"<p><b>Inside Front Cover Caption:</b> The cover image is based on the article <i>Critical role of apoptosis in MeCP2-mediated epithelial–mesenchymal transition of ARPE-19 cells</i> by Xiaohua Li et al., https://doi.org/10.1002/jcp.31429.\u0000\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"239 12","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.31514","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142861500","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pregnancy Entails a Metabolic Rewiring of Maternal Circulating Neutrophils","authors":"Guillermina Calo,&nbsp;Fátima Merech,&nbsp;Florencia Sabbione,&nbsp;Vanesa Hauk,&nbsp;Brenda Lara,&nbsp;Luciana Doga,&nbsp;Luciana D'eramo,&nbsp;Aldo Squassi,&nbsp;Rosanna Ramhorst,&nbsp;Analía Trevani,&nbsp;Daiana Vota,&nbsp;Claudia Pérez Leirós","doi":"10.1002/jcp.31502","DOIUrl":"10.1002/jcp.31502","url":null,"abstract":"<div>\u0000 \u0000 <p>Immunometabolism is an emerging growing field that focuses on the role of cellular metabolism in the regulation of immune cell function and fate. Thus, proliferation, differentiation, activation, and function of immune cell populations are modulated by reprogramming their fueling and metabolic pathways. Pregnancy entails a fine immune and metabolic regulation of the maternal−fetal interaction to assist the energetic demands of the fetus where trophoblast cells have a central role. Maternal neutrophil functional shaping by trophoblast cells has been proposed though their metabolic conditioning during pregnancy has not been studied yet. Here, we explored the effects of trophoblast-derived factors on the metabolic rewiring of neutrophils from nonpregnant women and its impact on central functions like reactive oxygen species (ROS) production, neutrophil extracellular trap (NET) release, and migration. In parallel, the immunometabolic status and function of neutrophils isolated from pregnant women (16−20 weeks) was compared with nonpregnant age-matched control samples. Trophoblast-derived factors induced glucose uptake and lipid droplet accumulation without activating ROS production or NET release. Conditioned media from trophoblast cells also inhibited PMA-induced NETosis partly by impairing glucose uptake in neutrophils. In turn, neutrophils from pregnant women had increased basal ROS production, lipid accumulation, and glucose uptake compared to neutrophils from nonpregnant women, accompanied by a higher release of PMA-induced NETs. Interestingly, PMA-induced NETs was blocked by a fatty acid oxidation inhibitor in neutrophils from pregnant women indicating the contribution of fatty acid metabolism to neutrophil activity during pregnancy. Results are consistent with immunometabolic mechanisms underlying the functional shaping of neutrophils during pregnancy and point out the contribution of trophoblast-derived factors to their metabolic profiling. These findings provide novel immunometabolic clues to understand immune homeostasis maintenance during pregnancy and raise the clinical potential of monitoring neutrophil metabolism during normal and complicated pregnancies.</p>\u0000 </div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142828657","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cover Image, Volume 239, Number 12, December 2024","authors":"Irene Bottillo,&nbsp;Andrea D'Alessandro,&nbsp;Maria Pia Ciccone,&nbsp;Gianluca Cestra,&nbsp;Gianluca Di Giacomo,&nbsp;Evelina Silvestri,&nbsp;Marco Castori,&nbsp;Francesco Brancati,&nbsp;Andrea Lenzi,&nbsp;Alessandro Paiardini,&nbsp;Silvia Majore,&nbsp;Giovanni Cenci,&nbsp;Paola Grammatico","doi":"10.1002/jcp.31513","DOIUrl":"https://doi.org/10.1002/jcp.31513","url":null,"abstract":"<p><b>Front Cover Caption:</b> The cover image is based on the article <i>An inherited TBX3 alteration in a prenatal case of ulnar-mammary syndrome: Clinical assessment and functional characterization in Drosophila melanogaster</i> by Giovanni Cenci et al., https://doi.org/10.1002/jcp.31440.\u0000\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"239 12","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.31513","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142861499","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring Metabolic Approaches for Epithelial Ovarian Cancer Therapy","authors":"Sangeeta Kumari,&nbsp;Shraddha Gupta,&nbsp;Aisha Jamil,&nbsp;Deyana Tabatabaei,&nbsp;Sergey Karakashev","doi":"10.1002/jcp.31495","DOIUrl":"10.1002/jcp.31495","url":null,"abstract":"<div>\u0000 \u0000 <p>Epithelial ovarian cancer (EOC) has the highest mortality rate among malignant tumors of the female reproductive system and the lowest survival rate. This poor prognosis is due to the aggressive nature of EOC, its late-stage diagnosis, and the tumor's ability to adapt to stressors through metabolic reprogramming. EOC cells sustain their rapid proliferation by altering the uptake, utilization, and regulation of carbohydrates, lipids, and amino acids. These metabolic changes support tumor growth and contribute to metastasis, chemotherapy resistance, and immune evasion. Targeting these metabolic vulnerabilities has shown promise in preclinical studies, with some therapies advancing to clinical trials. However, challenges remain due to tumor heterogeneity, adaptive resistance mechanisms, and the influence of the tumor microenvironment. This review provides a comprehensive summary of metabolic targets for EOC treatment and offers an overview of the current landscape of clinical trials focusing on ovarian cancer metabolism. Future efforts should prioritize combination therapies that integrate metabolic inhibitors with immunotherapies or chemotherapy. Advances in precision medicine and multi-omics approaches will be crucial for identifying patient-specific metabolic dependencies and improving outcomes. By addressing these challenges, metabolism-based therapies can significantly transform the treatment of this devastating disease.</p>\u0000 </div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142828655","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}