Pub Date : 2024-09-19DOI: 10.1007/s10528-024-10915-1
Ruonan Wang, He Meng, Xiaomeng Sun, Yihui Wang, Chunyu Ji, Yulin Jin, Yu Song
Severe Corona Virus Disease 2019 (COVID-19) patients may develop acute respiratory distress syndrome (ARDS). Modified Ginseng Baidu Powder (referred to as Baidu Powder) was used for respiratory system diseases caused by colds. To study the effect of Baidu Powder on protecting ARDS mice model and its underlying active ingredients and targets intervening in COVID-19. The optimal LPS concentration was selected for the induction of mouse ARDS model, and the protective effect of Baidu Powder prophylactic administration on LPS-induced ARDS mouse models was explored by mouse survival time analysis, lung wet/dry weight (W/D) ratio, pathological staining, and inflammatory factor detection. On the basis of pharmacodynamics, the network pharmacological analysis was used for target prediction for future mechanism study. 5 mg/kg LPS was selected for the construction of a mouse ARDS model, based on a mortality rate of 87% and the lung W/D ratio of 5.29 ± 0.23. Prophylactic administration of Baidu Powder at 125 g/L significantly reduced death, lung damage, inflammatory cell infiltration, and cytokine production (TNF-α, IL-6, and IL-10) caused by LPS-induced ARDS. The results of network pharmacological analysis showed that 42 target genes of Baidu Powder intervening in COVID-19 were involved in 30 biological processes related to COVID-19 and inflammation, and 11 signaling pathways related to lung diseases or inflammation. 5 mg/kg LPS can successfully establish a mice ARDS disease model; 125 g/L Baidu Powder prophylactic administration does not have toxicity and has a certain effect on protecting ARDS mouse models induced by LPS. Baidu Powder may intervene COVID-19-induced ARDS through multiple targets.
{"title":"Protective Effect of Modified Ginseng Baidu Powder Prophylactic Administration on LPS-Induced Acute Respiratory Distress Syndrome in Mice.","authors":"Ruonan Wang, He Meng, Xiaomeng Sun, Yihui Wang, Chunyu Ji, Yulin Jin, Yu Song","doi":"10.1007/s10528-024-10915-1","DOIUrl":"https://doi.org/10.1007/s10528-024-10915-1","url":null,"abstract":"<p><p>Severe Corona Virus Disease 2019 (COVID-19) patients may develop acute respiratory distress syndrome (ARDS). Modified Ginseng Baidu Powder (referred to as Baidu Powder) was used for respiratory system diseases caused by colds. To study the effect of Baidu Powder on protecting ARDS mice model and its underlying active ingredients and targets intervening in COVID-19. The optimal LPS concentration was selected for the induction of mouse ARDS model, and the protective effect of Baidu Powder prophylactic administration on LPS-induced ARDS mouse models was explored by mouse survival time analysis, lung wet/dry weight (W/D) ratio, pathological staining, and inflammatory factor detection. On the basis of pharmacodynamics, the network pharmacological analysis was used for target prediction for future mechanism study. 5 mg/kg LPS was selected for the construction of a mouse ARDS model, based on a mortality rate of 87% and the lung W/D ratio of 5.29 ± 0.23. Prophylactic administration of Baidu Powder at 125 g/L significantly reduced death, lung damage, inflammatory cell infiltration, and cytokine production (TNF-α, IL-6, and IL-10) caused by LPS-induced ARDS. The results of network pharmacological analysis showed that 42 target genes of Baidu Powder intervening in COVID-19 were involved in 30 biological processes related to COVID-19 and inflammation, and 11 signaling pathways related to lung diseases or inflammation. 5 mg/kg LPS can successfully establish a mice ARDS disease model; 125 g/L Baidu Powder prophylactic administration does not have toxicity and has a certain effect on protecting ARDS mouse models induced by LPS. Baidu Powder may intervene COVID-19-induced ARDS through multiple targets.</p>","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142278424","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}
Pub Date : 2024-09-18DOI: 10.1007/s10528-024-10901-7
Chen Wang, Jiajie Chen, Xu Wang, Xinyu Liang, Shulin Yu, Yu Gui, Xi Wen, Huabing Zhang, Shengxiu Liu
Infantile hemangioma (IH) is the most common benign vascular tumor during infancy and childhood and is characterized by abnormal vascular development. It is the most common vascular tumor and its related mechanisms and treatments remain a problem. IH-related biomarkers have been identified using transcriptome analysis and can be used to predict clinical outcomes. This study aimed to identify the key target genes for IH treatment and explore their possible roles in the IH pathophysiology. Gene records were acquired from the Gene Expression Omnibus database. Utilizing integrated weighted gene co-expression network examination, gene clusters were determined. Single-sample gene set enrichment analysis was performed to gauge immune infiltration. Essential genes were identified via Random Forest and Least Absolute Selection and Shrinkage Operator analyses. Ultimately, a set of five pivotal genes associated with the ailment was identified (NETO2, IDO1, KDR, MEG3, and TMSB15A). A nomogram for predicting IH diagnosis was constructed based on hub genes. The calibration curve showed valid agreement between the prediction and conclusion that the key genes in the model were clinically significant. Neuropilin and Tolloid-like 2 (NETO2) are closely associated with tumor development. The role value of NETO2 expression levels increased in hemangioma-derived endothelial cells (HemECs). After silencing NETO2, the growth and migration of cancer cells were significantly restrained. This study revealed the critical role of NETO2 in IH development, suggesting that targeting NETO2 may be effective in improving the therapeutic outcome of IH.
