EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #72622_C
PPARγ激活剂
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总览
罗格列酮（Rosiglitazone）是一种强效且选择性的PPARγ配体。它与PPARγ配体结合结构域结合，Kd值为43 nM（Lehmann et al.）。它激活基于荧光素酶的表达载体PPARγ1和PPARγ2，EC50值分别约为30 nM和100 nM （Lehmann et al.）。
维持和自我更新
·刺激小鼠胚胎神经干细胞增殖并抑制神经元分化（Wada et al.）。
分化
·诱导C3H10T1/2干细胞的脂肪细胞分化（Lehmann et al.）。
·促进血管生成祖细胞的内皮细胞分化，并抑制平滑肌细胞分化（Wang et al.）。
·刺激小鼠和人骨髓间充质干细胞的脂肪细胞分化，并降低成骨作用(Ali et al.; Benvenuti et al.; Lecka-Czernik et al.; Sorocéanu et al.)。
·增强 RANKL 和 M-CSF 刺激的小鼠骨髓细胞破骨细胞形成（Wu et al.）。
细胞类型
脂肪细胞，血管生成细胞，间充质干/祖细胞，神经干/祖细胞
种属
人，小鼠，非人灵长类，其他物种，大鼠
应用
分化，扩增
研究领域
神经科学，干细胞生物学
CAS 编号
122320-73-4
化学式
C₁₈H₁₉N₃O₃S
纯度
≥98%
通路
PPARγ
靶点
PPARγ
产品说明书及文档
请在《产品说明书》中查找相关支持信息和使用说明，或浏览下方更多实验方案。
应用领域
本产品专为以下研究领域设计，适用于工作流程中的高亮阶段。探索这些工作流程，了解更多我们为各研究领域提供的其他配套产品。
相关材料与文献
技术资料 (1)
文献 (8)
Divergent effects of selective peroxisome proliferator-activated receptor-gamma 2 ligands on adipocyte versus osteoblast differentiation.
Endocrinology 2002 JUN
Abstract
PPAR gamma is activated by diverse ligands and regulates the differentiation of many cell types. Based on evidence that activation of PPAR gamma 2 by rosiglitazone stimulates adipogenesis and inhibits osteoblastogenesis in U-33/gamma 2 cells,a model mesenchymal progenitor of adipocytes and osteoblasts,we postulated that the increase in marrow fat and the decrease in osteoblast number that occur during aging are due to increased PPAR gamma 2 activation. Here,we show that the naturally occurring PPAR gamma ligands 9,10-dihydroxyoctadecenoic acid,and 15-deoxy-Delta(12,14)-PGJ(2),also stimulate adipocytes and inhibit osteoblast differentiation of U-33/gamma 2 cells. Strikingly,9,10-epoxyoctadecenoic acid and the thiazolidine acetamide ligand GW0072 [(+/-)-(2S,5S)-4-(4-(4-carboxyphenyl)butyl)-2-heptyl-4-oxo-5-thaizolidineN,N-dibenzyl-acetamide] prevent osteoblast differentiation,but do not stimulate adipogenesis,whereas 9-hydroxyoctadecadienoic acid stimulates adipogenesis but does not affect osteoblast differentiation. The divergent effects of PPAR gamma 2 ligands on osteoblast and adipocyte differentiation were confirmed in primary murine bone marrow cultures using rosiglitazone and GW0072. These findings indicate that the proadipogenic and antiosteoblastogenic effects of PPAR gamma 2 are mediated by distinct regulatory pathways that can be differentially modulated depending on the nature of the ligand,and they support the idea that increased fatty acid oxidation during aging may inhibit osteoblast differentiation. Moreover,there may be selective PPAR gamma 2 modulators that block the adverse effects of fatty acid oxidation products while retaining beneficial activities such as insulin sensitization.
Rosiglitazone facilitates angiogenic progenitor cell differentiation toward endothelial lineage: a new paradigm in glitazone pleiotropy.
