产品号 #72692_C
Lysophosphatidic acid (LPA)1 and LPA2 agonist
概述
1-Oleoyl Lysophosphatidic Acid is a species of lysophosphatidic acid (LPA) containing oleic acid at the sn-1 position. LPA mediates a variety of biological responses including cell proliferation, smooth muscle contraction, platelet aggregation, neurite retraction, and cell motility (Moolenaar).
DIFFERENTIATION
· Stimulates neuronal differentiation in cultured mouse or rat neural progenitor cells (Cui and Qiao; Fukushima et al.; Spohr et al.).
· Inhibits human embryonic stem (ES) cell-derived neural stem cells (NSCs) from forming neurospheres and differentiating into neurons in vitro (Dottori et al.).
· Stimulates differentiation of human adipose tissue-derived mesenchymal stem cells to myofibroblast-like cells in vitro (Jeon et al.).
Alternative Names
Oleoyl-sn-3-glycerophosphate
Cell Type
Adipocytes, Mesenchymal Stem and Progenitor Cells, Neural Stem and Progenitor Cells
Species
Human, Mouse, Non-Human Primate, Other, Rat
Application
Differentiation
Area of Interest
Neuroscience, Stem Cell Biology
CAS Number
325465-93-8
Chemical Formula
C₂₁H₄₀O₇P · Na
Molecular Weight
458.5 g/mol
Purity
≥ 95%
Target
LPA
Protocols and Documentation
Find supporting information and directions for use in the Product Information Sheet or explore additional protocols below.
Applications
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Resources and Publications
Educational Materials (2)
Publications (9)
Lysophosphatidic acid inhibits neuronal differentiation of neural stem/progenitor cells derived from human embryonic stem cells. Stem cells (Dayton, Ohio) 2008 MAY
Abstract
Lysophospholipids are signaling molecules that play broad and major roles within the nervous system during both early development and neural injury. We used neural differentiation of human embryonic stem cells (hESC) as an in vitro model to examine the specific effects of lysophosphatidic acid (LPA) at various stages of neural development, from neural induction to mature neurons and glia. We report that LPA inhibits neurosphere formation and the differentiation of neural stem cells (NSC) toward neurons, without modifying NSC proliferation, apoptosis, or astrocytic differentiation. LPA acts through the activation of the Rho/ROCK and the phosphatidylinositol 3-kinase/Akt pathways to inhibit neuronal differentiation. This study is the first demonstration of a role for LPA signaling in neuronal differentiation of hESC. As LPA concentrations increase during inflammation, the inhibition of neuronal differentiation by LPA might contribute to the low level of neurogenesis observed following neurotrauma.
Lysophosphatidic acid receptor-dependent secondary effects via astrocytes promote neuronal differentiation. The Journal of biological chemistry 2008 MAR
Abstract
Lysophosphatidic acid (LPA) is a simple phospholipid derived from cell membranes that has extracellular signaling properties mediated by at least five G protein-coupled receptors referred to as LPA(1)-LPA(5). In the nervous system, receptor-mediated LPA signaling has been demonstrated to influence a range of cellular processes; however, an unaddressed aspect of LPA signaling is its potential to produce specific secondary effects, whereby LPA receptor-expressing cells exposed to, or primed�
Cancer-derived lysophosphatidic acid stimulates differentiation of human mesenchymal stem cells to myofibroblast-like cells. Stem cells (Dayton, Ohio) 2008 MAR
Abstract
Lysophosphatidic acid (LPA) is enriched in ascites of ovarian cancer patients and is involved in growth and invasion of ovarian cancer cells. Accumulating evidence suggests cancer-associated myofibroblasts play a pivotal role in tumorigenesis through secreting stromal cell-derived factor-1 (SDF-1). In the present study, we demonstrate that LPA induces expression of alpha-smooth muscle actin (alpha-SMA), a marker for myofibroblasts, in human adipose tissue-derived mesenchymal stem cells (hADSCs). The LPA-induced expression of alpha-SMA was completely abrogated by pretreatment of the cells with Ki16425, an antagonist of LPA receptors, or by silencing LPA(1) or LPA(2) isoform expression with small interference RNA (siRNA). LPA elicited phosphorylation of Smad2/3, and siRNA-mediated depletion of endogenous Smad2/3 or adenoviral expression of Smad7, an inhibitory Smad, abrogated the LPA induced expression of alpha-SMA and phosphorylation of Smad2/3. LPA-induced secretion of transforming growth factor (TGF)-beta1 in hADSCs, and pretreatment of the cells with SB431542, a TGF-beta type I receptor kinase inhibitor, or anti-TGF-beta1 neutralizing antibody inhibited the LPA-induced expression of alpha-SMA and phosphorylation of Smad2. Furthermore, ascites from ovarian cancer patients or conditioned medium from ovarian cancer cells induced expression of alpha-SMA and phosphorylation of Smad2, and pretreatment of the cells with Ki16425 or SB431542 abrogated the expression of alpha-SMA and phosphorylation of Smad2. In addition, LPA increased the expression of SDF-1 in hADSCs, and pretreatment of the cells with Ki16425 or SB431562 attenuated the LPA-stimulated expression of SDF-1. These results suggest that cancer-derived LPA stimulates differentiation of hADSCs to myofibroblast-like cells and increases SDF-1 expression through activating autocrine TGF-beta1-Smad signaling pathway.
PRODUCTS ARE FOR RESEARCH USE ONLY AND NOT INTENDED FOR HUMAN OR ANIMAL DIAGNOSTIC OR THERAPEUTIC USES UNLESS OTHERWISE STATED. FOR ADDITIONAL INFORMATION ON QUALITY AT STEMCELL, REFER TO WWW.STEMCELL.COM/COMPLIANCE.