婴幼儿血管瘤(IH)是婴幼儿时期最常见的良性血管肿瘤,其特点是血管发育异常。它是最常见的血管肿瘤,其相关机制和治疗方法仍是一个难题。目前已通过转录组分析确定了与IH相关的生物标志物,并可用于预测临床结果。本研究旨在确定IH治疗的关键靶基因,并探讨它们在IH病理生理学中可能发挥的作用。基因记录来自基因表达总库数据库。利用综合加权基因共表达网络检查,确定基因集群。进行单样本基因组富集分析以衡量免疫浸润。通过随机森林和最小绝对选择及收缩操作器分析确定了重要基因。最终,确定了一组与该疾病相关的五个关键基因(NETO2、IDO1、KDR、MEG3 和 TMSB15A)。根据枢纽基因构建了预测 IH 诊断的提名图。校准曲线显示,预测结果与模型中的关键基因具有临床意义的结论之间存在有效的一致性。Neuropilin and Tolloid-like 2(NETO2)与肿瘤的发展密切相关。NETO2表达水平在血管瘤衍生内皮细胞(HemECs)中的作用价值增加。沉默 NETO2 后,癌细胞的生长和迁移明显受到抑制。这项研究揭示了NETO2在IH发展过程中的关键作用,提示靶向NETO2可能有效改善IH的治疗效果。
{"title":"Identifying Potential Diagnostic and Therapeutic Targets for Infantile Hemangioma Using WGCNA and Machine Learning Algorithms","authors":"Chen Wang, Jiajie Chen, Xu Wang, Xinyu Liang, Shulin Yu, Yu Gui, Xi Wen, Huabing Zhang, Shengxiu Liu","doi":"10.1007/s10528-024-10901-7","DOIUrl":"https://doi.org/10.1007/s10528-024-10901-7","url":null,"abstract":"<p>Infantile hemangioma (IH) is the most common benign vascular tumor during infancy and childhood and is characterized by abnormal vascular development. It is the most common vascular tumor and its related mechanisms and treatments remain a problem. IH-related biomarkers have been identified using transcriptome analysis and can be used to predict clinical outcomes. This study aimed to identify the key target genes for IH treatment and explore their possible roles in the IH pathophysiology. Gene records were acquired from the Gene Expression Omnibus database. Utilizing integrated weighted gene co-expression network examination, gene clusters were determined. Single-sample gene set enrichment analysis was performed to gauge immune infiltration. Essential genes were identified via Random Forest and Least Absolute Selection and Shrinkage Operator analyses. Ultimately, a set of five pivotal genes associated with the ailment was identified (<i>NETO2</i>, <i>IDO1</i>, <i>KDR</i>, <i>MEG3</i>, and <i>TMSB15A</i>). A nomogram for predicting IH diagnosis was constructed based on hub genes. The calibration curve showed valid agreement between the prediction and conclusion that the key genes in the model were clinically significant. Neuropilin and Tolloid-like 2 (<i>NETO2</i>) are closely associated with tumor development. The role value of <i>NETO2</i> expression levels increased in hemangioma-derived endothelial cells (HemECs). After silencing <i>NETO2</i>, the growth and migration of cancer cells were significantly restrained. This study revealed the critical role of <i>NETO2</i> in IH development, suggesting that targeting <i>NETO2</i> may be effective in improving the therapeutic outcome of IH.</p>","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142260475","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}
Pub Date : 2024-09-17DOI: 10.1007/s10528-024-10911-5
Muhammad Zafar Saleem, Ghulam Zahra Jahangir, Ammara Saleem, Asma Zulfiqar, Khalid Ali Khan, Sezai Ercisli, Baber Ali, Muhammad Hamzah Saleem, Aroona Saleem
Recombinant antibodies, a prominent class of recombinant proteins, are witnessing substantial growth in research and diagnostics. Recombinant antibodies are being produced employing diverse hosts ranging from highly complex eukaryotes, for instance, mammalian cell lines (and insects, fungi, yeast, etc.) to unicellular prokaryotic models like gram-positive and gram-negative bacteria. This review delves into these production methods, highlighting approaches like antibody phage display that employs bacteriophages for gene library creation. Recent studies emphasize monoclonal antibody generation through hybridoma technology, utilizing hybridoma cells from myeloma and B-lymphocytes. Transgenic plants and animals have emerged as sources for polyclonal and monoclonal antibodies, with transgenic animals preferred due to their human-like post-translational modifications and reduced immunogenicity risk. Chloroplast expression offers environmental safety by preventing transgene contamination in pollen. Diverse production technologies, such as stable cell pools and clonal cell lines, are available, followed by purification via techniques like affinity chromatography. The burgeoning applications of recombinant antibodies in medicine have led to their large-scale industrial production.
