In Vitro Cellular & Developmental Biology. Animal最新文献

{"title":"miR- 34c- 5p targets ROCK1 expression to inhibit kidney injury in diabetic nephropathy rats through MAPK/ERK signaling pathway.","authors":"HuaJuan Wei, Ye Li, HongDe Liu, Li Pan, HuiLing Duo, ShaoYing Dong","doi":"10.1007/s11626-025-01039-w","DOIUrl":"https://doi.org/10.1007/s11626-025-01039-w","url":null,"abstract":"<p><p>This study was to investigate the mechanism of miR- 34c- 5p in alleviating kidney injury in diabetic nephropathy (DN) rats by targeting ROCK1 and MAPK/ERK signaling pathway. The rat model of DN was established and fasting blood glucose, 24-h proteinuria, blood urea nitrogen, and serum creatinine were measured to quantify kidney injury. Kidney tissue was dissected for H&E and TUNEL staining. Renal injury factor KIM- 1 was measured by Western blot analysis. Retinal Muller cells (RMCs) were treated with high glucose and transfected. Cell viability was detected by CCK- 8 and apoptosis by flow cytometry. Inflammatory factors in DN rats and RMCs were analyzed by ELISA. The targeting effect of miR- 34c- 54p on ROCK1 was demonstrated by RNA pull-down and dual-luciferase reporter gene. Finally, ROCK1, p-MEK1/2, and p-ERK were assessed by Western blot. Elevating miR- 34c- 5p could inhibit DN kidney injury and high glucose-induced cell injury, and reduce inflammation in kidney tissue of DN rats and RMCs. miR- 34c- 5p targeted to regulate ROCK1 expression, and restoring ROCK1 abolished the therapeutic effect of elevating miR- 34c- 5p. Phosphorylated MEK and ERK were increased in DN rats and RMCs induced by high glucose. miR- 34c- 5p can inhibit kidney injury induced by DN by targeting ROCK1, and the MAPK/ERK pathway may represent the pathological mechanism of DN.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144274764","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":"Enhancement of 5-fluorouracil efficacy in colorectal cancer cells through thymidylate synthase inhibition by sodium propionate.","authors":"Nayeon Kim, Yeoreum Lee, Taerim Kim, Jiyun Kim, Changwon Yang","doi":"10.1007/s11626-025-01058-7","DOIUrl":"https://doi.org/10.1007/s11626-025-01058-7","url":null,"abstract":"<p><p>5-Fluorouracil (5-FU) is a cornerstone chemotherapeutic agent commonly employed in colorectal cancer (CRC) treatment. Prolonged use of 5-FU can trigger drug resistance, primarily through the upregulation of thymidylate synthase (TS). Consequently, strategies targeting TS suppression could enhance 5-FU's therapeutic potential in resistant CRC cases. Short-chain fatty acids (SCFAs), derived from the fermentation of dietary fibers by gut microbiota, are implicated in various disease mechanisms, including cancer. Among SCFAs, sodium butyrate (NaB) is known to inhibit TS expression, reduce CRC cell viability, and promote apoptosis. However, the potential of sodium propionate (NaP), another SCFA, to exhibit similar effects remains under investigation. This study reveals that NaP, when combined with 5-FU, synergistically decreases CRC cell survival and enhances apoptosis. Furthermore, NaP counteracts the 5-FU-induced upregulation of TS, amplifying its inhibitory effects on drug-resistant CRC cells. These results suggest that NaP may serve as an effective adjunct in improving the therapeutic outcomes of 5-FU-based CRC treatments.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144234000","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":"miR-944 inhibits malignant progression of bladder cancer through ATIC/AKT/FOXO3 A axis mediated by SHMT1.","authors":"Zhiming Liu, Zhao Chen, Haibei Yang, Junning Liu, Maorong Cui, Weisheng Wang","doi":"10.1007/s11626-025-01050-1","DOIUrl":"https://doi.org/10.1007/s11626-025-01050-1","url":null,"abstract":"<p><p>To investigate the role of miR-944 in the progression of bladder cancer (BC) and explore its potential as a therapeutic target. In this study, we collected 12 pairs of BC tissues and paracancerous tissues and subcutaneously injected T24 cells into BALB/c nude mice at 1 × 10⁶/mouse to establish the BC animal model for experimental investigation. RT-qPCR and western blot were used to detect the expression of related genes and proteins, and the malignant progression of T24 cells and BC was detected by CCK-8, Transwell, scratch wound, and immunohistochemistry. This study found that miR-944 expression was low in BC clinical samples and cell lines. Overexpression of miR-944 inhibited the proliferation, migration, and invasion of BC cells and inhibited BC tumor growth in vivo. Mechanistically, overexpression of miR-944 downregulated ATIC by inhibiting SHMT1, thereby activating the AKT/FOXO3A signaling pathway and promoting the expression of autophagy-related proteins LC3II/I and Beclin1. At the same time, it can inhibit the expression of epithelial-mesenchymal transition (EMT)-related proteins vimentin, fibronectin, and N-cadherin, ultimately inhibiting the proliferation, migration, and invasion of BC cells, and increasing the apoptosis level of BC cells to improve the development of BC. Our study confirmed that the upregulation of miR-944 may become a new target for the treatment of BC.