Review Article

[Retracted] Mesenchymal Stem Cell-Derived Exosomes and Their Potential Agents in Hematological Diseases

Table 1

MSC-exosomes in hematological diseases.

DiseaseMSC sourcesExosomal cargoDisease modelBiological effectRef.

Refractory GVHDHuman BM-MSCsNMClinical caseReduced proinflammatory cytokine and improved clinical GvHD symptoms[37]
aGVHDImmortalized human embryonic stem cell-derived MSCsNMMouse GVHD modelEnhanced Treg production, alleviated GVHD symptoms, and increased survival by APC[95]
aGVHDHuman BM-MSCsmiR-125a-3pMouse GVHD modelProlonged the survival of mice with aGVHD and reduced the pathologic damage by suppressing the functional differentiation of T cells from a naive to an effect or phenotype[27]
aGVHDHuman UC-MSCsNMMouse GVHD modelLowered the number of CD3+CD8+ T cells; reduced levels of IL-2, TNF-α, and IFN-γ; increased the ratio of CD3+CD4+/CD3+CD8+ T cells; and rose serum levels of IL-10[96]
GVHDHuman UC-MSCsTGF-β, IFN-γ, IDO, IL-10In vitro cell experimentPromoted PBMCs to differentiate into Tregs via TGF-β and IFN-γ[94]
cGVHDHuman BM-MSCsNMMouse chronic GVHDBlocked Th17 differentiation and improved the Treg phenotype[97]
cGVHDHuman UC-MSCsNMMouse chronic GVHDPrevented skin fibrosis in the cGVHD mouse model by suppressing the activation of macrophages and B cell immune response[98]
MM/lymphoma/leukemiaYoung and elderly healthy donor BM-MSCsNMIn vitro cell experimentAntitumor effect existed in the supernatant and not in exosomes; the antiangiogenesis effect depends on the age of donors[43]
MMMM-derived BM-MSCsmiRNA-15a, IL-2, CCL-2, fibronectinMouse MM modelMM patient-derived BM-MSC exosomes promoted MM tumor growth while normal-derived exosomes inhibited the growth of MM cells[42]
MMHuman BM-MSCs and mouse BM-MSCsMCP-1, IP-10, SDF-1In vitro and in vivo MM modelFavored MM cell proliferation, migration, and survival and induce drug resistance to bortezomib[100]
MMNormal donors and MM BM-MSCsNMIn vitro cell experimentDecreased cells viability, proliferation, migration, and translation initiation with exosomes from normal donor BM-MSCs, whereas MM MSC-exosomes increased[101]
MMOld and young MM-derived BM-MSCsmiR-340In vivo model of hypoxic BM in MMInhibited MM-induced angiogenesis with exosomes from young BM-MSCs, and miR-340 inhibited angiogenesis in endothelial cells[103]
MMMM and normal tissue-derived MSCsLINC00461In vitro cell experimentLINC0046 was highly expressed in MSC exosomes and enhanced MM cell proliferation[102]
MMBortezomib-resistant or bortezomib-sensitive patient MSCslncPSMA3, PSMA3-AS1U266-luc+ xenograft modelsExosomal lncPSMA3-AS1 mediated resistance to proteasome inhibitors by regulating the stability of PSMA3[30]
AMLHuman BM-MSCsS100A4In vitro cell experimentUpregulated S100A4 and driven proliferation, invasion, and chemoresistance of leukemia cells[106]
AMLHuman BM-MSCsTGFB1, miR-155, miR-375Clinical sample analysisReleased TGFB1, miR155, and miR375 to mediate extrinsic chemoresistance within the niche in AML[33]
AMLHD or newly diagnosed AML patient BM-MSCsmiR-26a-5p, miR-101-3p, miR-23b-5p, miR-339-3p, miR-425-5pClinical sample analysisIdentified candidate miRNAs that provide new insights regarding leukemogenesis and new treatment strategies[39]
CMLHuman UC-MSCsNMIn vitro cell experimentEnhanced the sensitivity of K562 cells to imatinib (IM) via activation of the caspase signaling pathway[105]
CMLHuman BM-MSCsmiR-15aCML xenograft tumor modelInhibited CML cell proliferation, decreased their sensitivity to IM, and promoted IM resistance[32]
CLLHuman BM-MSCsNMIn vitro cell experimentRescued leukemic cells from spontaneous or drug-induced apoptosis, enhanced their migration, and induced gene expression modifications[40]
Hodgkin lymphomaMSC cell linesADAM10In vitro cell experimentInduced release of cytokines, like TNFα, sCD30, or CD30 shedding by HL cells[31]
MDSHD and MDS patient BM-MSCsmiR-10a, miR-15aIn vitro cell experimentMDS BM-MSC-derived cargoes overexpressed miR-10a and miR-15a and enhanced cell viability and clonogenic capacity of CD34+ cells[41]

NM: not mentioned; HD: health donor; aGVHD: acute GVHD; UC-MSC: umbilical cord MSC; MDS: myelodysplastic syndrome; miRNAs: microRNAs; MCP-1: monocyte chemoattractant protein 1; IP-10: interferon-inducible protein 10; SDF-1: stromal cell-derived factor 1; imatinib: IM.