重组抗体是一类重要的重组蛋白,在研究和诊断领域的应用正在大幅增长。重组抗体的宿主多种多样,既有高度复杂的真核生物,如哺乳动物细胞系(以及昆虫、真菌、酵母等),也有单细胞原核生物模型,如革兰氏阳性和革兰氏阴性细菌。本综述将深入探讨这些生产方法,重点介绍利用噬菌体创建基因库的抗体噬菌体展示等方法。最近的研究强调通过杂交瘤技术,利用骨髓瘤和 B 淋巴细胞的杂交瘤细胞产生单克隆抗体。转基因植物和动物已成为多克隆和单克隆抗体的来源,转基因动物因其类似人类的翻译后修饰和较低的免疫原性风险而受到青睐。叶绿体表达可防止花粉中的转基因污染,从而保证环境安全。目前有多种生产技术,如稳定细胞池和克隆细胞系,然后通过亲和层析等技术进行纯化。重组抗体在医学上的应用日益广泛,导致了大规模的工业化生产。
{"title":"Production Technologies for Recombinant Antibodies: Insights into Eukaryotic, Prokaryotic, and Transgenic Expression Systems","authors":"Muhammad Zafar Saleem, Ghulam Zahra Jahangir, Ammara Saleem, Asma Zulfiqar, Khalid Ali Khan, Sezai Ercisli, Baber Ali, Muhammad Hamzah Saleem, Aroona Saleem","doi":"10.1007/s10528-024-10911-5","DOIUrl":"https://doi.org/10.1007/s10528-024-10911-5","url":null,"abstract":"<p>Recombinant antibodies, a prominent class of recombinant proteins, are witnessing substantial growth in research and diagnostics. Recombinant antibodies are being produced employing diverse hosts ranging from highly complex eukaryotes, for instance, mammalian cell lines (and insects, fungi, yeast, etc.) to unicellular prokaryotic models like gram-positive and gram-negative bacteria. This review delves into these production methods, highlighting approaches like antibody phage display that employs bacteriophages for gene library creation. Recent studies emphasize monoclonal antibody generation through hybridoma technology, utilizing hybridoma cells from myeloma and B-lymphocytes. Transgenic plants and animals have emerged as sources for polyclonal and monoclonal antibodies, with transgenic animals preferred due to their human-like post-translational modifications and reduced immunogenicity risk. Chloroplast expression offers environmental safety by preventing transgene contamination in pollen. Diverse production technologies, such as stable cell pools and clonal cell lines, are available, followed by purification via techniques like affinity chromatography. The burgeoning applications of recombinant antibodies in medicine have led to their large-scale industrial production.</p>","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2024-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142260476","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}
Pub Date : 2024-09-14DOI: 10.1007/s10528-024-10905-3
Ling Hu, Linfeng Xie, Shan Huang, Qiu Li
LncRNA HAND2-AS1 is a novel cancer regulator, but the role and mechanisms of HAND2-AS1 involved with colon cancer (CC) progression remains unknown. The purpose of this research was to figure out how HAND2-AS1 regulates the progression of CC. Using qRT-PCR, we studied expression levels of miR-3118, HAND2-AS1, and ZG16 in CC tissues and cells. Protein levels of apoptosis-related proteins (Bax and Bcl-2) and ZG16 were quantified by western blotting. In vitro function analysis referred to western blotting, wound healing assay and CCK-8. The binding association among miR-3118, HAND2-AS1, and ZG16 was investigated using luciferase reporter and RIP assays. The functional role of HAND2-AS1 was analyzed using xenograft tumor models in vivo. In tissues and cells of CC, HAND2-AS1 was downregulated. We observed that HAND2-AS1 overexpression declined CC cell proliferation and migration while facilitating apoptosis. We further verified that when HAND2-AS1 is overexpressed it reduced CC tumor development in vivo. In CC cells and tissues, miR-3118 competed with HAND2-AS1 and was elevated. Further it was noted that the HAND2-AS1 when overexpressed, lessened the survival of CC cells, however overexpression of miR-3118 restored these changes. ZG16 was shown to be a target of miR-3118, it was found that ZG16 was downregulated in CC tissue and cells. We observed, high expression of ZG16 partially restored the enhanced malignant phenotype caused by miR-3118 overexpression. HAND2-AS1 inhibited CC progression by upregulating ZG16 expression through sponging miR-3118. Hence, HAND2-AS1/miR-3118/ZG16 axis could be a possible new target for CC treatment.
