Cell & developmental biology最新文献_第6页

Apoptosis in Bcl2l13 epididymal cells Bcl2l13附睾细胞的凋亡

Cell & developmental biology Pub Date : 2017-07-07 DOI: 10.4172/2168-9296.1000187

Donato Dalonzo, Hong Zhang

引用次数: 0

Microbial Growth in Planktonic Conditions 浮游条件下微生物的生长

Cell & developmental biology Pub Date : 2017-06-12 DOI: 10.4172/2168-9296.1000185

A. Schiraldi

引用次数: 8

Relationship of Metabolic Alterations and PD-L1 Expression in Cisplatin Resistant Lung Cancer. 顺铂耐药肺癌中代谢改变与 PD-L1 表达的关系

Cell & developmental biology Pub Date : 2017-06-01 Epub Date: 2017-04-28 DOI: 10.4172/2168-9296.1000183

M Wangpaichitr, H Kandemir, Y Y Li, C Wu, Djm Nguyen, L G Feun, M T Kuo, N Savaraj

{"title":"Relationship of Metabolic Alterations and PD-L1 Expression in Cisplatin Resistant Lung Cancer.","authors":"M Wangpaichitr, H Kandemir, Y Y Li, C Wu, Djm Nguyen, L G Feun, M T Kuo, N Savaraj","doi":"10.4172/2168-9296.1000183","DOIUrl":"10.4172/2168-9296.1000183","url":null,"abstract":"Despite numerous reports on immune checkpoint inhibitor for the treatment of non-small cell lung cancer (NSCLC), the response rate remains low but durable. Thus cisplatin still plays a major role in the treatment of NSCLC. While there are many mechanisms involved in cisplatin resistance, alteration in metabolic phenotypes with elevated levels of reactive oxygen species (ROS) are found in several cisplatin resistant tumors. These resistant cells become more reliant on mitochondria oxidative metabolism instead of glucose. Consequently, high ROS and metabolic alteration contributed to epithelial-mesenchymal transition (EMT). Importantly, recent findings indicated that EMT has a crucial role in upregulating PD-L1 expression in cancer cells. Thus, it is very likely that cisplatin resistance will lead to high expression of PD-L1/PD-1 which makes them vulnerable to anti PD-1 or anti PD-L1 antibody treatment. An understanding of the interactions between cancer cells metabolic reprogramming and immune checkpoints is critical for combining metabolism targeted therapies with immunotherapies.","PeriodicalId":9775,"journal":{"name":"Cell & developmental biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2017-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5557290/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35279945","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Mitochondrial Dysfunction and Mitophagy in Neurodegenerative Diseases 神经退行性疾病中的线粒体功能障碍和线粒体自噬

Cell & developmental biology Pub Date : 2017-05-18 DOI: 10.4172/2168-9296.1000184

Li‐Pin Kao, E. Wolvetang

{"title":"Mitochondrial Dysfunction and Mitophagy in Neurodegenerative Diseases","authors":"Li‐Pin Kao, E. Wolvetang","doi":"10.4172/2168-9296.1000184","DOIUrl":"https://doi.org/10.4172/2168-9296.1000184","url":null,"abstract":"Mitochondria are critical in providing energy for neuronal development. They provide the majority of intracellular energy and perform important metabolic functions such as the Krebs cycle. Mitochondria contain their own mitochondrial DNA in a circular form, similar to bacterial genomes. Mitochondrial genomes encode several essential genes of the eukaryotic respiratory machinery, but most respiratory machinery components and factors controlling mitochondrial biogenesis are encoded in the nucleus. Mitochondria and the nucleus cooperate and communicate via retrograde signals, such as energy supply and redox signaling. This poorly understood communication is essential for balancing intracellular energy production and demand. Mitochondrial mutations could lead to dysfunctions in ATP production, calcium homeostasis, reactive oxygen species generation, and apoptotic signaling. Thus, mitochondrial dysfunction has been reported and discussed as part of neurodegenerative etiologies. There is no doubt that mitochondrial dysfunction, abnormal mitochondrial dynamics, and mitophagic degradation occur in neurodegenerative diseases. Mitochondrial turnover maintains cellular homeostasis by eliminating defective mitochondria through a specific form of autophagy, an evolutionarily conserved eukaryotic response to stress conditions by which lysosome contents are used to breakdown cytoplasmic proteins and organelles. Both number of ‘healthy’ and ‘mutated’ mitochondria could be increased or decreased by fusion and fission. Selective uptake of mitochondria by autophagosomes is called mitophagy. Mitophagic events are highly selective processes controlled by oxidative stress and are accompanied by loss of membrane potential and ensuing mitochondrial degradation. This review discusses the role of mitochondria in neurodegenerative diseases. This review also explores the connection between neurodegeneration and mitophagy, a highly selective autophagic process of oxidative stress-induced mitochondrial degradation. It will further discuss the role of fusion and fission processes in maintaining homeostasis.","PeriodicalId":9775,"journal":{"name":"Cell & developmental biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2017-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89749326","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

