scholarly journals The Role ofHibiscus sabdariffaL. (Roselle) in Maintenance ofEx VivoMurine Bone Marrow-Derived Hematopoietic Stem Cells

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Zariyantey Abdul Hamid ◽  
Winnie Hii Lin Lin ◽  
Basma Jibril Abdalla ◽  
Ong Bee Yuen ◽  
Elda Surhaida Latif ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Stem Cells ◽  
Bone Marrow ◽  
Dna Damage ◽  
Ex Vivo ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Sod Activity ◽  
Hematopoietic Stem ◽  
Murine Bone Marrow

Hematopoietic stem cells- (HSCs-) based therapy requiresex vivoexpansion of HSCs prior to therapeutic use. However,ex vivoculture was reported to promote excessive production of reactive oxygen species (ROS), exposing HSCs to oxidative damage. Efforts to overcome this limitation include the use of antioxidants. In this study, the role ofHibiscus sabdariffaL. (Roselle) in maintenance of cultured murine bone marrow-derived HSCs was investigated. Aqueous extract of Roselle was added at varying concentrations (0–1000 ng/mL) for 24 hours to the freshly isolated murine bone marrow cells (BMCs) cultures. Effects of Roselle on cell viability, reactive oxygen species (ROS) production, glutathione (GSH) level, superoxide dismutase (SOD) activity, and DNA damage were investigated. Roselle enhanced the survival(P<0.05)of BMCs at 500 and 1000 ng/mL, increased survival of Sca-1+cells (HSCs) at 500 ng/mL, and maintained HSCs phenotype as shown from nonremarkable changes of surface marker antigen (Sca-1) expression in all experimental groups. Roselle increased(P<0.05)the GSH level and SOD activity but the level of reactive oxygen species (ROS) was unaffected. Moreover, Roselle showed significant cellular genoprotective potency against H2O2-induced DNA damage. Conclusively, Roselle shows novel property as potential supplement and genoprotectant against oxidative damage to cultured HSCs.

scholarly journals Reactive oxygen species contribute to dysfunction of bone marrow hematopoietic stem cells in aged C57BL/6 J mice

2015 ◽  
Vol 22 (1) ◽  
Author(s):  
Marcella L. Porto ◽  
Bianca P. Rodrigues ◽  
Thiago N. Menezes ◽  
Sara L. Ceschim ◽  
Dulce E. Casarini ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Stem Cells ◽  
Bone Marrow ◽  
Hematopoietic Stem Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Hematopoietic Stem

scholarly journals Microwaves from mobile phone induce reactive oxygen species but not DNA damage, preleukemic fusion genes and apoptosis in hematopoietic stem/progenitor cells

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Matus Durdik ◽  
Pavol Kosik ◽  
Eva Markova ◽  
Alexandra Somsedikova ◽  
Beata Gajdosechova ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Flow Cytometry ◽  
Dna Damage ◽  
Mobile Phone ◽  
Progenitor Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Fusion Genes ◽  
Microscopy Imaging ◽  
Hematopoietic Stem

Abstract Exposure to electromagnetic fields (EMF) has been associated with the increased risk of childhood leukemia, which arises from mutations induced within hematopoietic stem cells often through preleukemic fusion genes (PFG). In this study we investigated whether exposure to microwaves (MW) emitted by mobile phones could induce various biochemical markers of cellular damage including reactive oxygen species (ROS), DNA single and double strand breaks, PFG, and apoptosis in umbilical cord blood (UCB) cells including CD34+ hematopoietic stem/progenitor cells. UCB cells were exposed to MW pulsed signals from GSM900/UMTS test-mobile phone and ROS, apoptosis, DNA damage, and PFG were analyzed using flow cytometry, automated fluorescent microscopy, imaging flow cytometry, comet assay, and RT-qPCR. In general, no persisting difference in DNA damage, PFG and apoptosis between exposed and sham-exposed samples was detected. However, we found increased ROS level after 1 h of UMTS exposure that was not evident 3 h post-exposure. We also found that the level of ROS rise with the higher degree of cellular differentiation. Our data show that UCB cells exposed to pulsed MW developed transient increase in ROS that did not result in sustained DNA damage and apoptosis.

scholarly journals Fe3O4@GO magnetic nanocomposites protect mesenchymal stem cells and promote osteogenic differentiation of rat bone marrow mesenchymal stem cells

2020 ◽  
Vol 8 (21) ◽  
pp. 5984-5993
Author(s):  
He Zhang ◽  
Sirong Li ◽  
Yufeng Liu ◽  
Yijun Yu ◽  
Shichao Lin ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Osteogenic Differentiation ◽  
Reactive Oxygen ◽  
Magnetic Nanocomposites ◽  
Oxygen Species ◽  
Marrow Mesenchymal Stem Cells ◽  
Rat Bone

Fe3O4@GO/BMP2 protecting mesenchymal stem cells by regulating reactive oxygen species and promoting osteogenic differentiation of cells.

scholarly journals Proton beam radiation induces DNA damage and cell apoptosis in glioma stem cells through reactive oxygen species

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
R. Alan Mitteer ◽  
Yanling Wang ◽  
Jennifer Shah ◽  
Sherika Gordon ◽  
Marcus Fager ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Stem Cells ◽  
Dna Damage ◽  
Proton Beam ◽  
Cell Apoptosis ◽  
Reactive Oxygen ◽  
Glioma Stem Cells ◽  
Oxygen Species ◽  
Beam Radiation ◽  
Proton Beam Radiation

Reactive oxygen species in hematopoietic stem cells affect culture outcomes under inflammatory conditions