LncRNA HAND2-AS1是一种新型癌症调控因子,但HAND2-AS1在结肠癌(CC)进展中的作用和机制仍不清楚。本研究的目的是弄清HAND2-AS1如何调控CC的进展。通过 qRT-PCR,我们研究了 miR-3118、HAND2-AS1 和 ZG16 在 CC 组织和细胞中的表达水平。蛋白水平(Bax和Bcl-2)和ZG16通过Western印迹进行定量。体外功能分析参考了 Western 印迹、伤口愈合试验和 CCK-8。利用荧光素酶报告和 RIP 试验研究了 miR-3118、HAND2-AS1 和 ZG16 之间的结合关系。利用体内异种移植肿瘤模型分析了HAND2-AS1的功能作用。在CC的组织和细胞中,HAND2-AS1被下调。我们观察到,HAND2-AS1过表达会降低CC细胞的增殖和迁移,同时促进细胞凋亡。我们进一步证实,当HAND2-AS1过表达时,会减少CC肿瘤在体内的发展。在CC细胞和组织中,miR-3118与HAND2-AS1竞争并升高。此外,研究还发现,HAND2-AS1过表达会降低CC细胞的存活率,而miR-3118的过表达则会恢复这些变化。ZG16被证明是miR-3118的靶标,研究发现ZG16在CC组织和细胞中被下调。我们观察到,ZG16的高表达部分恢复了miR-3118过表达导致的恶性表型增强。HAND2-AS1通过疏导miR-3118,上调ZG16的表达,从而抑制了CC的进展。因此,HAND2-AS1/miR-3118/ZG16轴可能是治疗CC的新靶点。
{"title":"LncRNA HAND2-AS1 Inhibited Colon Cancer Progression By Regulating miR-3118/ZG16 Axis","authors":"Ling Hu, Linfeng Xie, Shan Huang, Qiu Li","doi":"10.1007/s10528-024-10905-3","DOIUrl":"https://doi.org/10.1007/s10528-024-10905-3","url":null,"abstract":"<p>LncRNA HAND2-AS1 is a novel cancer regulator, but the role and mechanisms of HAND2-AS1 involved with colon cancer (CC) progression remains unknown. The purpose of this research was to figure out how HAND2-AS1 regulates the progression of CC. Using qRT-PCR, we studied expression levels of miR-3118, HAND2-AS1, and ZG16 in CC tissues and cells. Protein levels of apoptosis-related proteins (Bax and Bcl-2) and ZG16 were quantified by western blotting. In vitro function analysis referred to western blotting, wound healing assay and CCK-8. The binding association among miR-3118, HAND2-AS1, and ZG16 was investigated using luciferase reporter and RIP assays. The functional role of HAND2-AS1 was analyzed using xenograft tumor models in vivo<i>.</i> In tissues and cells of CC, HAND2-AS1 was downregulated. We observed that HAND2-AS1 overexpression declined CC cell proliferation and migration while facilitating apoptosis. We further verified that when HAND2-AS1 is overexpressed it reduced CC tumor development in vivo. In CC cells and tissues, miR-3118 competed with HAND2-AS1 and was elevated. Further it was noted that the HAND2-AS1 when overexpressed, lessened the survival of CC cells, however overexpression of miR-3118 restored these changes. ZG16 was shown to be a target of miR-3118, it was found that ZG16 was downregulated in CC tissue and cells. We observed, high expression of ZG16 partially restored the enhanced malignant phenotype caused by miR-3118 overexpression. HAND2-AS1 inhibited CC progression by upregulating ZG16 expression through sponging miR-3118. Hence, HAND2-AS1/miR-3118/ZG16 axis could be a possible new target for CC treatment.</p>","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2024-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142260477","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}
Pub Date : 2024-09-12DOI: 10.1007/s10528-024-10910-6
Farhana Begum, Karpagavel Lakshmanan
Diabetic nephropathy (DN) is one of the common complications of type 2 diabetes mellitus (T2DM), and oxidative stress plays a key role in the pathogenesis of DN. Studies have demonstrated that antioxidants (MnSOD, CAT, and GPx1) may reduce the complications associated with T2DM. The purpose of the study is to correlate the role of antioxidant gene polymorphisms in the pathogenesis of DN among T2DM individuals in the South Indian population. It clarifies the importance of early manifestation and reliable genetic indicators modulating the oxidative stress mechanism in DN. The study participants were divided and grouped as Group 1: Control, Group 2: T2DM without DN, and Group 3: T2DM with DN (n = 100 in each group). The levels of plasma glucose, HbA1c, renal profile, SOD, CAT, GPx1, MDA, and TAS were assessed. MnSOD (rs4880), CAT (rs1049982), and GPx1 (rs1050450) polymorphisms were genotyped via Tetra-arms PCR. The genotypes of GPx1 depict a significant role in the progression of DN in T2DM patients (co-dominant [OR: 2.134; 95% CI (1.202–3.788), p < 0.01], dominant [OR: 2.015; 95% CI (1.117–3.634), p = 0.02], and recessive model [OR: 2.215; 95% CI (1.235–3.972), p = 0.008]); whereas rs4880 and rs1049982 polymorphisms are not associated with DN progression. As a result, GPx1 (rs1050450) polymorphism could be a diagnostic risk factor for developing DN in T2DM patients. Moreover, the genotypes of rs4880 and rs1049982 polymorphism show significant difference in the antioxidant parameters compared to the genotypes of rs1050450. In contradiction to earlier studies, the current study demonstrates that the genotypes of rs1050450 (GPx1) can be considered as an influential component for higher susceptibility and risk of developing DN in T2DM patients among the South Indian population.
