Fatma F. Elsayed , Dina M. Abo-elmatty , Zakaria El -khayat , Emad Tolba , Alaa S. Wahba , Jihan Hussien
{"title":"The role of eicosapentaenoic acid-loaded nanoparticles on alleviating drug resistance in xenograft breast cancer model","authors":"Fatma F. Elsayed , Dina M. Abo-elmatty , Zakaria El -khayat , Emad Tolba , Alaa S. Wahba , Jihan Hussien","doi":"10.1016/j.prostaglandins.2025.107042","DOIUrl":"10.1016/j.prostaglandins.2025.107042","url":null,"abstract":"<div><h3>Background</h3><div>Multidrug resistance (MDR) is a major dilemma in the effective chemotherapy treatment of breast cancer. Potential strategies to combat MDR include inhibiting efflux pumps such as ATP-binding cassette (ABC) transporters and calcium channel pumps like transient receptor potential (TRP) channels and blocking the metastatic pathway by inhibiting the antiapoptotic proteins like Bcl-2, while enhancing the apoptotic proteins like caspase-3.</div></div><div><h3>Results</h3><div>The results demonstrated that treatment with either EPA or EPA/PCL led to a marked suppression of doxorubicin resistance, as evidenced by a significant reduction in tumor size, measured by caliper, in the treated groups over the course of the experiment. Furthermore, the combination of EPA or EPA-loaded PCL with DOX modulated the expression of drug resistance genes and apoptotic pathways by targeting transient receptor potential canonical 5 (TRPC5), P-glycoprotein (P-gp), and Bcl-2, while simultaneously enhancing the expression of caspase-3. Additionally, nano-characterization of the PCL particles using transmission electron microscopy (TEM), dynamic light scattering (DLS), and zeta potential analysis demonstrated their favorable stability and physicochemical properties.</div></div><div><h3>Conclusion</h3><div>The present study investigated the effect of eicosapentaenoic acid (EPA)-loaded polycaprolactone (PCL) in overcoming drug resistance when used in combination with doxorubicin (DOX), as compared to DOX alone and EPA in its original form. Interestingly, it reveals a promising approach to ameliorate the resistance of Doxorubicin in breast cancer.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"181 ","pages":"Article 107042"},"PeriodicalIF":2.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145363879","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}
Dustin G. Brown , Jonathan Manke , Michael Armstrong , Sangya Yadav , John O. Marentette , James R. Roede , Eszter K. Vladar , Nichole Reisdorph , Vanessa V. Phelan
{"title":"Impact of overexpression of wild-type CFTR and elexacaftor-tezacaftor-ivacaftor on oxylipin production by the CFBE41o- bronchial epithelial cell line","authors":"Dustin G. Brown , Jonathan Manke , Michael Armstrong , Sangya Yadav , John O. Marentette , James R. Roede , Eszter K. Vladar , Nichole Reisdorph , Vanessa V. Phelan","doi":"10.1016/j.prostaglandins.2025.107043","DOIUrl":"10.1016/j.prostaglandins.2025.107043","url":null,"abstract":"<div><div>A hallmark of cystic fibrosis (CF) is dysregulated lipid metabolism marked by an imbalance of pro-inflammatory to pro-resolving metabolites. Despite the breadth of evidence associating mutation of the cystic fibrosis conductance regulator (CFTR) with dysregulation of the production of oxylipins, oxidized lipid mediators with specialized functions generated during inflammation, few studies have directly measured whether overexpression of wild-type (WT) CFTR is sufficient to equilibrate oxylipin levels in CF models. In this study, targeted lipidomics was used to compare the oxylipin profiles of the parental CFBE41o- immortalized bronchial epithelial cell line homozygous for F508del CFTR, the most common CFTR mutation in people with CF, with the same cell line overexpressing WT CFTR (CFBE41o- o/e WT CFTR). Overexpression of WT CFTR in the CFBE41o- background resulted in decreased production of prostaglandins and increased production of precursors of specialized pro-resolving mediators, including 14,15-epoxyeicosatrienoic acid (14(15)-EET) compared to the parent CFBE41o- cell line, likely due to a decrease in production of inducible