Autologous stem cell transplantation in HIV-positive patients affected by relapsed/partially responding lymphoma: let it be

Zanet, Ernesto; Michieli, Mariagrazia; Tirelli, Umberto

doi:10.1080/17474086.2016.1194751

Cited by 1 publication

(1 citation statement)

References 13 publications

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“…Due to an efficient granulocyte-mobilizing effect, recombinant human G-CSF (rhG-CSF) is now widely used clinically in various conditions such as neutropenia due to chemotherapy and myeloablative therapy followed by HSC transplantation and in HIV infection [17,18]. More recently, it has been tested as an alternative and/or support to MSCs in studies with ischemic conditions including the myocardium and brain [19,20] and for degenerative conditions of the central nervous system [21].…”

Section: Introductionmentioning

confidence: 99%

Modulation of Adipose-Derived Mesenchymal Stem/Stromal Cell Transcriptome by G-CSF Stimulation

Ávila-Portillo

Aristizábal

Riveros

et al. 2020

Stem Cells International

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Mesenchymal stem/stromal cells (MSCs) exhibit multidifferentiation potential, paralleled with immunomodulatory and trophic properties that make them viable alternative tools for the treatment of degenerative disorders, allograft rejection, autoimmune diseases, and tissue regeneration. MSC functional attributes can be modulated by exposing them to inflammatory-stimulating microenvironments (i.e., priming) before their therapeutic use. Granulocyte-colony stimulating factor (G-CSF) is a cytokine that plays key roles in immune response and hematopoiesis modulation through direct effects on hematopoietic progenitors’ proliferation, survival, and mobilization. Despite the established roles of MSCs supporting hematopoiesis, the effects of G-CSF on MSCs biology have not been thoroughly explored. This study reveals that G-CSF has also direct effects on adipose-derived MSCs (ADSCs), modulating their functions. Herein, microarray-based transcriptomic analysis shows that G-CSF stimulation in vitro results in modulation of various signaling pathways including ones related with the metabolism of hyaluronan (HA), conferring a profile of cell mobilization to ADSCs, mediated in a cell-intrinsic fashion in part by reducing CD44 expression and HA synthesis-related genes. Collectively, these data suggest a direct modulatory effect of G-CSF on ADSC function, potentially altering their therapeutic capacity and thus the design of future clinical protocols.

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