2015 ◽  
Vol 6 ◽  
pp. 1 ◽  
Author(s):  
Takashi Ishida ◽  
Satoshi Yamazaki ◽  
Hiromitsu Nakauchi ◽  
Masaaki Higashihara ◽  
Makoto Otsu ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Stem Cells ◽  
Hematopoietic Stem Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Hematopoietic Stem ◽  
Inflammatory Conditions

scholarly journals Evidence that Growth factor independence 1b regulates dormancy and peripheral blood mobilization of hematopoietic stem cells

Blood ◽  
2010 ◽  
Vol 116 (24) ◽  
pp. 5149-5161 ◽  
Author(s):  
Cyrus Khandanpour ◽  
Ehssan Sharif-Askari ◽  
Lothar Vassen ◽  
Marie-Claude Gaudreau ◽  
Jinfang Zhu ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Stem Cells ◽  
Growth Factor ◽  
Hematopoietic Stem Cells ◽  
Reactive Oxygen ◽  
Hematologic Malignancies ◽  
Oxygen Species ◽  
Hematopoietic Stem ◽  
Adhesion Protein ◽  
Adult Mice

Abstract Donor-matched transplantation of hematopoietic stem cells (HSCs) is widely used to treat hematologic malignancies but is associated with high mortality. The expansion of HSC numbers and their mobilization into the bloodstream could significantly improve therapy. We report here that adult mice conditionally deficient for the transcription Growth factor independence 1b (Gfi1b) show a significant expansion of functional HSCs in the bone marrow and blood. Despite this expansion, Gfi1bko/ko HSCs retain their ability to self-renew and to initiate multilineage differentiation but are no longer quiescent and contain elevated levels of reactive oxygen species. Treatment of Gfi1bko/ko mice with N-acetyl-cystein significantly reduced HSC numbers indicating that increased reactive oxygen species levels are at least partially responsible for the expansion of Gfi1b-deficient HSCs. Moreover, Gfi1b−/− HSCs show decreased expression of CXCR4 and Vascular cell adhesion protein-1, which are required to retain dormant HSCs in the endosteal niche, suggesting that Gfi1b regulates HSC dormancy and pool size without affecting their function. Finally, the additional deletion of the related Gfi1 gene in Gfi1bko/ko HSCs is incompatible with the maintenance of HSCs, suggesting that Gfi1b and Gfi1 have partially overlapping functions but that at least one Gfi gene is essential for the generation of HSCs.

Oncogenic Nras Grants Apoptosis Resistance to Hematopoietic Stem Cells

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 2451-2451
Author(s):  
Kevin B Yang ◽  
Victor Ng ◽  
Gina Ney ◽  
Lu Liu ◽  
Xi Jin ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Stem Cells ◽  
Hematopoietic Stem Cells ◽  
Reactive Oxygen ◽  
Clonal Expansion ◽  
Oxygen Species ◽  
Leukemic Stem Cells ◽  
Apoptosis Resistance ◽  
Hematopoietic Stem ◽  
Pkc Signaling

Abstract Genetic lesions hijack the regulatory programs of hematopoietic stem cells and progenitors (HSC/P) to transform them into leukemic stem cells (LSC). These initiating mutations confer a competitive advantage to promote clonal expansion of pre-leukemic stem cells (pre-LSC). Pre-LSCs are believed to serve as a reservoir for leukemia relapses and a cure for leukemia likely depends on the eliminating of pre-LSCs. Better understanding of how mutations dysregulate HSCs to transform them into pre-LSCs will identify new therapeutic targets to eliminate pre-LSCs. Activating RAS mutations are highly prevalent in hematopoietic malignancies. We have previously shown that a single allele of oncogenic NrasG12D promotes clonal expansion in hematopoietic stem cells (HSCs) through increased proliferation and self-renewal, but the role apoptosis plays in the clonal dominance of NrasG12D HSCs remains unclear. Here we report that oncogenic NRasG12D protects HSCs from cellular stress. Upon cytokine starvation and γ-irradiation, HSCs fromMx1-cre; LSL-NrasG12D/+ mice display reduced apoptosis as measured by Annexin V staining and Caspase 3/7 activation. This NRasG12D-mediated HSC survival is not dependent on autophagy since Bafilomycin A, an inhibitor previously shown to inhibit autophagy in HSCs, did not rescue the phenotype. Moreover, NrasG12D HSCs exhibits decreased levels of cellular reactive oxygen species (ROS), and restoration of ROS levels with buthionine sulfoximine significantly blocked the survival of NrasG12D HSCs. We next sought to identify the signaling activated by NRasG12D to promote HSC survival. Although our previous studies show that STAT5 is required for NRasG12D-mediated HSC proliferation, STAT5 is dispensable for NRasG12D-mediated HSC survival. We then determined whether inhibition of the canonical Ras effector pathways blocks NRasG12D-mediated HSC survival. To our surprise, inhibition of PI3K/AKT, MEK/ERK, or mTOR signaling did not abrogate the pro-survival effect of NRasG12D in HSCs. However, inhibition of protein kinase C (PKC) with two structurally independent inhibitors rescued the pro-survival phenotype of NrasG12D/+ HSCs. PKC inhibition also led to increased ROS levels in NrasG12D mutant HSCs, suggesting that NRasG12D reduces ROS and protects HSCs from stress through activation of PKC signaling. Taken together, we discover that in addition to increasing HSC proliferation, oncogenic NRasG12D promotes HSC survival under stress conditions. Furthermore, we reveal a pathway NRasG12D relies on to evade apoptosis and manage reactive oxygen species in HSCs independent of the STAT5 signaling that governs cell proliferation. Targeting PKC signaling, alone or in combination with STAT5 signaling, may have therapeutic benefit in eliminating pre-LSCs. Disclosures No relevant conflicts of interest to declare.

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