COX-2 associated with inflammation and an increase in COX-1 and PPARγ associated with resolution of inflammation. Additionally, highly effective modulator therapy (HEMT) improves pulmonary health for people with CF (PwCF) by targeting the underlying biochemical dysfunction of mutant CFTR. However, its impact on dysregulated lipid metabolism remains under-investigated. Despite inducing production and trafficking of F508del CFTR, treatment of the CFBE41o- parental cell line monolayers with the HEMT elexacaftor-tezacaftor-ivacaftor (ETI) increased levels of the prostaglandin E2 (PGE<sub>2</sub>). This disparity in cellular response by CFBE41o- cells to overexpression of WT CFTR and exposure to ETI was due to differences in production of prostaglandin biosynthetic and regulatory proteins upstream of oxylipin biosynthesis.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"181 ","pages":"Article 107043"},"PeriodicalIF":2.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145490048","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}
Jianyang Liu , Helena Idborg , Marina Korotkova , Per-Johan Jakobsson
{"title":"Pro-inflammatory differentiation by GM-CSF reduces prostanoid release and phagocytic activity in murine bone marrow-derived macrophages","authors":"Jianyang Liu , Helena Idborg , Marina Korotkova , Per-Johan Jakobsson","doi":"10.1016/j.prostaglandins.2025.107044","DOIUrl":"10.1016/j.prostaglandins.2025.107044","url":null,"abstract":"<div><div>Murine bone marrow-derived macrophages (BMDMs) are widely used to study macrophage functions <em>in vitro</em>. Granulocyte-macrophage colony-stimulating factor (GM-CSF) and macrophage colony-stimulating factor (M-CSF) are routinely used to differentiate monocytes into M1- and M2-like macrophages, respectively. Although macrophage-derived eicosanoids regulate both inflammation and its resolution, the impact of these differentiation factors on eicosanoid production remains poorly understood. Additionally, eicosanoid secretion and transportation has never been characterised in these macrophage populations. In the present study, we show that BMDMs differentiated in the presence of GM-CSF (hereafter referred to as GM-BMDMs) produce markedly lower levels of arachidonic acid (AA)-derived prostanoids following lipopolysaccharide (LPS) activation than macrophages differentiated with M-CSF (hereafter referred to as M-BMDMs). Moreover, we found that GM-BMDMs failed to rapidly release LPS-induced prostanoids. Mechanistically, this delayed release of prostanoids likely arises from reduced expression of the prostaglandin efflux transporter multidrug resistance protein-4 (MRP4) alongside a concomitant upregulation of the influx prostaglandin transporter (PGT). Our results also highlight that analyses of both cell pellets and supernatants are essential when comparing oxylipin profiles between M1- and M2-like macrophages. We next studied the phagocytic capacity of GM-BMDMs and found that GM-BMDMs display a blunted increase in phagocytosis of fluorescent <em>E. coli</em> bioparticles after LPS stimulation compared to M-BMDMs. Pharmacological inhibition of microsomal prostaglandin E synthase-1 (mPGES-1), but not cyclooxygenase-2 (COX-2), promotes phagocytic capacity, suggesting that mPGES-1 inhibitors may be superior to COX-2 inhibitors for suppressing inflammation. Collectively, our findings reveal that GM-CSF not only modulates the production and trafficking of prostanoids but also constrains phagocytic activity in response to LPS, which can be enhanced by mPGES-1 inhibition.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"181 ","pages":"Article 107044"},"PeriodicalIF":2.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145565057","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}
Wenhui Bao , Shuangyi Zhang , Jiamin Zhao , Zhiguo Gong , Yunjie Bai , Yanqin Dong , Wei Mao , Bo Liu
