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ScRNASeq of splenic CD3+ cells from immunodeficient mice injected with progenitor T-cells generated from naïve, non-expanded or SR1-expanded human cord blood-derived CD34+ cells

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE135929 | GEO | 2019/10/15

REPOSITORIES: GEO

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5' scRNAseq of splenic CD3+ cells from immunodeficient mice injected with progenitor T-cells generated from naïve, non-expanded or SR1-expanded human cord blood-derived CD34+ cells

Project description:We report the gene expression profile of single cell peripheral CD3+ cells from immunodeficient mice injected with human progenitor T-cells (proT-cells). ProT-cell subsets were generated in vitro using human umbilical cord blood-derived CD34+ cells that were either non-expanded (naive), or expanded in vitro with the hydrocarbon receptor antagonist, StemRegenin-1 (SR1).

2019-10-15 | GSE135927 | GEO

3' V(D)J scRNASeq of splenic CD3+ cells from immunodeficient mice injected with progenitor T-cells generated from naïve, non-expanded or SR1-expanded human cord blood-derived CD34+ cells

2019-10-15 | GSE135928 | GEO

scRNASeq of splenic CD3+ cells from immunodeficient mice injected with progenitor T-cells generated from naïve, non-expanded or SR1-expanded human cord blood-derived CD34+ cells

Project description:scRNASeq of splenic CD3+ cells from immunodeficient mice injected with progenitor T-cells generated from naïve, non-expanded or SR1-expanded human cord blood-derived CD34+ cells

| PRJNA560655 | ENA

5' scRNAseq of splenic CD3+ cells from immunodeficient mice injected with progenitor T-cells generated from naïve, non-expanded or SR1-expanded human cord blood-derived CD34+ cells

Project description:5' scRNAseq of splenic CD3+ cells from immunodeficient mice injected with progenitor T-cells generated from naïve, non-expanded or SR1-expanded human cord blood-derived CD34+ cells

| PRJNA560656 | ENA

3' V(D)J scRNASeq of splenic CD3+ cells from immunodeficient mice injected with progenitor T-cells generated from naïve, non-expanded or SR1-expanded human cord blood-derived CD34+ cells

Project description:3' V(D)J scRNASeq of splenic CD3+ cells from immunodeficient mice injected with progenitor T-cells generated from naïve, non-expanded or SR1-expanded human cord blood-derived CD34+ cells

| PRJNA560657 | ENA

Coinhibition of activated p38 MAPKα and mTORC1 potentiates stemness maintenance of HSCs from SR1-expanded human cord blood CD34<sup>+</sup> cells via inhibition of senescence.

Project description:The stemness of ex vivo expanded hematopoietic stem cells (HSCs) is usually compromised by current methods. To explore the failure mechanism of stemness maintenance of human HSCs, which were expanded from human umbilical cord blood (hUCB) CD34+ cells, by differentiation inhibitor Stem Regenin 1 (SR1), an antagonist of aryl hydrocarbon receptor, we investigated the activity of p38 mitogen-activated protein kinase α (p38 MAPKα, p38α) and mammalian target of rapamycin complex 1 (mTORC1), and their effect on SR1-expanded hUCB CD34+ cells. Our results showed that cellular senescence occurred in the SR1-expanded hUCB CD34+ cells in which p38α and mTORC1 were successively activated. Furthermore, their coinhibition resulted in a further decrease in hUCB CD34+ cell senescence without an effect on apoptosis, promoted the maintenance of expanded phenotypic HSCs without differentiation inhibition, increased the hematopoietic reconstitution ability of multiple lineages, and potentiated the long-term self-renewal capability of HSCs from SR1-expanded hUCB CD34+ cells in NOD/Shi-scid/IL-2Rγnull mice. Our mechanistic study revealed that senescence inhibition by our strategy was mainly attributed to downregulation of the splicesome, proteasome formation, and pyrimidine metabolism signaling pathways. These results suggest that coinhibition of activated p38α and mTORC1 potentiates stemness maintenance of HSCs from SR1-expanded hUCB CD34+ cells via senescence inhibition. Thus, we established a new strategy to maintain the stemness of ex vivo differentiation inhibitor-expanded human HSCs via coinhibition of multiple independent senescence initiating signal pathways. This senescence inhibition-induced stemness maintenance of ex vivo expanded HSCs could also have an important role in other HSC expansion systems.

