In Vitro Cellular & Developmental Biology. Animal最新文献

{"title":"Role of PDGFRα-mediated signalling in anoikis resistance in glioblastoma: in vitro study.","authors":"Sneha Raut, Meet Makwana, Prakash Pillai","doi":"10.1007/s11626-025-01075-6","DOIUrl":"https://doi.org/10.1007/s11626-025-01075-6","url":null,"abstract":"<p><p>Anoikis resistance, the evasion of programmed cell death when cells detach from the extracellular matrix (ECM), is a critical feature of glioblastoma (GBM) malignancy, contributing to tumor survival, spread, and resistance to therapy. We focused on the role of growth factor receptors, particularly platelet-derived growth factor receptor-α (PDGFRα), and integrin expression patterns in mediating this resistance. We first cultured cells under non-adherent conditions using polyHEMA-treated plates to induce anoikis resistance. We performed assays like cell survival, migration, and sphere formation. To delineate the role of PDGFRα signalling in anoikis resistance, we further employed pharmacological inhibitors of key signalling molecules such as AG1295 (PDGFRα blocker), HS173 (PI3K inhibitor), U0126 (ERK inhibitor), and AG490 (JAK-STAT inhibitor) which led to a decrease in cell survival, proliferation, and migration. These findings highlight the critical role of PDGFRα and associated signalling pathways in mediating anoikis resistance in GBM, offering potential therapeutic targets for intervention.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144682557","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adhesion extracellular matrix proteins improve in vitro cellular and functional properties of enriched caprine adult dermal fibroblast.","authors":"Juhi Pathak, Shiva Pratap Singh, Manisha Pathak, Vishal Khandelwal, Yogesh Kumar Soni, Manoj Kumar Singh","doi":"10.1007/s11626-025-01065-8","DOIUrl":"https://doi.org/10.1007/s11626-025-01065-8","url":null,"abstract":"","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144682555","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Functions of ectodysplasin A2 receptor (EDA2R) in inducing capacitation of sperm in mice.","authors":"Oluwakemi I Anjorin, Takahiro Yamanaka, Masayuki Shimada","doi":"10.1007/s11626-025-01084-5","DOIUrl":"https://doi.org/10.1007/s11626-025-01084-5","url":null,"abstract":"<p><p>Sperm capacitation, a prerequisite for fertilization, is regulated not only by intrinsic signaling but also by paracrine factors within the female tract. Analysis of previously published RNA-seq datasets identified the ectodysplasin-A2 receptor (EDA2R), an X-linked member of the TNF-receptor superfamily, as a candidate regulator of this process. This study was conducted to test the hypothesis that the EDA-A2/EDA2R axis is a regulator that directly regulates sperm capacitation during fertilization process. Western blotting and immunofluorescence showed that EDA2R was localized in late spermatogenic cells and in the midpiece of epididymal sperm. Incubation of mouse sperm in HTF medium containing the corresponding ligand EDA-A2 (0-1 µg/mL) resulted in a dose-dependent improvement in the amplitude of lateral head displacement and curvilinear velocities. Ligand exposure promoted the appearance of capacitation hallmarks: tyrosine phosphorylation level was elevated within 30 min and the proportion of FITC-PNA positive, acrosome-reacted cells increased at 30 and 60 min (p < 0.05). The EDA-A2 treated sperm yielded a higher cleavage rate (78.5% vs. 48.3%) and a higher blastocyst formation rate (97.6% vs. 88.4%) after in vitro fertilization. qPCR in hormonally synchronized females revealed transient ovarian and prolonged oviductal Eda-a2 upregulation surrounding ovulation, suggesting that the ligand is present at the site of sperm-oocytes fertilization. These results clarify that EDA-A2/EDA2R is a rapid physiological driver of sperm capacitation. This provides a tractable cytokine axis for optimizing assisted reproduction.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144682556","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bone marrow-derived mesenchymal stem cells and their extracellular vesicles suppress splenocyte activation and ameliorate experimental autoimmune encephalomyelitis.","authors":"Sina Vakili, Majid Reza Farrokhi, Mahsa Motamed, Morteza Jafarinia, Shima Shapoori","doi":"10.1007/s11626-025-01077-4","DOIUrl":"https://doi.org/10.1007/s11626-025-01077-4","url":null,"abstract":"<p><p>Multiple sclerosis (MS) is a neurodegenerative and autoimmune disease affecting the central nervous system (CNS). Recently, mesenchymal stem cells (MSCs) and their extracellular vesicles (EVs) have been extensively studied as a potential treatment for MS. In this study, we