{"title":"Association of MnSOD, CAT, and GPx1 Gene Polymorphism with Risk of Diabetic Nephropathy in South Indian Patients: A Case–Control Study","authors":"Farhana Begum, Karpagavel Lakshmanan","doi":"10.1007/s10528-024-10910-6","DOIUrl":"https://doi.org/10.1007/s10528-024-10910-6","url":null,"abstract":"<p>Diabetic nephropathy (DN) is one of the common complications of type 2 diabetes mellitus (T2DM), and oxidative stress plays a key role in the pathogenesis of DN. Studies have demonstrated that antioxidants (MnSOD, CAT, and GPx1) may reduce the complications associated with T2DM. The purpose of the study is to correlate the role of antioxidant gene polymorphisms in the pathogenesis of DN among T2DM individuals in the South Indian population. It clarifies the importance of early manifestation and reliable genetic indicators modulating the oxidative stress mechanism in DN. The study participants were divided and grouped as Group 1: Control, Group 2: T2DM without DN, and Group 3: T2DM with DN (n = 100 in each group). The levels of plasma glucose, HbA1c, renal profile, SOD, CAT, GPx1, MDA, and TAS were assessed. MnSOD (rs4880), CAT (rs1049982), and GPx1 (rs1050450) polymorphisms were genotyped via Tetra-arms PCR. The genotypes of GPx1 depict a significant role in the progression of DN in T2DM patients (co-dominant [OR: 2.134; 95% CI (1.202–3.788), <i>p</i> < 0.01], dominant [OR: 2.015; 95% CI (1.117–3.634), <i>p</i> = 0.02], and recessive model [OR: 2.215; 95% CI (1.235–3.972), <i>p</i> = 0.008]); whereas rs4880 and rs1049982 polymorphisms are not associated with DN progression. As a result, GPx1 (rs1050450) polymorphism could be a diagnostic risk factor for developing DN in T2DM patients. Moreover, the genotypes of rs4880 and rs1049982 polymorphism show significant difference in the antioxidant parameters compared to the genotypes of rs1050450. In contradiction to earlier studies, the current study demonstrates that the genotypes of rs1050450 (GPx1) can be considered as an influential component for higher susceptibility and risk of developing DN in T2DM patients among the South Indian population.</p>","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142219730","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}
Bergenia ciliata (Haw.) Sternb. is a perennial medicinal herb distributed in Indian Himalayan Region (IHR). A total of eight populations of B. ciliata were collected from diverse locales of IHR, and 17 EST-SSR markers were used in this study. The present study revealed moderate genetic diversity at the locus level with the mean number of alleles (Na = 7.823), mean number effective of alleles (Ne = 3.375), mean expected heterozygosity (He = 0.570), and mean Shannon's diversity index (I = 1.264). The MSR (He = 0.543, I = 1.067) and DRJ populations (He = 0.309, I = 0.519) revealed the highest and lowest genetic diversity at the population level, respectively. AMOVA analysis showed that 81.76% of genetic variation was within populations, 10.55% was among populations, and 7.69% was among the regions. In addition, a moderate to high level of differentiation was found among the populations (FST = 0.182), which could be indicative of low to moderate gene flow (Nm = 0.669) in the B. ciliata populations. UPGMA and PCoA analysis revealed that eight populations could be differentiated into two groups, while the structure analysis of the 96 individuals differentiated into three groups. The Mantel test showed a positive relationship between genetic and geographical distance. The findings of this study will provide the development of conservation and germplasm management strategies for this valuable medicinal species.