{"title":"Prostaglandin E2 is a crucial intermediator of 17β-estradiol-induced growth factor expression in bovine endometrial cells and explants","authors":"Wenhui Bao , Shuangyi Zhang , Jiamin Zhao , Zhiguo Gong , Yunjie Bai , Yanqin Dong , Wei Mao , Bo Liu","doi":"10.1016/j.prostaglandins.2025.107041","DOIUrl":"10.1016/j.prostaglandins.2025.107041","url":null,"abstract":"<div><div>Estradiol is a critical hormone that regulates morphological and functional changes in the bovine endometrium throughout the estrous cycle. Prostaglandin E<sub>2</sub> (PGE<sub>2</sub>), a well-established inflammatory mediator, also plays an essential role in endometrial physiology. Whether PGE<sub>2</sub> acts as an intermediary in estradiol-related activities within the bovine endometrium remains unclear. The results revealed that 17β-estradiol at 10<sup>−10</sup> M and 10<sup>−9</sup> M induced PGE<sub>2</sub> secretion in endometrial explants, whereas a higher concentration (10<sup>−7</sup> M) downregulated PGE₂ secretion. In endometrial epithelial cells, 17β-estradiol at concentrations ranging from 10<sup>−10</sup> to 10<sup>−8</sup> M stimulated PGE<sub>2</sub> secretion. In endometrial stromal cells, 17β-estradiol at 10<sup>−10</sup> to 10<sup>−7</sup> M concentrations promoted PGE<sub>2</sub> production. PGE<sub>2</sub> synthesis was inhibited by the mPGES-1 inhibitor MF63 [2-(6-chloro-1H-phenanthro[9,10-<em>d</em>]imidazol-2-yl) isophthalonitrile] in the presence of 17β-estradiol (10<sup>−9</sup> M), highlighting mPGES-1 as a key enzyme in 17β-estradiol-induced PGE<sub>2</sub> production in the bovine endometrium. Furthermore, both the mRNA and protein levels of endometrial growth factors, including fibroblast growth factor 2 (FGF-2), vascular endothelial growth factor A (VEGFA), matrix metalloproteinase-2 (MMP-2), and MMP-9, were increased by 17β-estradiol (10<sup>−9</sup> M). This effect was reversed by pretreatment with the mPGES-1 inhibitor MF63 in endometrial cells and explants. Notably, supplementation with exogenous PGE<sub>2</sub> restored the expression of these growth factors in the presence of both 17β-estradiol (10<sup>−9</sup> M) and MF63. In conclusion, mPGES-1-derived PGE<sub>2</sub> serves as a crucial mediator of the 17β-estradiol-induced expression of FGF-2, VEGFA, MMP-2, and MMP-9 in the bovine endometrium, underscoring its significant role in regulating endometrial function.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"181 ","pages":"Article 107041"},"PeriodicalIF":2.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145204482","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}
Matthew Stevenson, Bryan Chen, Ankita Srivastava, Christopher E. Hall, Louis Ragolia
{"title":"Lipocalin-type prostaglandin D₂ synthase (L-PGDS) deficiency disrupts heme catabolism and iron homeostasis in mice","authors":"Matthew Stevenson, Bryan Chen, Ankita Srivastava, Christopher E. Hall, Louis Ragolia","doi":"10.1016/j.prostaglandins.2025.107046","DOIUrl":"10.1016/j.prostaglandins.2025.107046","url":null,"abstract":"<div><div>Efficient recycling of red blood cells (RBCs) requires not only heme cleavage but also stabilization of reactive intermediates generated during iron liberation. Lipocalin-type Prostaglandin D₂ Synthase (<span>L</span>-PGDS, β-trace protein), best known for prostaglandin synthesis, possesses structural and biochemical features consistent with a buffering role in heme catabolism. Here, we show that <span>L</span>-PGDS knockout mice exhibit elevated plasma, increased total splenic iron, reduced total hepatic iron, decreased plasma free heme/hemin, and modest RBC enlargement, consistent with disrupted iron release. Transcript–protein mismatches in key iron regulators, including NRF2 and FPN, further suggest redox imbalance and impaired iron sensing. Despite normal Hmox1 expression, these mice display widespread evidence of inefficient porphyrin clearance. Combined with prior findings that <span>L</span>-PGDS binds ferric biliverdin and is upregulated during heme overload, our results support a model in which <span>L</span>-PGDS buffers porphyrin intermediates to facilitate their safe processing and clearance. This study identifies <span>L</span>-PGDS as a putative auxiliary factor in heme catabolism, with implications for iron recycling, erythropoiesis, and systemic iron homeostasis. All data in this report are from male mice.