Linoleic Acid Induces Mouse Embryonic Stem Cell Proliferation Via Ca&lt;sup&gt;2+&lt;/sup&gt;/PKC, PI3K/Akt, and MAPKs

Kim, Min Hee; Kim, Miok; Kim, Yun Hee; Kim, Jin Sang; Han, Ho Jae

doi:10.1159/000204090

Cited by 39 publications

(27 citation statements)

References 62 publications

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“…Such difference was due to the presence of linoleic acid in SPE-IV (3.38% of total lipids analyzed) and its absence in aMEM. Notably, from literature, the linoleic acid is known to have a crucial role on membrane fluidity and integrity and was reported to induce mouse embryonic stem cell proliferation (Kim et al, 2009). Interestingly, it was also reported that one of the major and biologically active products of cell peroxidation of n-6 fatty acids, such as linoleic acid, is the aldehyde 4-hydroxynonenal that can trigger the desensitization of PDGFRB to its own agonist together with both a progressive inhibition of its phosphorylation and a partial removal from the cell surface as observed in SPE-IV (Vindis et al, 2007).…”

Section: Lipid Membrane Composition Analysismentioning

confidence: 99%

Diet composition transiently modulates proliferative and potency features of human cord blood-derived mesenchymal stem cells

Ragni

Parazzi

Crosti

et al. 2014

The International Journal of Biochemistry & Cell Biology

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Section: Lipid Membrane Composition Analysismentioning

confidence: 99%

Diet composition transiently modulates proliferative and potency features of human cord blood-derived mesenchymal stem cells

Ragni

Parazzi

Crosti

et al. 2014

The International Journal of Biochemistry & Cell Biology

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“…In mouse embryonic stem cells, LA regulates various cell cycle proteins via p44/42 MAPK signaling [18]. Interestingly, unsaturated fatty acids promote the activation of ERK1/2 mainly via FFA1, leading to an anti-lipoapoptotic effect on NIT-1 cells [19].…”

Section: Introductionmentioning

confidence: 99%

Agonist-induced activation of human FFA1 receptor signals to extracellular signal-regulated kinase 1 and 2 through Gq- and Gi-coupled signaling cascades

Qian

Chun

et al. 2017

Cell Mol Biol Lett

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BackgroundFFA1 is abundantly expressed in the liver, skeletal muscle, monocytes and nervous system, but is particularly abundant in pancreatic β cells. It is widely believed that FFA1 exerts its regulatory roles in a variety of physiological and pathological functions. In response to oleic acid, FFA1 has been shown to induce the activation of extracellular signal-regulated kinase 1 and 2 (ERK1/2) through a mechanism involving EGFR transactivation in a breast cancer cell line. However, the underlying molecular mechanism for ERK1/2 activation mediated by n-6 free fatty acid (LA) in HEK293 cells remains to be further elucidated.MethodsA FLAG-FFA1 vector was stably expressed in HEK293 cells. Western blot analysis was applied to investigate the change in LA-induced ERK1/2 phosphorylation change in response to kinase inhibitors. Arrestin-2/3-specific siRNA was used to analyze the effect of arrestin-2/3 knockdown on FFA1-mediated ERK1/2 activation.ResultsWe proved that activation of ERK1/2 by LA was rapid, peaking at 5 min. Further experiments proved that FFA1 couples to a Gq protein and activates PI-PLC, which induces the IP3/Ca2+ and DAG/PKC signal pathways, both of which are involved in ERK1/2 activation. We also showed that there is no EGFR transactivation, arrestin-2/3 or Gβγ pathway participation in ERK1/2 phosphorylation. Treating cells with PTX abolished ERK1/2 activation at a late time point (≥20 min), indicating a critical role for Gi subunits in FFA1-mediated ERK1/2 activation.ConclusionsOur study provides a detailed delineation of the LA-mediated activation of ERK1/2 in HEK293 cells that are stably transfected with human FFA1. We also present evidence of Gi/Gq-induced synergism in the regulation of ERK1/2 phosphorylation. These observations may provide new insights into the pharmacological effects of FFA1 and the physiological functions modulated by FFA1-mediated activation of ERK1/2.Electronic supplementary materialThe online version of this article (doi:10.1186/s11658-017-0043-3) contains supplementary material, which is available to authorized users.

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“…Hormones modulate mammary stem cells (LaMarca and Rosen, 2008). Dietary factors stimulate mouse embryonic and hematopoietic stem cell activity (Hinge et al, 2009;Kim et al, 2009). It remains largely unknown, however, whether stem cells and their progeny respond to systemic changes uniformly or more specifically.…”

Section: Introductionmentioning

confidence: 99%

Specific roles of Target of rapamycin in the control of stem cells and their progeny in theDrosophilaovary

et al. 2010

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Stem cells depend on intrinsic and local factors to maintain their identity and activity, but they also sense and respond to changing external conditions. We previously showed that germline stem cells (GSCs) and follicle stem cells (FSCs) in the Drosophila ovary respond to diet via insulin signals. Insulin signals directly modulate the GSC cell cycle at the G2 phase, but additional unknown dietary mediators control both G1 and G2. Target of rapamycin, or TOR, is part of a highly conserved nutrient-sensing pathway affecting growth, proliferation, survival and fertility. Here, we show that optimal TOR activity maintains GSCs but does not play a major role in FSC maintenance, suggesting differential regulation of GSCs versus FSCs. TOR promotes GSC proliferation via G2 but independently of insulin signaling, and TOR is required for the proliferation, growth and survival of differentiating germ cells. We also report that TOR controls the proliferation of FSCs but not of their differentiating progeny. Instead, TOR controls follicle cell number by promoting survival, independently of either the apoptotic or autophagic pathways. These results uncover specific TOR functions in the control of stem cells versus their differentiating progeny, and reveal parallels between Drosophila and mammalian follicle growth.

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Linoleic Acid Induces Mouse Embryonic Stem Cell Proliferation Via Ca<sup>2+</sup>/PKC, PI3K/Akt, and MAPKs

Abstract: LA stimulated cell proliferation via Ca2+, PLC/PKC, PI3K/Akt, and p44/42 MAPKs signaling pathways in mouse ES cells.

Cited by 39 publications

References 62 publications

Diet composition transiently modulates proliferative and potency features of human cord blood-derived mesenchymal stem cells

Diet composition transiently modulates proliferative and potency features of human cord blood-derived mesenchymal stem cells

Agonist-induced activation of human FFA1 receptor signals to extracellular signal-regulated kinase 1 and 2 through Gq- and Gi-coupled signaling cascades

Specific roles of Target of rapamycin in the control of stem cells and their progeny in theDrosophilaovary

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