The Hormone Exocytosis in Prolactinoma and Normal Adenohypophysis Cell Cultures by the Effects of Hypocalcaemia 低钙对泌乳素瘤和正常腺垂体细胞激素分泌的影响

Cell & developmental biology Pub Date : 2017-03-28 DOI: 10.4172/2168-9296.1000182

K. Sepp, A. László, M. Radács, A. Serester, Z. Valkusz, M. Gálfi, Z. Molnár

{"title":"The Hormone Exocytosis in Prolactinoma and Normal Adenohypophysis Cell Cultures by the Effects of Hypocalcaemia","authors":"K. Sepp, A. László, M. Radács, A. Serester, Z. Valkusz, M. Gálfi, Z. Molnár","doi":"10.4172/2168-9296.1000182","DOIUrl":"https://doi.org/10.4172/2168-9296.1000182","url":null,"abstract":"The biological systems are opened, complex objects, which can regularly exchange feedbacks with their environment. The calcium ion is a universal messenger, which can regulate several cellular functions e.g. exocytosis machinery. The primary aim of this study was to investigate the response mechanisms of normal adenohypophysis and adenohypophyseal prolactinoma cell populations at different extracellular Ca2+ levels with an otherwise isoionic milieu of all other essential ions. We focused on prolactin (PRL) and adrenocorticotrophic hormone (ACTH) release. In our experimental study, female Wistar rats (n=10) were treated with estrone-acetate (150 μg/kg b.w/week) for 6 months to induce prolactinomas in the adenohypophysis. Primary, monolayer cell cultures were prepared by enzymatic and mechanical digestion. PRL and ACTH hormone presence was measured by radioimmunoassay or immuno- chemiluminescence assay. Repeated measurements of ACTH and PRL hormone release in different treatment groups on cell cultures during 80 minutes were compared using marginal models. Differences between the effects of hypocalcaemia on normal adenohypophysis cultures and prolactinoma cell populations were investigated. Significant alteration (p<0.001, n=12) in hormone exocytosis was detected in Ca2+ treated adenohypophyseal and prolactinoma cell cultures, compared to untreated groups. Diminution of Ca2+ may inhibit the SNARE mediated fusion of hormone containing vesicles to plasma membrane. In conclusion, the main finding of this study is that a strict correlation exists among certain biophysical properties, especially extracellular Ca2+ milieu and hormone vesicle exocytosis.","PeriodicalId":9775,"journal":{"name":"Cell & developmental biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2017-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73239889","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Silencing miR-16 Expression Promotes Angiotensin II Stimulated Vascular Smooth Muscle Cell Growth. 沉默miR-16表达可促进血管紧张素II刺激血管平滑肌细胞生长。

Cell & developmental biology Pub Date : 2017-03-01 Epub Date: 2017-03-24 DOI: 10.4172/2168-9296.1000181