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"181 ","pages":"Article 107046"},"PeriodicalIF":2.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145576170","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":"The association of Cytochrome 4F2 rs2108622 genetic variant and non-genetic factors with essential hypertension among Jordanian patients attending the University of Jordan Hospital","authors":"Enas Yousef Alkasasbeh , Yazun Bashir Jarrar , Wiam Khalil , Hussein Alhawari , Malek Zihlif","doi":"10.1016/j.prostaglandins.2025.107045","DOIUrl":"10.1016/j.prostaglandins.2025.107045","url":null,"abstract":"<div><h3>Background</h3><div>Essential hypertension (EH) contributes to death and morbidity. CYP4 genes influence EH via 20-hydroxyeicosatetraenoic acid production. Identifying genetic risk factors may reveal biomarkers for EH among Jordanian patients.</div></div><div><h3>Aim</h3><div>To determine the prevalence of <em>CYP4F2 rs2108622</em> genetic variants, determine their influence on the systolic (SBP) and diastolic blood pressure (DBP), and their association with the risk of EH disease among Jordanian patients.</div></div><div><h3>Methods</h3><div>This case-control study consisted of 200 Jordanian individuals recruited from Jordan University Hospital, divided into two groups: 100 hypertensive patients (cases) and 100 non-hypertensive individuals (controls). The data for demographic, anthropometric, blood pressure measurements, glycaemic, and lipid profile measurements were collected from participants during their hospital visits and from the hospital’s computer’s record. The genotyping of <em>CYP4F2 rs2108622</em> genetic variant was done using PCR-RFLP.</div></div><div><h3>Results</h3><div>EH patients had a significantly higher mean age (45.82 ± 10.6 years, <em>P</em> < 0.001) and BMI (30.84 ± 5.27 kg/m², <em>P</em> = 0.001) compared to controls. Obesity was significantly associated with EH (OR = 3.18, <em>P</em> = 0.01). The CT genotype of <em>CYP4F2 rs2108622</em> was more frequent among EH patients (79 %) than controls (66 %) (<em>P</em> < 0.001) and was associated with increased EH risk (CT vs TT: OR = 3.02, <em>P</em> = 0.01; CT vs CC: OR = 2.71, <em>P</em> = 0.025). Genotype variations also showed significant associations with SBP (<em>P</em> = 0.019) and DBP (<em>P</em> = 0.017).</div></div><div><h3>Conclusion</h3><div>It can be concluded from this study that age, BMI and heterozygous <em>CYP4F2 rs2108622</em> genotype are significantly associated with the occurrence of EH among Jordanians. The <em>CYP4F2 rs2108622</em> genotype can be considered as a potential candidate biomarker of the development of EH. However, more studies with larger sample size are needed to validate the finding of this study.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"181 ","pages":"Article 107045"},"PeriodicalIF":2.5,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145582439","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}
Mona A. El-Bana , Jihan Hussein , Sherien M. El-Daly , Heba H. Metwaly , Mahmoud A. Abdel-Monem , Enayat A. Omara , Dalia Medhat
{"title":"Exploring the diverse signaling mechanisms of 17β-estradiol deficiency and replacement: Impacts on cognitive dysfunction in a post-menopausal experimental model","authors":"Mona A. El-Bana , Jihan Hussein , Sherien M. El-Daly , Heba H. Metwaly , Mahmoud A. Abdel-Monem , Enayat A. Omara , Dalia Medhat","doi":"10.1016/j.prostaglandins.2025.107024","DOIUrl":"10.1016/j.prostaglandins.2025.107024","url":null,"abstract":"<div><div>This study aimed to investigate brain signaling mechanisms affected by estradiol deficiency during menopause and how these pathways are modified with 17β-estradiol replacement to mitigate menopause-related changes, particularly in cognitive function and neuroinflammation, which are linked to the risk of dementia. Forty female white albino rats were divided into four groups: control, sham, ovariectomized (OVX), and OVX rats treated with 17β-estradiol. Cognitive tests using the Morris Water Maze assessed spatial