| S-EPMC7695631 | biostudies-literature

The induced APL cells generated by the transplantation of PML-RARA-transduced human CD34+ hematopoietic cells into immunodeficient mice

Project description:A humanized in vivo APL model has been established utilizing the retroviral transduction of PML-RARA into human CD34+ hematopoietic cells and the transplantation of these cells into immunodeficient mice. The resultant leukemia recapitulated human APL phenotypically, and was clustered in the same category as human APL samples in the gene expression analysis. CD34+ cells from human cord blood were retrovirally transduced with PML-RARA. They were then intravenously injected into a tail vein of nine- to 20-week-old NOD/Shi-SCID/IL-2Rγnull (NOG) mice which were irradiated with 220 cGy of X-rays. Three to four months later, the CD45+/ CD33+/ EGFP+ cells were sorted from the bone marrow for a microarray analysis. Two human APL/M3 AML samples were utilized for a comparison with these cells.

2014-11-04 | E-GEOD-49344 | biostudies-arrayexpress

The induced APL cells generated by the transplantation of PML-RARA-transduced human CD34+ hematopoietic cells into immunodeficient mice

2014-11-04 | GSE49344 | GEO

Transgene-free iPSCs generated from small volume peripheral blood nonmobilized CD34+ cells.

Project description:A variety of somatic cells can be reprogrammed to induced pluripotent stem cells (iPSCs), but CD34(+) hematopoietic stem cells (HSCs) present in nonmobilized peripheral blood (PB) would be a convenient target. We report a method for deriving iPSC from PB HSCs using immunobead purification and 2- to 4-day culture to enrich CD34(+) HSCs to 80% ± 9%, followed by reprogramming with loxP-flanked polycistronic (human Oct4, Klf4, Sox2, and c-Myc) STEMCCA-loxP lentivector, or with Sendai vectors. Colonies arising with STEMCCA-loxP were invariably TRA-1-60(+), yielding 5.3 ± 2.8 iPSC colonies per 20 mL PB (n = 17), where most colonies had single-copy STEMCCA-loxP easily excised by transient Cre expression. Colonies arising with Sendai were variably reprogrammed (10%-80% TRA-1-60(+)), with variable yield (6 to >500 TRA-1-60(+) iPSC colonies per 10 mL blood; n = 6). Resultant iPSC clones expressed pluripotent cell markers and generated teratomas. Genomic methylation patterns of STEMCCA-loxP-reprogrammed clones closely matched embryonic stem cells. Furthermore, we showed that iPSCs are derived from the nonmobilized CD34(+) HSCs enriched from PB rather than from any lymphocyte or monocyte contaminants because they lack somatic rearrangements typical of T or B lymphocytes and because purified CD14(+) monocytes do not yield iPSC colonies under these reprogramming conditions.

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Nanofiber-expanded human CD34+ cells heal cutaneous wounds in streptozotocin-induced diabetic mice.

Project description:Despite advances in diabetic wound care, the significant number of amputations that occur every year demands more effective therapeutics. Herein, we offer an aminated polyethersulfone nanofiber-expanded human umbilical cord blood-derived CD34+ cells (henceforth CD34+ cells) effective therapy, tested in cutaneous wounds developed in streptozotocin-induced diabetic NOD/SCID mice. We show that systemic administration of CD34+ cells homed to the wound site and significantly accelerated wound closure. Wound closure was associated with improved re-epithelialization and increased neovascularization; and with decreased sustained pro-inflammatory activity of NF-κB and its downstream effector molecules TNF-α, IL-1β, and IL-6 at the wound bed. This finding was further supported by the observation of a decreased number of myeloperoxidase positive neutrophils, and concomitantly increased levels of IL-10. In addition, improved granulation tissue formation was observed along with higher collagen deposition and myofibroblasts and decreased expressions of MMP-1. Mechanistically, CD34+ cells reduced the level of MMP-1 expression by inhibiting recruitment of NF-κB to the MMP-1 promoter site in dermal fibroblasts. In summary, we provide evidence of a novel nanofiber-expanded CD34+ stem cell therapeutic development for treating diabetic wounds by defining their cellular and molecular mechanisms.

| S-EPMC6557810 | biostudies-other

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