Qingqing Gu, Guannan Zhao, Yinan Wang, Biao Xu, Junming Yue

{"title":"Silencing miR-16 Expression Promotes Angiotensin II Stimulated Vascular Smooth Muscle Cell Growth.","authors":"Qingqing Gu, Guannan Zhao, Yinan Wang, Biao Xu, Junming Yue","doi":"10.4172/2168-9296.1000181","DOIUrl":"https://doi.org/10.4172/2168-9296.1000181","url":null,"abstract":"miRNAs are a class of non-coding endogenous small RNAs that control gene expression at the posttranscriptional level and involved in cell proliferation, migration and differentiation. Dysregulation of miRNA expression is involved in a variety of human diseases including cardiovascular diseases. miRNAs have been shown to regulate vascular smooth muscle cell (VSMC) function and play vital roles in hypertension, restenosis and atherosclerosis. Here we reported that miR-16 as one of miRNAs in the miR-15 family was highly expressed in vascular smooth muscle cells (VSMCs) and involved in angiotensin II (Ang II) mediated VSMC signaling pathways. Ang II downregulated miR-16 expression in VSMCs. Lentiviral vector mediated miR-16 knockdown promoted Ang II-induced cell proliferation and migration. Moreover, silencing miR-16 enhanced Ang II induced cell cycle associated gene expression and promoted Ang II-activated cell proliferative pathways ERK1/2 and p38. Our finding demonstrated for the first time that miR-16 was a potential therapeutic target by participating in the Ang II-associated multiple signaling pathways in cardiovascular diseases.","PeriodicalId":9775,"journal":{"name":"Cell & developmental biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2017-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4172/2168-9296.1000181","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35523839","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 6

Treatments for Sickle Cell Disease: A Global Problem in Cell and Developmental Biology 镰状细胞病的治疗:细胞和发育生物学中的一个全球性问题

Cell & developmental biology Pub Date : 2017-02-28 DOI: 10.4172/2168-9296.1000E141

R. Broyles

{"title":"Treatments for Sickle Cell Disease: A Global Problem in Cell and Developmental Biology","authors":"R. Broyles","doi":"10.4172/2168-9296.1000E141","DOIUrl":"https://doi.org/10.4172/2168-9296.1000E141","url":null,"abstract":"Copyright: © 2017 Broyles RH. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Sickle cell disease (SCD) is the world’s most common genetic disorder, being most prevalent among populations in the regions where malaria has been endemic [1]. SCD is caused by a point mutation (A → T) in the sixth codon of the β-globin gene on chromosome 11, resulting in the substitution of the amino acid valine for glutamic acid in the expressed protein. The result is that the mutated hemoglobin S (HbS) polymerizes and precipitates within the red blood cells (RBCs) during deoxygenation or dehydration, altering the RBC’s form from a flexible biconcave disc to a rigid elongated cell that is often in the shape of a crescent or sickle. Sickling results in a vascular train wreck, producing abnormally increased adhesion to other blood cells and to the vascular walls, hyper-coagulation, hemolysis, hypoxia, widespread inflammation, organ damage, and premature death. There are approximately 340,000 deaths per year attributed to the effects of SCD, most of the deaths being children under five years of age. Although the molecular basis of sickle cell has been understood for over sixty years [2,3], there is still no treatment that is highly effective and available to the millions of affected individuals worldwide.","PeriodicalId":9775,"journal":{"name":"Cell & developmental biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2017-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88259640","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cflarb Complemented the Function of Cflara to Allow Cflara Knock out Zebrafish To Normal Development Cflara补充了Cflara的功能，使Cflara敲昏斑马鱼恢复正常发育

Cell & developmental biology Pub Date : 2017-02-28 DOI: 10.4172/2168-9296.1000180