learning and memory, while neurotransmitter levels were analyzed via HPLC. Serum levels of estrogen, Nerve Growth Factor (NGF), amyloid precursor protein(Aβ), and Postsynaptic Density Protein 95 (PSD-95) were measured using ELISA. Additionally, RT-PCR was used to evaluate the expression of gap junction protein connexin-43 (Cx43), Lipoprotein receptor-related protein (LRP1), and receptor for advanced glycation end products (RAGE), and aromatase expression was assessed via immunohistochemistry. Results showed that estrogen deficiency in OVX rats led to significant impairments in cognition, neurotransmitter signaling, and neurotrophic factors. Reduced NGF and altered PSD-95 levels indicated compromised neuronal health and synaptic plasticity. Increased aromatase expression reflected reduced local estrogen synthesis, potentially contributing to cognitive deficits. Upregulated RAGE and altered LRP1 expression suggested inflammatory and neurodegenerative processes, while decreased Cx43 expression and modified Aβ processing indicated impaired intercellular communication. Overall, the findings highlight the detrimental effects of estrogen deficiency on brain function and suggest that 17β-estradiol replacement may mitigate menopause-related cognitive decline and neuroinflammation.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"180 ","pages":"Article 107024"},"PeriodicalIF":2.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144660066","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":"Role of lysophosphatidic acid in the regulation of immune cells and hematological malignancies","authors":"Vishal Kumar Gupta , Kriti Gupta , Pratishtha Sonker , Manoj Mishra , Ajay Kumar","doi":"10.1016/j.prostaglandins.2025.107028","DOIUrl":"10.1016/j.prostaglandins.2025.107028","url":null,"abstract":"<div><div>Lysophosphatidic acid (LPA), a small bioactive glycerophospholipid, has been reported to play an indispensable role in the regulation of a wide range of cellular processes, including cell proliferation, morphology, differentiation, invasion, migration, and apoptosis. Besides, it has a diverse role in the development, differentiation, migration, and trafficking of immune cells. The role of LPA in the functioning of immune cells, such as macrophages, natural killer cells, T cells, and B cells has been poorly understood and is still a major thrust area for immunological research. Further, accumulating experimental evidence indicates the pro-tumoral action of LPA in various cancers, including hematological malignancies. Hematological malignancies or blood cancers are a group of neoplastic conditions derived from the cells of hematopoietic tissues. LPA is reported to promote the development and progression of cancers of hematological origin through altering apoptosis, invasion and migration, metabolism, and anti-tumor immune response. But still, the mechanistic pathways by which LPA supports the development and progression of hematological malignancies are not well explored. The present review aims to provide an elaborate survey on the role of LPA in the functioning of immune cells and its implication in hematological malignancies.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"180 ","pages":"Article 107028"},"PeriodicalIF":2.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144922990","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}
Juanjuan Zhu , Bingbing Wang , Sanaz Asemani , Shiwei Bao , Niannian Tian
{"title":"Corrigendum to “The association between vitamin D deficiency and childhood obesity and its impact on children’s serum calcium, alkaline phosphatase, and bone age” [Prostaglandins Other Lipid Mediat. 176 (2024) 106920]","authors":"Juanjuan Zhu , Bingbing Wang , Sanaz Asemani , Shiwei Bao , Niannian Tian","doi":"10.1016/j.prostaglandins.2025.107025","DOIUrl":"10.1016/j.prostaglandins.2025.107025","url":null,"abstract":"","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"180 ","pages":"Article 107025"},"PeriodicalIF":2.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144668262","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}