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144180948","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":"Spatiotemporal distribution of YAP and importin-β in nucleus and cytosol after wounding of adjacent cells.","authors":"Boyuan Xiao, Saori Sasaki, Naoki Takeishi, Toshihiro Sera, Susumu Kudo","doi":"10.1007/s11626-025-01054-x","DOIUrl":"https://doi.org/10.1007/s11626-025-01054-x","url":null,"abstract":"<p><p>Yes-associated protein (YAP), an important downstream mediator of the Hippo pathway, exhibits nuclear translocation when it is dephosphorylated. However, its interplay with other intracellular substances has not yet been clarified. Here, we explored mechano-induced YAP nuclear translocations and its interplay with importin-β (Impβ), one of the nucleocytoplasmic transport receptors, through live imaging of the spatiotemporal distribution of intracellular YAP and Impβ following mechanical stimulation, represented by the release of intercellular tension. YAP nuclear translocation was impeded by inhibition of Impβ and F-actin polymerization. Specifically, inhibiting F-actin polymerization not only impeded the nuclear import of YAP but also prevented its translocation from the near regions, adjacent to the wounded cell, toward the nucleus. These results provide a fundamental basis for further research into mechanotransduction, particularly mechano-induced YAP translocation, and may potentially be exploited as a therapeutic target for wound healing.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144173687","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":"NEURL1 acts as a candidate suppressor in bladder cancer by down-regulating PDE9A.","authors":"Yu Qiu, Huijie Ruan, Decai Ji, Na Cao","doi":"10.1007/s11626-025-01047-w","DOIUrl":"https://doi.org/10.1007/s11626-025-01047-w","url":null,"abstract":"<p><p>Bladder cancer is a common malignancy in the genitourinary system with its incidence rate among the world's highest. Neuralized E3 ubiquitin protein ligase 1 (NEURL1) belongs to the RING E3 ubiquitin ligase family, and its role in bladder cancer has not been reported yet. We aimed to explore the expression and roles of NEURL1 in bladder cancer. The NEURL1 expression was determined in clinical samples of bladder cancer. We stably overexpressed NEURL1 and NEURL1 with the RING domain deletion in human bladder cancer cell lines 5637 and RT-112 to investigate its functions. NEURL1 was confirmed to be significantly down-regulated in clinical bladder tumor specimens. NEURL1 overexpression significantly inhibited the growth, colony formation, and Ki-67 protein expression in both bladder cancer cells. The overexpression of NEURL1 also increased the apoptosis rate and cleaved caspase-3 protein expression in 5637 and RT-112 cells. As expected, the RING-deleted NEURL1 had no such effect. Moreover, NEURL1 overexpression facilitated the apoptosis of 5637/RT-112 cells under cisplatin conditions. NEURL1 promotes ubiquitination and proteasomal degradation of PDE9A. PDE9A protein expression was notably increased in bladder tumors from clinical specimens. Overexpressed NEURL1 inhibited PDE9A protein expression in both cell lines, whereas NEURL1 with the RING domain deletion did not. The addition of proteasome inhibitors MG-132 reversed the decrease in PDE9A expression by NEURL1 overexpression. Cell viability was inhibited and apoptosis was increased in the 5637 and RT-112 cells with stable knockdown of PDE9A. NEURL1 may be involved in the bladder cancer progression by increasing apoptosis, thereby leading to tumor cell growth inhibition.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144181428","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":"Photobiomodulation therapy: a promising treatment for insulin resistance in type 2 diabetes.","authors":"Jaber Zafari, Hanieh Sadeghi, Hossein Abbasinia, Nabaa Najjar, Saeid Jamali, Fatemeh Javani Jouni","doi":"10.1007/s11626-025-01051-0","DOIUrl":"https://doi.org/10.1007/s11626-025-01051-0","url":null,"abstract":"<p><p>Type 2 diabetes mellitus (T2DM) affects over 90% of diabetic patients and is characterized by insulin resistance (IR), primarily due to impaired GLUT4 function and abnormalities in insulin signaling within adipose and skeletal muscle cells. Dysfunctional adipose tissue elevates triglyceride and fatty acid levels, worsening IR. Photobiomodulation therapy (PBMT), which employs low-power light, has emerged as a