{"title":"Exploration of Genetic Variation and Population Structure in Bergenia ciliata for its Conservation Implications.","authors":"Harish Chandra Singh, Vandana Tiwari, Baleshwar Meena, Avinash Tiwari, Tikam Singh Rana","doi":"10.1007/s10528-024-10908-0","DOIUrl":"https://doi.org/10.1007/s10528-024-10908-0","url":null,"abstract":"<p><p>Bergenia ciliata (Haw.) Sternb. is a perennial medicinal herb distributed in Indian Himalayan Region (IHR). A total of eight populations of B. ciliata were collected from diverse locales of IHR, and 17 EST-SSR markers were used in this study. The present study revealed moderate genetic diversity at the locus level with the mean number of alleles (Na = 7.823), mean number effective of alleles (Ne = 3.375), mean expected heterozygosity (He = 0.570), and mean Shannon's diversity index (I = 1.264). The MSR (He = 0.543, I = 1.067) and DRJ populations (He = 0.309, I = 0.519) revealed the highest and lowest genetic diversity at the population level, respectively. AMOVA analysis showed that 81.76% of genetic variation was within populations, 10.55% was among populations, and 7.69% was among the regions. In addition, a moderate to high level of differentiation was found among the populations (F<sub>ST</sub> = 0.182), which could be indicative of low to moderate gene flow (Nm = 0.669) in the B. ciliata populations. UPGMA and PCoA analysis revealed that eight populations could be differentiated into two groups, while the structure analysis of the 96 individuals differentiated into three groups. The Mantel test showed a positive relationship between genetic and geographical distance. The findings of this study will provide the development of conservation and germplasm management strategies for this valuable medicinal species.</p>","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142118688","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}
Pub Date : 2024-09-02DOI: 10.1007/s10528-024-10909-z
Sareh Al-Dahimavi, Reza Safaralizadeh, Mohammad Khalaj-Kondori
Multiple sclerosis (MS) is an inflammatory and neurodegenerative disorder affecting white and gray matter. This study aimed to investigate the association between clinical outcomes in MS patients and the levels of certain molecules in their serum, including ACTH, IL-17, and specific miRNAs: miR-26a, miR-34a, miR-155-5p, and miR-146a. Fifty healthy people and 75 blood samples from MS patients were selected. MS patients had higher expression levels of IL-17, miR-26a, miR-34a, and miR-146a compared to healthy individuals (p < 0.0001). There was no significant difference in miR-155-5p expression between the two groups (p = 0.203). MS patients also had higher serum levels of ACTH compared to the normal population (p < 0.0001). In MS patients, there was a negative correlation between IL-17 and miR-155-5p expression levels (p = 0.048, r = - 0.229). Similarly, a significant negative correlation was observed between ACTH and miR-155-5p in the control group (p = 0.044, r = - 0.286). The study's analysis revealed no significant difference in the expression of miR-155-5p between MS patients and normal individuals; the study's examination revealed that the expression level of IL-17, miR-26a, miR-34a, and miR-146a was higher in MS patients than in normal individuals.
{"title":"Evaluating the Serum Level of ACTH and Investigating the Expression of miR-26a, miR-34a, miR-155-5p, and miR-146a in the Peripheral Blood Cells of Multiple Sclerosis Patients.","authors":"Sareh Al-Dahimavi, Reza Safaralizadeh, Mohammad Khalaj-Kondori","doi":"10.1007/s10528-024-10909-z","DOIUrl":"https://doi.org/10.1007/s10528-024-10909-z","url":null,"abstract":"<p><p>Multiple sclerosis (MS) is an inflammatory and neurodegenerative disorder affecting white and gray matter. This study aimed to investigate the association between clinical outcomes in MS patients and the levels of certain molecules in their serum, including ACTH, IL-17, and specific miRNAs: miR-26a, miR-34a, miR-155-5p, and miR-146a. Fifty healthy people and 75 blood samples from MS patients were selected. MS patients had higher expression levels of IL-17, miR-26a, miR-34a, and miR-146a compared to healthy individuals (p < 0.0001). There was no significant difference in miR-155-5p expression between the two groups (p = 0.203). MS patients also had higher serum levels of ACTH compared to the normal population (p < 0.0001). In MS patients, there was a negative correlation between IL-17 and miR-155-5p expression levels (p = 0.048, r = - 0.229). Similarly, a significant negative correlation was observed between ACTH and miR-155-5p in the control group (p = 0.044, r = - 0.286). The study's analysis revealed no significant difference in the expression of miR-155-5p between MS patients and normal individuals; the study's examination revealed that the expression level of IL-17, miR-26a, miR-34a, and miR-146a was higher in MS patients than in normal individuals.</p>","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142118687","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}
Pub Date : 2024-08-30DOI: 10.1007/s10528-024-10903-5
Junli Pan, Quanxi Li, Junli Zhu
Sorafenib resistance has become a big hurdle for treating advanced HCC; thus, identifying novel targets to overcome sorafenib resistance is of great importance. Thanks to the massive progress in the sequencing and data analysis, high-throughput screening of novel targets in HCC development has been extensively used in recent years. In present study, we harnessed the public dataset and aimed to identify novel targets related to sorafenib resistance in HCC via bioinformatics analysis and in vitro validation. This study examined three GEO datasets (GSE140202, GSE143233, GSE182593) and identified 20 common DEGs. Functional enrichment analysis suggested these DEGs might play a role in regulating drug resistance pathways. PPI network analysis pinpointed 14 hub genes, with EFNB2 showing high connectivity to other genes. Subsequent in vitro experiments demonstrated that EFNB2 was up-regulated in sorafenib-resistant HCC cells. EFNB2 suppression sensitized HepG2 and Huh7 sorafenib-resistant cells. Furthermore, EFNB2 knockdown increased caspase-3/-7 activities and hindered EMT in sorafenib-resistant HCC cells. Conversely, EFNB2 overexpression promoted sorafenib resistance, decreased caspase-3/-7 activity, and enhanced EMT in HCC cells. Overall, this study identified 14 promising genes potentially linked to sorafenib resistance in HCC, with EFNB2 emerging as a potential contributor to this resistance mechanism.