S. Huh, Kyu-Seok Hwang, S. Koppula, C. Kim, Cheol‐Hee Kim, Chan Gil Kim

{"title":"Cflarb Complemented the Function of Cflara to Allow Cflara Knock out Zebrafish To Normal Development","authors":"S. Huh, Kyu-Seok Hwang, S. Koppula, C. Kim, Cheol‐Hee Kim, Chan Gil Kim","doi":"10.4172/2168-9296.1000180","DOIUrl":"https://doi.org/10.4172/2168-9296.1000180","url":null,"abstract":"Cellular FLICE-inhibitory protein (cFLIP, cflara) is a regulator of death receptor (DR)-induced apoptosis and NF-κB activation. cFLIP is known to prevent activation of the caspase cascade by binding to FADD/caspase-8. Up-regulated cFLIP has been identified in many tumor types, and therefore restoring apoptosis by silencing cFLIP may be one of the more potent strategies in cancer therapeutics. The zebrafish cFLIP gene, cflara, has 2 death effector domains (DEDs) and a single caspase-like domain. Expression of cflara was detected in the zebrafish embryo by RT-PCR and whole-mount in situ hybridization. To study the in vivo function of cflara, we generated a cflara knockout mutant zebrafish using transcription activator-like effector nucleases (TALENs). Frame shift mutation is caused by a 10-bp deletion in the first DED domain. By inbreeding the F1 generation, a homozygous mutant fish was produced and confirmed by PCR. Knockout of cflara leads to abnormal heart development and embryonic lethality in mice. However, mutant zebrafish did not show any differences from wild type in heartbeat rate, survival rate or development. Zebrafish have analogues of both cflara and cflarb. Quantitative PCR showed that cflarb mRNA levels of mutant zebrafish were higher than those in the wild type. In a chemical exposure experiment, mutant zebrafish larvae showed a longer survival rate compared with wild type after CoCl2 treatment. However, no significant difference was observed from cisplatin treatment. This data suggests that cflarb may contribute to normal development and causes a difference in chemical resistance.","PeriodicalId":9775,"journal":{"name":"Cell & developmental biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2017-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79907133","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Characterization of Cell Cycle Phase-Based Micrornas in Pluripotency and Differentiation 细胞周期期微rna在多能性和分化中的特性研究

Cell & developmental biology Pub Date : 2017-01-25 DOI: 10.4172/2168-9296.1000178

X. Ming, T. Wan, Lin Chen, M. Garcia-Barceló, C. Lo, X. Q. Wang

{"title":"Characterization of Cell Cycle Phase-Based Micrornas in Pluripotency and Differentiation","authors":"X. Ming, T. Wan, Lin Chen, M. Garcia-Barceló, C. Lo, X. Q. Wang","doi":"10.4172/2168-9296.1000178","DOIUrl":"https://doi.org/10.4172/2168-9296.1000178","url":null,"abstract":"In addition to signaling pathways, transcription factors and epigenetic regulators, microRNAs (miRNAs) are emerging as important regulators of human pluripotent stem cells (hPSCs). Pluripotent miRNAs that regulate G1-S transition and pluripotency factors to maintain self-renewal have been identified. However, only 4-5 clusters of miRNAs have been identified in human embryonic stem cells (hESCs). We performed cell cycle phase-based (G1, S, and G2/M phases) miRNA array in pluripotent and differentiated hESCs. We demonstrated that embryonic stem cell-cell cycle (ESCC) regulating miRNAs were all highly expressed in three cell cycle phases of undifferentiated hESCs suggesting a non-cell phase regulated mechanism. From cell phase-dependent miRNAs, G2/M-miRNAs was extracted by principle component analysis (PCA) as a significant component in pluripotent hESCs, whereas G1-miRNAs was a significant component in differentiated hESCs. The results indicate that G2/M-miRNAs might function to maintain pluripotency and G1-miRNAs might function to enhance differentiation. By miRNA target site prediction, G2/M-phase miRNA displayed potential target sites on differentiation factors GATA6 and GATA4, G1-phase miRNAs displayed potential target sites on pluripotency gene OCT4, NANOG, and SOX2, which warrant further confirmation and functional study. By statistical and computation analysis of the miRNA array data, we demonstrated that the G2/M-miRNAs could potentially repress differentiation factors to maintain pluripotency, and G1-miRNAs could potentially target pluripotency genes to enhance differentiation.","PeriodicalId":9775,"journal":{"name":"Cell & developmental biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2017-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76314653","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The Acquisition of Mathematical Language in Biomedical Articles 生物医学文章中数学语言的习得

Cell & developmental biology Pub Date : 2017-01-01 DOI: 10.13140/RG.2.2.18390.75841

D. Lu

引用次数: 8