potential treatment by enhancing glucose metabolism and reducing inflammation through the activation of the PI3K/AKT signaling pathway. Key factors influencing IR include FOXO1, GFAT-2, and PTP1B, which play significant roles in insulin signaling and glucose homeostasis. In this study, 3T3-L1 preadipocytes were cultured in high glucose DMEM with FBS and antibiotics, with differentiation induced using dexamethasone and insulin, followed by laser treatment. The viability of preadipocytes and adipocytes was assessed using the MTT assay, while oil red O staining quantified lipid droplet formation. An insulin resistance model was established, and glucose levels and gene expression were analyzed through qRT-PCR. The findings indicated that PBMT did not adversely affect cell viability and significantly reduced triglyceride levels and glucose uptake in IR models. Additionally, PBMT altered gene expression related to adipogenesis, suggesting its potential in managing IR and adipocyte function. Overall, while the mechanisms of PBMT require further investigation, the therapy shows promise in alleviating insulin resistance and its associated metabolic consequences.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144173684","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":"In vitro model of equine cartilage degradation; using cartilage pellets differentiated from bone marrow-derived mesenchymal stem cells.","authors":"Thippaporn Euppayo, Puntita Siengdee, Pakorn Limlenglert, Korakot Nganvongpanit, Gen Watanabe, Yoshinori Kasashima, Katsuhiko Arai","doi":"10.1007/s11626-025-01049-8","DOIUrl":"https://doi.org/10.1007/s11626-025-01049-8","url":null,"abstract":"<p><p>The self-renewal capacity of chondrocytes in osteoarthritis (OA) joints is limited, and mesenchymal stem cells (MSCs) are crucial in disease treatment. This study established an OA model from equine bone marrow-derived mesenchymal stem cells (eBMSCs). The eBMSCs were cultured and differentiated into chondrocytes to generate cartilage pellets, which were induced for 7 d with inflammatory cytokines, interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) to mimic OA conditions. Treated culture medium was collected to estimate enzyme activity (MMP-2, MMP-3, and MMP-9) using zymography, and the cartilage pellets were collected to estimate both anabolic gene (COL2A1) and catabolic gene expression (MMP2, MMP3, and MMP9) using qRT-PCR. Cartilage degradation was observed when induced with IL-1β + TNF-α on cartilage pellets. IL-1β + TNF-α decreased the expression levels of COL2A1 and MMP2 genes, and enhanced their enzymatic activities, while Alcian blue-positive glycosaminoglycan in cartilage pellets induced by IL-1β + TNF-α groups decreased. These results suggested that IL-1β + TNF-α induced on cartilage pellets from eBMSCs could be used as an in vitro OA model in horses.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144158364","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":"SERPINA3 is expressed in human adipocytes and modulated by TNF-α and vitamin B6.","authors":"Nataly Guzmán-Herrera, Bertha Ruíz-Madrigal, Jaime Parés-Hipólito, Luis A Salazar-Olivo","doi":"10.1007/s11626-025-01053-y","DOIUrl":"https://doi.org/10.1007/s11626-025-01053-y","url":null,"abstract":"<p><p>SERPINA3G participates in the antiadipogenesis and insulin resistance induced by TNF-α in 3T3-F442A murine cells. Here, we show that the human orthologue SERPINA3 is expressed in human subcutaneous and visceral adipose depots of normal-weight individuals and that TNF-α and RA induced the overexpression of SERPINA3 mRNA in cultured human subcutaneous and visceral adipocytes, although only TNF-α induced the expression of serpin A3 protein. We also demonstrate that vitamin B6 abrogated the expression of the SERPINA3 gene and diminished the anti-adipogenic effects of TNF-α on mature adipocytes. Our results indicate that SERPINA3 is expressed in human adipose tissues and modulates the antiadipogenic effects of TNF-α, and suggest serpin A3 could be a promissory target in the inflammatory processes linked to obesity and other adipose dysfunctions.