{"title":"Unveiling EFNB2 as a Key Player in Sorafenib Resistance: Insights from Bioinformatics Analysis and Functional Validation in Hepatocellular Carcinoma.","authors":"Junli Pan, Quanxi Li, Junli Zhu","doi":"10.1007/s10528-024-10903-5","DOIUrl":"https://doi.org/10.1007/s10528-024-10903-5","url":null,"abstract":"<p><p>Sorafenib resistance has become a big hurdle for treating advanced HCC; thus, identifying novel targets to overcome sorafenib resistance is of great importance. Thanks to the massive progress in the sequencing and data analysis, high-throughput screening of novel targets in HCC development has been extensively used in recent years. In present study, we harnessed the public dataset and aimed to identify novel targets related to sorafenib resistance in HCC via bioinformatics analysis and in vitro validation. This study examined three GEO datasets (GSE140202, GSE143233, GSE182593) and identified 20 common DEGs. Functional enrichment analysis suggested these DEGs might play a role in regulating drug resistance pathways. PPI network analysis pinpointed 14 hub genes, with EFNB2 showing high connectivity to other genes. Subsequent in vitro experiments demonstrated that EFNB2 was up-regulated in sorafenib-resistant HCC cells. EFNB2 suppression sensitized HepG2 and Huh7 sorafenib-resistant cells. Furthermore, EFNB2 knockdown increased caspase-3/-7 activities and hindered EMT in sorafenib-resistant HCC cells. Conversely, EFNB2 overexpression promoted sorafenib resistance, decreased caspase-3/-7 activity, and enhanced EMT in HCC cells. Overall, this study identified 14 promising genes potentially linked to sorafenib resistance in HCC, with EFNB2 emerging as a potential contributor to this resistance mechanism.</p>","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142103088","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}
The treatment of triple-negative breast cancer (TNBC) has been associated with challenges due to the lack of expression of ER, PR, and HER2 receptors in tumor cells. This study aimed to identify genes with potential therapeutic targets in TNBC. Data from the cancer genome atlas regarding breast cancer (BC) were downloaded. After initial preprocessing, cancer samples were categorized into four groups: TNBC, HER2-positive, luminal A, and luminal B. Gene expression differences between these groups were calculated, focusing on genes that showed differential expression in TNBC. A protein-protein interaction network was conducted to identify hub genes among the candidate genes related to TNBC. The protein expression of candidate genes was assessed using immunohistochemistry data from the human protein atlas. Drug resistance and sensitivity associated with hub genes were identified using data from PharmacoDB. TNBC samples and the RT-qPCR method were used to confirm the results. Our findings revealed that eight genes, namely PLK1, KIF4A, CDCA5, UBE2C, CDT1, SKA3, AURKB, and PTTG1, had significant upregulation at the RNA level in TNBC subgroup compared to other subgroups and could be considered hub genes in TNBC. Compared to other subgroups, their expression level in TNBC samples had high sensitivity and specificity. RT-qPCR results also demonstrated a significant increase in levels of SKA3 and PTTG1 in the TNBC compared to healthy tissue and other subgroups. The protein expression of these genes was notably high in some BC samples. PharmacoDB data showed that some candidate genes were closely linked to drug sensitivity of GSK 461364 and IKK 16. The results of this study showed a significant increase in the expression level of PLK1, KIF4A, CDCA5, UBE2C, CDT1, SKA3, AURKB, and PTTG1 in TNBC compared to other BC subgroups. These genes show considerable promise as therapeutic targets for the TNBC subgroup.