examined the impact of therapy using EVs derived from murine bone marrow MSCs (BMSC-EVs) on the proliferation of splenocytes, frequency of regulatory T cells (Tregs), and cytokine secretion in mice induced with experimental autoimmune encephalomyelitis (EAE), comparing the effects with those of their parent cells. After inducing EAE in 30 mice, the animals were divided into three groups and treated with PBS, BMSCs, or BMSC-EVs. The mice were sacrificed on day 30 post-immunization, and their splenocytes were isolated for further analysis. The proliferation of splenocytes was assessed by measuring the fluorescent intensity of CFSE dye using a FACSCalibur flow cytometer, the frequency of Treg cells was determined by flow cytometry, and cytokine levels of tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β, IL-6, IL-10, and transforming growth factor-beta (TGF-β) were measured using enzyme-linked immunosorbent assay (ELISA). The results showed that treatment with BMSC and BMSC-EV both significantly reduced splenocyte proliferation, increased Treg cell frequency, and shifted cytokine profiles toward reduced pro-inflammatory (TNF-α, IL-1β, IL-6) and increased anti-inflammatory (IL-10, TGF-β) cytokines compared to untreated EAE controls, with comparable efficacy between BMSCs and BMSC-EVs. These findings emphasize the capability of BMSC-EVs to serve as a cell-free therapy for immune response modulation in EAE.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144649312","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cyto-genotoxic assessment of bisphenol P through expression of DNA damage/repair genes in MDBK cell line.","authors":"Muhammad Muddassir Ali, Samra Afzal, Maryam Javed, Imran Rashid, Furqan Awan, Asad Ullah, Tanveer Majeed, Hadeer Darwish, Ahmed Noureldeen, Jawaher Albaqami, Khalid Mehmood","doi":"10.1007/s11626-025-01068-5","DOIUrl":"https://doi.org/10.1007/s11626-025-01068-5","url":null,"abstract":"<p><p>Bisphenol P (BPP) is a recognized endocrine disruptor with detrimental effects on human health. This study aimed to evaluate BPP's cytotoxic and genotoxic effects on Madin-Darby bovine kidney (MDBK) cells by examining changes in gene expression, genotoxicity, and cell survival. Various assays were employed, including the MTT assay, comet assay, micronucleus assay, and real-time PCR for gene expression analysis. Among the series of concentrations (0.5 µM, 1 µM, 2 µM, 4 µM, 8 µM, 16 µM, 32 µM, 64 µM, 128 µM, and 256 µM), the treatment with 32 µM BPP (LC₅₀) resulted in 50% cell viability after 24 h via MTT assay. The comet assay revealed a significant increase in comet tail length in BPP-treated groups compared to controls, indicating DNA with the highest damage at the 3xLC_50/2 dose concentration of BPP. The frequency of micronuclei (MNi) was higher than binuclei. A significantly higher level of cytokinesis-block proliferation index (CBPI) was also observed at higher doses than in the negative control group. Gene expression analysis indicated increased levels of OGG1 and HPRT1 in BPP-treated cells compared to untreated controls, with a dose-dependent elevation in OGG1 expression involved in DNA damage response. This study concluded that BPP exhibits both cytotoxic and genotoxic effects on MDBK cells. Expression of DNA repair genes (OGG1, HPRT1) served as biomarkers for genotoxicity. Furthermore, it is recommended that additional studies on BPP's molecular toxicity and its cross-species effects should be explored further to combat its harmful effects.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144608244","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"α-Cyperone affects the development and chemosensitivity of breast cancer by modulating TRIM24.","authors":"Xiaojun Zhang, Fang Wang, Yuna Dai, Zhaoyu Gao, Jianchao He","doi":"10.1007/s11626-025-01067-6","DOIUrl":"https://doi.org/10.1007/s11626-025-01067-6","url":null,"abstract":"<p><p>Breast cancer (BC) refers to a malignant neoplasm that takes place in the epithelial tissue of the breast. α-Cyperone (α-CYP) is one of the principal active components of Cyperus rotundus. However, research on the role of α-CYP in the development of BC is still lacking. This study investigates the effect and underlying mechanism of α-CYP in the progression of BC. Our findings revealed that both low-dose and high-dose α-CYP inhibited the colony formation ability of MCF-7 and BT474 cells, accompanied by the decrease in Ki67 expression and the obstruction of the cell cycle. Moreover, α-CYP treatment increased the activity of caspase-3, which leads to an increase in apoptosis. Moreover, the combination of α-CYP and cisplatin (DDP) remarkably suppressed cell viability and further facilitated apoptosis, indicating that α-CYP could enhance the sensitivity of chemotherapeutic agents in BC cells. Further, α-CYP treatment decreased TRIM24 expression through the ubiquitin-proteasome pathway. Notably, α-CYP counteracted the robust proliferation of BC cells triggered by TRIM24 overexpression. Taken together, this study confirmed that α-CYP is an effective anticancer component for BC treatment. α-CYP inhibits proliferation and induces apoptosis of BC cells via the modulation of TRIM24.