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144158442","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":"Fenofibrate maintains the integrity of the blood-brain barrier during cerebral ischemia-reperfusion injury by inhibiting Egr- 1.","authors":"Weifeng Shan, Haiyan Lan, Yini Wu, Qiaomin Xu, Minji You, Jimin Wu","doi":"10.1007/s11626-025-01044-z","DOIUrl":"https://doi.org/10.1007/s11626-025-01044-z","url":null,"abstract":"<p><p>Blood-brain barrier (BBB) damage and dysfunction are critical pathological features associated with cerebral ischemia-reperfusion injury in stroke. Fenofibrate, a lipid-regulating drug, has an unclear role in BBB function during stroke. This study investigates the effects of fenofibrate on BBB disruption and cerebrovascular endothelial cells induced by ischemia-reperfusion. Cerebral ischemia-reperfusion injury (CIRI) models were established using the middle cerebral artery occlusion (MCAO) method. Blood-brain barrier (BBB) integrity was assessed using Evans blue dye. The permeability of human brain microvascular endothelial cells (HBMVECs) was evaluated using fluorescein isothiocyanate (FITC)-dextran permeation assays and trans-endothelial electrical resistance (TEER) measurements. Additionally, real-time polymerase chain reaction (PCR), immunohistochemistry, enzyme-linked immunosorbent assay (ELISA), and Western blot analysis were performed. We found that the administration of fenofibrate improved brain endothelial dysfunction by reducing the expression of vascular cell adhesion molecule- 1 (VCAM- 1) and E-selectin in MCAO mice. Furthermore, fenofibrate restored the expression of the tight junction protein occludin in the cortices of MCAO mice. Notably, fenofibrate alleviated BBB dysfunction in MCAO mice. In vitro studies demonstrated that fenofibrate ameliorated endothelial monolayer permeability under oxygen-glucose deprivation/reoxygenation (OGD/R) conditions and inhibited the expression of VCAM- 1 and E-selectin in HBMVECs. Moreover, fenofibrate restored occludin expression following OGD/R. We identified a novel mechanism whereby fenofibrate suppressed the elevation of Egr- 1 induced by OGD/R; however, overexpression of Egr- 1 abrogated the protective effects of fenofibrate on the upregulation of VCAM- 1 and E-selectin and the downregulation of occludin induced by OGD/R. Furthermore, overexpression of early growth response- 1 (Egr- 1) negated the protective effects of fenofibrate on endothelial monolayer permeability and trans-endothelial electrical resistance (TEER). Our findings suggest that fenofibrate may be a promising therapeutic agent for stroke treatment.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144158357","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":"Synergistic effects of micropatterned substrates and transforming growth factor-β1 on differentiation of human mesenchymal stem cells into vascular smooth muscle cells through modulation of Krϋppel-like factor 4.","authors":"Sakhavat Abolhasani, Davood Fattahi, Yasin Ahmadi, Behnaz Valipour, Majid Ghasemian, Masoumeh Rajabibazl, Khalil Maleki Chollou","doi":"10.1007/s11626-025-01033-2","DOIUrl":"https://doi.org/10.1007/s11626-025-01033-2","url":null,"abstract":"<p><p>The functionality and structural integrity of the cardiovascular system are critically dependent on vascular smooth muscle cells (VSMCs). Human mesenchymal stem cells (hMSCs) have significant potential for differentiating into VSMCs, making them a valuable resource in regenerative medicine and the development of vascular grafts. This study explored the synergistic effects of micropatterned substrates and TGF-β1 on the differentiation of hMSCs into VSMCs. HMSCs were cultured on both micropatterned and flat substrates for a duration of 6 days, with some groups receiving TGF-β1 treatment, after which cell morphology and the expression of specific smooth muscle markers were evaluated through Western blotting, immunofluorescence staining, and RT-qPCR. Results indicated that hMSCs on micropatterned substrates treated with TGF-β1 exhibited significantly elevated protein levels of smooth muscle myosin heavy chain (MYH11) compared with hMSCs on flat substrates without TGF-β1 (p < 0.001). Additionally, MYH11 expression was markedly enhanced in samples cultured on micropatterned substrates with TGF-β1. Furthermore, hMSCs treated with TGF-β1 on flat substrates exhibited increased cadherin-11 mRNA expression compared with both micropatterned and flat substrates lacking TGF-β1 (p < 0.05). Interestingly, KLF4 protein levels were significantly higher in hMSCs on flat substrates without TGF-β1 compared to those cultured on micropatterned substrates with TGF-β1 treatment (p < 0.001). In conclusion, this study demonstrated that the combination of micropatterned substrates and TGF-β1 treatment preferentially enhances MYH11 expression, indicative of advanced smooth muscle cell organization, along with modulating KLF4 levels and upregulating cadherin-11 expression in hMSCs. These findings provide critical insights into the differentiation pathways of MSCs into VSMCs and may inform the design of improved vascular grafts that better replicate the properties of native blood vessels.</p>","PeriodicalId":13340,"journal":{"name":"In Vitro Cellular & Developmental Biology. Animal","volume":" ","pages":""},"PeriodicalIF":1.5,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144127500","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}