Circulation 2004 MAR
Abstract
BACKGROUND: Peroxisome proliferator-activated receptor-gamma (PPAR-gamma) agonists inhibit vascular smooth muscle proliferation and migration and improve endothelial function. It is unknown whether PPAR-gamma agonists favorably modulate bone marrow (BM)-derived angiogenic progenitor cells (APCs) to promote endothelial lineage differentiation and early reendothelialization after vascular intervention. METHODS AND RESULTS: C57/BL6 mice,treated with or without rosiglitazone (8 mg/kg per day),a PPAR-gamma agonist,underwent femoral angioplasty. Rosiglitazone treatment attenuated neointimal formation (intima/media ratio: 0.98+/-0.12 [rosiglitazone] versus 3.1+/-0.5 [control]; Ptextless0.001; n=10 per group). Using a BM transplantation model,we identified that 58+/-12% of the cells within the neointima at 4 weeks were derived from the BM. Pure endothelial marker-positive,pure alpha-smooth muscle actin (alphaSMA)-positive,or double-positive APCs could be found both in mouse BM and in human peripheral blood after culture in conditional medium enriched with vascular endothelial growth factor. Rosiglitazone caused a 6-fold (Ptextless0.001) increase in colony formation by human endothelial progenitor cells,promoted the differentiation of APCs toward the endothelial lineage in mouse BM in vivo (0.66+/-0.06% [control] to 0.95+/-0.08% [rosiglitazone]; Ptextless0.05) and in human peripheral blood in vitro (13.2+/-1.5% [control] to 28.4+/-3.3% [rosiglitazone]; Ptextless0.05),and inhibited the differentiation toward the smooth muscle cell lineage. Within the neointima,rosiglitazone also stimulated APCs to differentiate into mature endothelial cells and caused earlier reendothelialization compared with controls (31+/-5 versus 8+/-2 CD31-positive cells per millimeter of neointimal surface on day 14; Ptextless0.01). CONCLUSIONS: Similar to embryonic stem cell-derived progenitors,the adult BM and peripheral blood harbor APCs that are at least bipotential and able to differentiate into endothelial and smooth muscle lineages. The PPAR-gamma agonist rosiglitazone promotes the differentiation of these APCs toward the endothelial lineage and attenuates restenosis after angioplasty.
Rosiglitazone impacts negatively on bone by promoting osteoblast/osteocyte apoptosis.
The Journal of endocrinology 2004 OCT
Abstract
Thiazolidinediones (TZDs) increase peripheral tissue insulin sensitivity in patients with type 2 diabetes mellitus by activating the nuclear receptor peroxisome proliferator-activated receptor gamma (PPARgamma). In bone marrow stromal cell cultures and in vivo,activation of PPARgamma by high doses (20 mg/kg/day) of TZDs has been reported to alter stem cell differentiation by promoting commitment of progenitor cells to the adipocytic lineage while inhibiting osteoblastogenesis. Here,we have examined the in vivo effects of low-dose rosiglitazone (3 mg/kg/day) on bone,administered to mice by gavage for 90 days. Rosiglitazone-treated mice had increased weight when compared with controls,with no significant alterations in serum levels of glucose,calcium or parathyroid hormone (PTH). Bone mineral density (BMD) at the lumbar vertebrae (L1-L4),ilium/sacrum,and total body was diminished by rosiglitazone treatment. Histologically,bone was characterized by decreased trabecular bone volume and increased marrow space with no significant change in bone marrow adipocity. Decreased osteoblast number and activity due to increased apoptotic death of osteoblasts and osteocytes was apparent while osteoclast parameters and serum levels of osteocalcin,alkaline phosphatase activity,and leptin were unaltered by rosiglitazone treatment. Therefore,the imbalance in bone remodeling that follows rosiglitazone administration arises from increased apoptotic death of osteogenic cells and diminished bone formation leading to the observed decrease in trabecular bone volume and BMD. These novel in vivo effects of TZDs on bone are of clinical relevance as patients with type 2 diabetes mellitus and other insulin resistant states treated with these agents may potentially be at increased risk of osteoporosis.
更多信息
| 物种 | 人, 其它物种, 大鼠, 小鼠, 非人灵长类 |
|---|---|
| Cas Number | 122320-73-4 |
| Chemical Formula | C₁₈H₁₉N₃O₃S |
| 纯度 | ≥ 98% |
| Target | PPARγ |
| Pathway | PPARγ |
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