巻号一覧
後続誌
53 巻 (2009)
- 4 号 p. 99-
- 3 号 p. 49-
- 2 号 p. 17-
- 1 号 p. 1-
53 巻, 4 号
選択された号の論文の4件中1～4を表示しています
- |<
- <
- 1
- >
- >|
シンポジウム：疾病と再生医療
-
湯浅 慎介2009 年 53 巻 4 号 p. 99-101
発行日: 2009年
公開日: 2009/12/26
ジャーナル フリーInduced pluripotent stem (iPS) cells have recently been established by transfecting mouse and human fibroblasts with the transcription factors known to be expressed in embryonic stem (ES) cells. These cells have great potential in regenerative medicine as they have the capacity to differentiate into all three germ layer-derived cells and are syngeneic. The differentiation of ES cells and iPS cells into cardiomyocytes mimics the early processes involved in heart development. Recent studies describe the contribution of various humoral factors to heart development during embryogenesis. The exposure of ES cells and iPS cells to such growth factors is hypothesized to augment differentiation into cardiomyocytes. These progresses in basic science have the potential for providing the foundations for future regenerative medicine.
抄録全体を表示PDF形式でダウンロード (215K) -
加古 英介, 金子 奈穂子, 祖父江 和哉, 澤本 和延2009 年 53 巻 4 号 p. 103-107
発行日: 2009年
公開日: 2009/12/26
ジャーナル フリーA growing number of studies highlight the potential of cell transplantation as a novel therapeutic strategy for a wide range of brain diseases. However, there are many unsolved problems for this therapy to become scientifically/socially acceptable and clinically available.
Endogenous neural stem cells continuously generate new neurons in the subventricular zone and dentate gyrus in the adult brain. Recent studies suggest that these cells are capable of contributing to the regeneration processes after various brain insults. In this review article, we discuss problems and potential of regenerative medicine with or without cell transplantation for brain regeneration.
抄録全体を表示PDF形式でダウンロード (520K) -
服部 浩一, 田代 良彦, Beate Heissig2009 年 53 巻 4 号 p. 109-114
発行日: 2009年
公開日: 2009/12/26
ジャーナル フリーVascular endothelial growth factor (VEGF) regulates vasculogenesis and angiogenesis by signaling through two tyrosine kinase receptors, VEGF receptor-1(VEGFR1) and VEGFR2. Whereas VEGF/VEGFR2 signaling contributes to the regulation of endothelial cell lineage differentiation and proliferation, VEGF/VEGFR1 signaling in hematopoietic lineage cells can promote the mobilization of hematopoietic stem cells and induce bone marrow regeneration. These data suggest that there is a significant interaction between post-natal angiogenesis and hematopoiesis.
We reported that the activation of VEGF/VEGFR and chemokine stromal cell-derived factor-1(CXCL12)/CXCR4 signal pathways induce the mobilization of bone marrow-derived hematopoietic lineage cells. It was shown that these pathways regulate bone marrow cell differentiation and proliferation by activating matrix metalloproteinases (MMP) causing MMP-mediated hematopoietic factor, Kit ligand processing. Moreover, we have also reported that CXCL12 and VEGF are released from bone marrow-derived inflammatory cells like neutrophils or platelets.
It was demonstrated that CXCR4 positive and VEGFR1 positive lineage cells, also called hemangiocytes, can produce angiopoetin-2 which can recruit hematopoietic stem cells from the bone marrow and work as molecular HUB by augmenting revascularization in the “neo-vascular niche”. Recently, we showed that activation of the fibrinolytic system resulted in the constitutive activation of MMPs causing Kit ligand release, which promoted bone marrow regeneration after myelosuppression. These data imply that the fibrinolytic system might also play a role in regulating neoangiogenesis during tissue regeneration. Here, we will introduce recent studies from our group and several novel concepts in our current understanding of the regulation of angiogenesis.
抄録全体を表示PDF形式でダウンロード (1072K) -
上野 康晴, 内藤 貴子, 谷口 英樹2009 年 53 巻 4 号 p. 115-119
発行日: 2009年
公開日: 2009/12/26
ジャーナル フリーStem cell are defined as having robust self-renewal and multilineage differentiation potential. It is thought that the self-renewal capability of stem cells can be established when both of the gene clusters involved in maintaining the undifferentiated state and cell differentiation state are expressed neutrally.
In present study, we first investigated the role of Polycomb group (PcG) genes in the hepatic stem/progenitor cells. As a result, we revealed that forced expression of Bmi1 promoted the self-renewal of hepatic stem/progenitor cells. The transplantation of Bmi1 introduced cells clonally expanded from single hepatic stem/progenitor cells produced the tumor, which exhibited the histologic features of combined hepatocellular and cholangiocarcinoma. These observations imply that Bmi1 act as a positive regulator of self-renewal capability in hepatic stem cells.
Moreover, to investigate the role of PcG protein complex in self-renewal of the hepatic stem cells, we performed functional analyses of Ring1B that is essential for gene silencing by coupling with Bmi1 directly. When performed functional analysis of Ring1B in hepatic stem/progenitor cells derived from Ring1B-KO mouse with single cell-based colony assay, self-renewal capability of hepatic stem/progenitor was inhibited. Moreover, cyclin-dependent kinase inhibitor, ink4a and arf genes that were thought to be target genes of Bmi1, were depressed in Ring1B-KO cells.
These results indicate that Bmi1 and Ring1B are critical factor to self-renewal of hepatic stem/progenitor cells in the developing murine liver by suppressing a negative cell cycle regulators including Ink4a/Arf.
抄録全体を表示PDF形式でダウンロード (2480K)
- |<
- <
- 1
- >
- >|