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Single-cell RNA sequencing on cord blood-derived HPSCs cultured with or without liproxstatin-1 supplementation in chemically-defined conditions

ABSTRACT: The aim for this dataset is to demonstrate that blockade of ferroptosis with the small molecule liproxstatin-1 can significantly augment the expansion of human HSCs derived from either cord blood or adult sources using diverse methods, including widely applied serum-free cultures and recently reported chemically-defined conditions. We find that human HSCs treated with liproxstatin-1 display increased ribosome biogenesis and cholesterol biosynthesis, accompanied by elevated 7-dehydrocholesterol levels - a potent endogenous inhibitor of ferroptosis. This study demonstrates the effectiveness of mitigating ferroptosis to enhance human HSC expansion in the setting of therapeutic genome modifications, paving the path to clinical applications.

ORGANISM(S): Homo sapiens

PROVIDER: GSE276160 | GEO | 2025/10/13

REPOSITORIES: GEO

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Effect of ferrostatin-1 and liproxstatin-1 during TNF-induced HT-29 cells apoptosis

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Single-cell RNA sequencing on cord blood-derived HPSCs cultured with or without liproxstatin-1 supplementation in chemically-defined conditions

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2026-01-12 | GSE296239 | GEO

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Project description:Background: Autologous fat grafting is hampered by unpredictable graft survival, which is potentially regulated by ferroptosis. Glutathione (GSH), a powerful antioxidant used in tissue preservation, has ferroptosis-regulating activity; however, its effects on fat grafts are unclear. This study investigated the effects and mechanisms of GSH in fat graft survival. Methods: Human lipoaspirates were transplanted subcutaneously into the backs of normal saline-treated (control) or GSH-treated nude mice. Graft survival was evaluated by magnetic resonance imaging and histology. RNA sequencing was performed to identify differentially expressed genes and enriched pathways. GSH activity was evaluated in vitro using an oxygen and glucose deprivation (OGD) model of adipose-derived stem cells. Results: Compared with control group, GSH induced better outcomes, including superior graft retention, appearance, and histological structures. RNA sequencing suggested enhanced negative regulation of ferroptosis in the GSH-treated grafts, which showed reduced lipid peroxides, better mitochondrial ultrastructure, and SLC7A11/GPX4 axis activation. In vitro, OGD-induced ferroptosis was ameliorated by GSH, which restored cell proliferation, reduced oxidative stress, and upregulated ferroptosis defense factors. Conclusions: Our study confirms that ferroptosis participates in regulating fat graft survival and that GSH exerts a protective effect by inhibiting ferroptosis. GSH-assisted lipotransfer is a promising therapeutic strategy for future clinical application.

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2023-10-18 | E-MTAB-12241 | biostudies-arrayexpress

Global Gene Expression of hematopoietic stem cells expressing endogenous NrasG12D/G12D, NrasG12D/+, Nras+/+

Project description:Oncogenic NRAS mutations are frequently identified in human myeloid leukemias. In mice, expression of endogenous oncogenic Nras (NrasG12D/+) in hematopoietic cells leads to expansion of myeloid progenitors, increased long-term reconstitution of bone marrow cells, and a chronic myeloproliferative neoplasm (MPN). However, acute expression of NrasG12D/+ in a pure C57BL/6 background does not induce hyperactivated GM-CSF signaling or increased proliferation in myeloid progenitors. It is thus unclear how NrasG12D/+ signaling promotes leukemogenesis. Here we show that hematopoietic stem cells (HSCs) expressing NrasG12D/+ serve as MPN initiating cells. They undergo moderate hyperproliferation with increased self-renewal. The aberrant NrasG12D/+ HSC function is associated with hyperactivation of ERK1/2 in HSCs. Conversely, downregulation of MEK/ERK by pharmacological and genetic approaches attenuates the cycling of NrasG12D/+ HSCs and prevents the expansion of NrasG12D/+ HSCs and myeloid progenitors. Our data delineate critical mechanisms of oncogenic Nras signaling in HSC function and leukemogenesis. three NrasG12D/G12D HSCs samples, three NrasG12D/+ HSCs samples, two Nras+/+ HSCs control samples.

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