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144600273","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"5-Methoxytryptophan improves cerebrovascular injury induced by chronic kidney disease through NF-κB pathway.","authors":"Xiaoyan Zhou, Yan Sun, Guoshuai Yang","doi":"10.1007/s11626-025-01057-8","DOIUrl":"https://doi.org/10.1007/s11626-025-01057-8","url":null,"abstract":"<p><p>5-Methoxytryptophan (5-MTP), a candidate biomarker for chronic kidney disease (CKD), has an undefined role in cerebrovascular pathophysiology. To investigate this, we employed a folic acid (FA)-induced CKD to simulate cerebrovascular complications in vivo. Additionally, in vitro models of cerebral ischemia and cerebrovascular endothelial cell injury were established. 5-MTP was administered to rats and cells, along with nuclear factor-κB (NF-κB) expression. The pathological characteristics of kidney and brain tissue were observed by histological staining. Cell proliferation was assessed using the Cell Counting Kit 8, while tube formation and migration were examined using tube formation and wound healing assays. Cell apoptosis was detected using both TdT-mediated dUTP-biotin nick end labeling and flow cytometry. Levels of renal injury markers, blood biomarkers of cerebrovascular disease, and inflammatory cytokines were measured using biochemical assays. Quantitative real-time PCR and Western blot were used to detect the mRNA and protein expression, respectively. Key findings revealed that FA successfully induced CKD in rats, which subsequently exacerbated cerebrovascular dysfunction. 5-MTP reduced the levels of proteinuria, N-acetyl-beta-D-glucosaminidase, nephrin, endothelin-1, von Willebrand factor, and thrombomodulin; improved the degree of renal fibrosis and structural damage to the brain tissue; and inhibited cell apoptosis in rats. In vitro, 5-MTP promoted cell proliferation, tube formation, migration, and the upregulation of B-cell lymphoma-2 and caspase-3 expression. This treatment also led to an increase in interleukin (IL)-10 levels while suppressing cell apoptosis, Bcl-2-associated X protein (Bax), and cleaved caspase-3 expression. Furthermore, it reduced the IL-6 and tumor necrosis factor-alpha levels. NF-κB overexpression reversed the effects of 5-MTP in vitro and in vivo. Our results demonstrate that 5-MTP ameliorated CKD-induced cerebrovascular injury through the NF-κB pathway, indicating its potential as an innovative and efficacious therapeutic target for CKD-induced cerebrovascular dysfunction.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144591160","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ginsenoside Rg1 mitigates myocardial ischemia/reperfusion injury by inhibiting NLRP3-mediated pyroptosis.","authors":"Qian-Hui Li, Jun-Xian Shen, Shuai-Lei Xu, Kang-Zhen Zhang","doi":"10.1007/s11626-025-01070-x","DOIUrl":"https://doi.org/10.1007/s11626-025-01070-x","url":null,"abstract":"<p><p>Nucleotide-binding oligomerisation domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome activation and pyroptosis exert the pivotal influence on myocardial ischemia/reperfusion (I/R) injury. Ginsenoside Rg1 (Rg1) reportedly has multiple pharmacological actions. However, the cardioprotective potential and underlying mechanism of Rg1 in treating myocardial I/R injury in the context of pyroptosis have not been comprehensively investigated. A rat model of myocardial I/R injury was established by blocking the left anterior descending coronary artery for 30 min followed by reperfusion for 120 min. The prevention of Rg1 against I/R-caused damage and the potential mechanisms were explored. In our study, NLRP3 overexpression abolished the cardioprotective effect of Rg1, and Rg1 treatment improved myocardial function and changes in histological morphology and suppressed I/R-induced cytotoxicity as well as cardiomyocyte pyroptosis by reducing the pyroptosis-related proteins. These results indicate that Rg1 mitigated I/R-induced myocardial damage and pyroptosis by dramatically suppressing NLRP3 inflammasome activation and may provide new insights for the treatment of ischemic heart disease.