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Comparison of Healing Effect of DMSP in Green Sea Algae and Mesenchymal Stem Cells on Various Inflammatory Disorders
Published in Se-Kwon Kim, Marine Biochemistry, 2023
The clinical test with Muse cells will be initiated for patients with acute myocardial infarction at Gifu University Hospital by a research group of Prof. M. Dezawa in Tohoku University and Prof. S. Hamaguchi of Gihu University and other institutions. Human Bone marrow-derived Muse cell allografts and xenografts are proven to ameliorate the damaged tissue and function of acute heart infarction in rabbits by intravenous injection. SIP-S1PR2 axis mediates homing of Muse cells into damaged heart for long-lasting tissue repair and functional recovery after acute myocardial infarction (Uchida et al., 2015; Yamada et al., 2018).
Splicing deregulation, microRNA and notch aberrations: fighting the three-headed dog to overcome drug resistance in malignant mesothelioma
Published in Expert Review of Clinical Pharmacology, 2022
Dario P. Anobile, Giulia Montenovo, Camilla Pecoraro, Marika Franczak, Widad Ait Iddouch, Godefridus J Peters, Chiara Riganti, Elisa Giovannetti
Intracellular S1P is involved in epigenetic regulation of NF-kB signaling, by regulating its target proteins: HDACs and the E3 ubiquitin ligase tumor-necrosis factor receptor-associated factor 2 (TRAF2) [53]. S1P is also involved in calcium homeostasis, suppression of apoptosis, cell motility and cell growth [74]. On the other side, ABC transporters and Sphingolipid Transporter 2 allow S1P to be exported outside the cell where it acts as ligand for five G protein-coupled receptors (S1PR1-5). In addition, S1P regulates several extracellular processes, including growth and differentiation, survival, immune defense, angiogenesis, cytoskeletal rearrangements, and motility [74]. Therefore, S1P can be involved in several pathologic processes including cancer due to its role in angiogenesis, cell survival/proliferation and lymphocyte trafficking [53], as well as in metastasis through the release of the S1P receptor (S1P2) in exosomes [75].
S1P in the development of atherosclerosis: roles of hemodynamic wall shear stress and endothelial permeability
Published in Tissue Barriers, 2021
Christina M Warboys, Peter D Weinberg
S1P is a highly bioactive lipid signaling mediator that is produced following phosphorylation of sphingosine by sphingosine kinase. Serum S1P levels are regulated by the actions of S1P phosphatase and S1P lyase that dephosphorylate or degrade S1P, respectively. S1P is produced by erythrocytes, leukocytes and activated platelets29 although EC are the major source of plasma S1P under physiological conditions.30 Circulating S1P levels range between 200 and 1000 nM with the majority bound to high-density lipoprotein. S1P can also circulate bound to albumin and other lipoproteins but to a lesser extent.31 At target cells, S1P binds to and activates the S1P family of G-protein coupled receptors (S1PR1–S1PR5) that couple to different G proteins to elicit a variety of cellular responses.32 Endothelial cells express only S1PR1, which couples exclusively to Gαi and S1PR3, which couples to Gαi, Gαq/11, Gα12/13, although S1PR1 is expressed at significantly greater levels.33 There is conflicting evidence regarding the expression of S1PR2 in EC. S1PR2 is expressed at low levels in bovine microvascular EC34 but is undetectable in human umbilical vein EC (HUVEC).33
Intravital imaging of megakaryocytes
Published in Platelets, 2020
David Stegner, Katrin G. Heinze
Zhang and colleagues reported that the directional formation of proplatelets from vessel-adjacent MKs into the vessel lumen depends on sphingosine-1-phosphate (S1P) – S1PR1 (one of the sphingosine-1-phosphate receptors) signaling [32]. With the help of 2P-IVM, the authors noted an increase in the size of S1PR1-deficient MKs, which was not accompanied by an altered MK localization or motility. However, intra-vascular PPF was dramatically reduced in S1PR1-deficient MKs and these MKs displayed PPF within the interstitial space of the BM. Consequently, the authors concluded that the release of proplatelets depends on S1PR1 [32] suggesting that the final stages of thrombopoiesis depend on S1P signaling. However, a more recent study [89] challenged these findings and observed no thrombocytopenia in mice lacking S1P1 in the hematopoietic system, which in stark contrast to the initial report [32]. Niazi and colleagues concluded that S1P would rather inhibit megakaryopoiesis through S1P1 and S1P2 [89]. Clearly, more studies are required to address this controversy.