{"title":"Therapeutic Potential of PLK1, KIF4A, CDCA5, UBE2C, CDT1, SKA3, AURKB, and PTTG1 Genes in Triple-Negative Breast Cancer: Correlating Their Expression with Sensitivity to GSK 461364 and IKK 16 Drugs.","authors":"Najmeh Bashari, Mohammadamin Naghizadeh, Mehrnaz Kalhor Chegini, Ensieh Sagheb Sadeghi, Atefeh Zamani, Mohammad Mahdevar","doi":"10.1007/s10528-024-10907-1","DOIUrl":"https://doi.org/10.1007/s10528-024-10907-1","url":null,"abstract":"<p><p>The treatment of triple-negative breast cancer (TNBC) has been associated with challenges due to the lack of expression of ER, PR, and HER2 receptors in tumor cells. This study aimed to identify genes with potential therapeutic targets in TNBC. Data from the cancer genome atlas regarding breast cancer (BC) were downloaded. After initial preprocessing, cancer samples were categorized into four groups: TNBC, HER2-positive, luminal A, and luminal B. Gene expression differences between these groups were calculated, focusing on genes that showed differential expression in TNBC. A protein-protein interaction network was conducted to identify hub genes among the candidate genes related to TNBC. The protein expression of candidate genes was assessed using immunohistochemistry data from the human protein atlas. Drug resistance and sensitivity associated with hub genes were identified using data from PharmacoDB. TNBC samples and the RT-qPCR method were used to confirm the results. Our findings revealed that eight genes, namely PLK1, KIF4A, CDCA5, UBE2C, CDT1, SKA3, AURKB, and PTTG1, had significant upregulation at the RNA level in TNBC subgroup compared to other subgroups and could be considered hub genes in TNBC. Compared to other subgroups, their expression level in TNBC samples had high sensitivity and specificity. RT-qPCR results also demonstrated a significant increase in levels of SKA3 and PTTG1 in the TNBC compared to healthy tissue and other subgroups. The protein expression of these genes was notably high in some BC samples. PharmacoDB data showed that some candidate genes were closely linked to drug sensitivity of GSK 461364 and IKK 16. The results of this study showed a significant increase in the expression level of PLK1, KIF4A, CDCA5, UBE2C, CDT1, SKA3, AURKB, and PTTG1 in TNBC compared to other BC subgroups. These genes show considerable promise as therapeutic targets for the TNBC subgroup.</p>","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142103079","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}
Epigenetic alterations, changes in gene expression without DNA sequence modifications, are associated with various health disorders, including reproductive health issues. These alterations can be influenced by environmental factors such as pesticides. This study aimed to explore the relationship between exposure to Organochlorine Pesticides (OClPs) and the histone modification mark H3K9ac in the placenta and fetal tissue, in the context of unexplained recurrent miscarriage (URM). In the case-control study, serum samples from 73 women with URM and 30 healthy women were examined for the presence of OClPs, which include 2,4-DDT, 2,4-DDE, 4,4-DDT, 4,4-DDE, α-HCH, β-HCH, and γ-HCH, using gas chromatography. Western blot analysis was used to assess H3K9ac expression in placental and fetal tissues. In the URM group, significant increases were observed in the values of α-HCH, β-HCH, 2,4-DDE, and 4,4-DDE, as well as in the concentration of total OClPs (Ʃ3HCH, Ʃ2DDE, Ʃ2DDT, and Ʃ7OClP), compared to controls. While H3K9ac levels in fetal tissue showed no significant difference, a notable decrease was found in the placental tissue of the URM. In the placenta tissue of URM, logistic regression analysis also revealed a significant inverse correlation between the toxins α-HCH, 2,4-DDE, 4,4-DDE, 4,4-DDT, total OClPs, and reduced H3K9ac expression. Our findings suggest that OClPs exposure may contribute to URM by reducing H3K9ac expression in the placenta, potentially affecting placental growth and immune tolerance. This underscores the need for further investigation into the involved mechanisms and potential therapeutic interventions, and the importance of OClPs regulation for reproductive health protection.
{"title":"Impact of Organochlorine Pesticides Exposure on Histone Modification H3K9ac: Implications for Unexplained Recurrent Miscarriage.","authors":"Sanaz Faramarz, Gholamreza Asadikaram, Mojtaba Abbasi-Jorjandi, Moslem Abolhassani, Katayoun Alidousti, Parvin Mangolian Shahrbabaki, Hossein Pourghadamyari","doi":"10.1007/s10528-024-10904-4","DOIUrl":"https://doi.org/10.1007/s10528-024-10904-4","url":null,"abstract":"<p><p>Epigenetic alterations, changes in gene expression without DNA sequence modifications, are associated with various health disorders, including reproductive health issues. These alterations can be influenced by environmental factors such as pesticides. This study aimed to explore the relationship between exposure to Organochlorine Pesticides (OClPs) and the histone modification mark H3K9ac in the placenta and fetal tissue, in the context of unexplained recurrent miscarriage (URM). In the case-control study, serum samples from 73 women with URM and 30 healthy women were examined for the presence of OClPs, which include 2,4-DDT, 2,4-DDE, 4,4-DDT, 4,4-DDE, α-HCH, β-HCH, and γ-HCH, using gas chromatography. Western blot analysis was used to assess H3K9ac expression in placental and fetal tissues. In the URM group, significant increases were observed in the values of α-HCH, β-HCH, 2,4-DDE, and 4,4-DDE, as well as in the concentration of total OClPs (Ʃ3HCH, Ʃ2DDE, Ʃ2DDT, and Ʃ7OClP), compared to controls. While H3K9ac levels in fetal tissue showed no significant difference, a notable decrease was found in the placental tissue of the URM. In the placenta tissue of URM, logistic regression analysis also revealed a significant inverse correlation between the toxins α-HCH, 2,4-DDE, 4,4-DDE, 4,4-DDT, total OClPs, and reduced H3K9ac expression. Our findings suggest that OClPs exposure may contribute to URM by reducing H3K9ac expression in the placenta, potentially affecting placental growth and immune tolerance. This underscores the need for further investigation into the involved mechanisms and potential therapeutic interventions, and the importance of OClPs regulation for reproductive health protection.</p>","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":null,"pages":null},"PeriodicalIF":2.1,"publicationDate":"2024-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142015913","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}