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144583816","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dexmedetomidine preserves neuronal function by promoting mitochondrial biogenesis through the AMPK/PGC-1α pathway.","authors":"Li Wang, Meng Zhang, Shaowei Wang, Zhen Xing, Tong Jia, Xiaojia Sun, Hui Liu, Jie Yao, Yanlin Chen","doi":"10.1007/s11626-025-01059-6","DOIUrl":"https://doi.org/10.1007/s11626-025-01059-6","url":null,"abstract":"<p><p>Mitochondrial dysfunction, often linked to the deregulation of mitochondrial biogenesis, plays a significant role in the progression of neurological diseases. Dexmedetomidine (Dex), a selective alpha-2 adrenergic agonist utilized for anesthesia and sedation, has a largely unexplored impact on mitochondrial function. In this study, cells were treated with Dex at concentrations of 10 μg/mL and 20 μg/mL. Mitochondrial function was assessed by measuring mitochondrial membrane potential, adenosine triphosphate (ATP) production, and oxygen consumption rates. The expression levels of key mitochondrial genes and proteins were analyzed using quantitative polymerase chain reaction (qPCR) and Western blot. To investigate the role of AMP-activated protein kinase α (AMPK), cells were co-treated with the AMPK inhibitor Compound C. Our results demonstrate that treating cells with Dex significantly enhances mitochondrial membrane potential, ATP production, and oxygen consumption rates. Additionally, Dex increases the expression of vital mitochondrial genes, including Mitochondrially Encoded NADH: Ubiquinone Oxidoreductase Core Subunit 6 (mtND6), Mitochondrially Encoded Cytochrome c Oxidase II (mtCO2), and Mitochondrially Encoded ATP Synthase 6 (mtATP6), while also improving the mtDNA-to-nDNA ratio. The treatment raises Messenger Ribonucleic Acid (mRNA) and protein levels of essential mitochondrial biogenesis regulators such as Nuclear Respiratory Factor 1(Nrf1), Mitochondrial Transcription Factor A (TFAM), Peroxisome Proliferator-Activated Receptor Gamma Coactivator-1α (PGC-1α), and phosphorylated AMP-Activated Protein Kinase α (p-AMPKα). However, when cells are co-treated with the AMPK inhibitor compound C, these positive effects are lost, highlighting the necessity of AMPK activation for the mitochondrial enhancements induced by Dex. These findings suggest a promising therapeutic potential for Dex in supporting neuronal function through mitochondrial pathways.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144583815","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Xuebijing inhibits alveolar macrophage M1 polarization by regulating ROS-mediated NLRP3 inflammasome signaling.","authors":"Xuelian Chen, Fan Zhang, Zhiguo Zhou, Dixuan Jiang, Long Wen","doi":"10.1007/s11626-025-01063-w","DOIUrl":"https://doi.org/10.1007/s11626-025-01063-w","url":null,"abstract":"<p><strong>Background: </strong>Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are devastating acute pulmonary conditions with high mortality rates and limited effective treatment options. This study aimed to investigate the therapeutic potential of XBJ on ALI and its potential mechanism.</p><p><strong>Methods: </strong>We developed an in vitro model of lipopolysaccharide (LPS)-induced ALI and evaluated the effects of XBJ pre-treatment on oxidative stress, inflammatory responses, and the polarization state of alveolar macrophages.</p><p><strong>Results: </strong>LPS exposure significantly elevated the levels of reactive oxygen species (ROS) and oxidants 8-hydroxy-2'-deoxyguanosine (8-OHDG) and malondialdehyde (MDA) in alveolar macrophages. It also elevated the concentrations of pro-inflammatory cytokines, including tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and IL-23. XBJ and quercetin significantly mitigated the increase in these indicators. Moreover, XBJ and quercetin both downregulated the expression of key proteins in the NLRP3 inflammasome pathway in the ALI model. Similar to the ROS inhibitor N-acetylcysteine (NAC), XBJ and quercetin significantly decreased M1 polarization markers like CD86 and inducible nitric oxide synthase (iNOS), while increasing M2 polarization markers such as CD206 and arginase-1 (Arg-1). Notably, the overexpression of NLRP3 was able to reverse the inhibitory effect of XBJ on macrophage M1 polarization.</p><p><strong>Conclusion: </strong>XBJ inhibits the M1 polarization of alveolar macrophages by targeting ROS-mediated NLRP3 inflammasome signaling, thereby reducing the inflammatory response. These results indicate that XBJ may offer a novel therapeutic strategy for ALI/ARDS by modulating macrophage polarization and inflammation.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560036","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}