Topic
Cellular differentiation
About: Cellular differentiation is a research topic. Over the lifetime, 90966 publications have been published within this topic receiving 6099252 citations. The topic is also known as: Cellular differentiation & GO:0030154.
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TL;DR: In this paper, the authors showed that blocking the recruitment of these vascular precursors might provide a novel approach to blocking tumour angiogenesis by inhibiting the vasculature recruitment.
Abstract: Summary Tumours recruit neighbouring blood vessels and vascular endothelial cells to support their own blood supply. Recent evidence has indicated, however, that tumours are also capable of mobilizing bone-marrow-derived endothelial precursor cells, inducing them to migrate to the tumour and become incorporated into the developing vasculature. Tumour-derived angiogenic factors promote the recruitment of these cells, which include circulating endothelial progenitor cells and haematopoietic stem and progenitor cells. As clinical trials with anti-angiogenic agents have been confronted with therapeutic hurdles, inhibiting the recruitment of these vascular precursors might provide a novel approach to blocking tumour angiogenesis.
697 citations
Ludwig Institute for Cancer Research1, Howard Hughes Medical Institute2, Salk Institute for Biological Studies3, Morgridge Institute for Research4, University of Texas at Dallas5, University of California, San Diego6, University of Wisconsin-Madison7, University of California, Los Angeles8, Tsinghua University9, University of California, Santa Barbara10
TL;DR: It is found that promoters that are active in early developmental stages tend to be CG rich and mainly engage H3K27me3 upon silencing in nonexpressing lineages, while promoters for genes expressed preferentially at later stages are often CG poor and primarily employ DNA methylation upon repression.
697 citations
TL;DR: A TH-17 cell–associated microRNA, miR-326, is identified whose expression was highly correlated with disease severity in patients with multiple sclerosis and mice with experimental autoimmune encephalomyelitis, and its overexpression led to more TH- 17 cells and severe EAE.
Abstract: Interleukin 17 (IL-17)-producing T helper cells (T H -17 cells) are increasingly recognized as key participants in various autoimmune diseases, including multiple sclerosis. Although sets of transcription factors and cytokines are known to regulate T H -17 differentiation, the role of noncoding RNA is poorly understood. Here we identify a T H -17 cell–associated microRNA, miR-326, whose expression was highly correlated with disease severity in patients with multiple sclerosis and mice with experimental autoimmune encephalomyelitis (EAE). In vivo silencing of miR-326 resulted in fewer T H -17 cells and mild EAE, and its overexpression led to more T H -17 cells and severe EAE. We also found that miR-326 promoted T H -17 differentiation by targeting Ets-1, a negative regulator of T H -17 differentiation. Our data show a critical role for microRNA in T H -17 differentiation and the pathogenesis of multiple sclerosis.
696 citations
TL;DR: BAFF overexpression rescued only self-reactive B cells normally deleted with relatively low stringency and facilitated their migration into otherwise forbidden microenvironments, which is likely to underlie the autoimmunity associated with BAFF overeexpression.
695 citations
TL;DR: Results indicate that ISL1, by virtue of its requirement for the formation of dorsal mesenchyme, is necessary for the development of the dorsal exocrine pancreas, and also thatISL1 function in pancreatic endodermal cells is required for the generation of all endocrine islet cells.
Abstract: The mammalian pancreas is a specialized derivative of the primitive gut endoderm and controls many homeostatic functions through the activity of its component exocrine acinar and endocrine islet cells. The LIM homeodomain protein ISL1 is expressed in all classes of islet cells in the adult1,2 and its expression in the embryo is initiated soon after the islet cells have left the cell cycle. ISL1 is also expressed in mesenchymal cells that surround the dorsal but not ventral evagination of the gut endoderm, which together comprise the pancreatic anlagen. To define the role of ISL1 in the development of the pancreas, we have now analysed acinar and islet cell differentiation in mice deficient in ISL1 function3. Dorsal pancreatic mesenchyme does not form in ISL1-mutant embryos and there is an associated failure of exocrine cell differentiation in the dorsal but not the ventral pancreas. There is also a complete loss of differentiated islet cells. Exocrine, but not endocrine, cell differentiation in the dorsal pancreas can be rescued in vitro by provision of mesenchyme derived from wild-type embryos. These results indicate that ISL1, by virtue of its requirement for the formation of dorsal mesenchyme, is necessary for the development of the dorsal exocrine pancreas, and also that ISL1 function in pancreatic endodermal cells is required for the generation of all endocrine islet cells.
695 citations