Reliability of ROS and RNS detection in hematopoietic stem cells − potential issues with probes and target cell population

Vlaski‐Lafarge, Marija; Ivanović, Zoran

doi:10.1242/jcs.171496

Cited by 17 publications

(9 citation statements)

References 121 publications

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“…The possible response may be in a mtROS-driven mechanism, which has been suggested as a critical regulator of stem cell fate. These reports assume the physiological mtROS concentration in the micro-environmental low O 2 as being crucial for the maintenance of stemness while the enhancement of mtROS over this niche-relevant level leads to the commitment and differentiation [52][53][54][55]. In fact, this physiological mtROS level corresponds to the "steady state" in situ mtROS levels as ones found at physiologically relevant O 2 concentrations [22,35,38].…”

Section: Discussionmentioning

confidence: 97%

α-Tocopherol Acetate Attenuates Mitochondrial Oxygen Consumption and Maintains Primitive Cells within Mesenchymal Stromal Cell Population

Lončarić

Rodríguez

Debeissat

et al. 2021

Stem Cell Rev and Rep

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We present here the data showing, in standard cultures exposed to atmospheric O 2 concentration, that alpha-tocopherol acetate (α-TOA) has a positive impact on primitive cells inside mesenchymal stromal cell (MstroC) population, by maintaining their proliferative capacity. α-TOA decreases the O 2 consumption rate of MStroC probably by impacting respiratory chain complex II activity. This action, however, is not associated with a compensatory increase in glycolysis activity, in spite of the fact that the degradation of HIF-1α was decreased in presence of α-TOA. This is in line with a moderate enhancement of mtROS upon α-TOA treatment. However, the absence of glycolysis stimulation implies the inactivity of HIF-1α which might -if it were active -be related to the maintenance of stemness. It should be stressed that α-TOA might act directly on the gene expression as well as the mtROS themselves, which remains to be elucidated.

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Section: Discussionmentioning

confidence: 97%

α-Tocopherol Acetate Attenuates Mitochondrial Oxygen Consumption and Maintains Primitive Cells within Mesenchymal Stromal Cell Population

Lončarić

Rodríguez

Debeissat

et al. 2021

Stem Cell Rev and Rep

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“…Separate previous studies indicate that NADPH oxidases Nox4 or Nox2 or that mitochondria is the major source of ROS that serve as signaling molecules to promote switching from a quiescent to an angiogenic phenotype in ECs (1,11,13,18,44,50,56,58,62 this question, we applied several methods to measure intracellular redox status due to limitation of each ROS measurement (15,24,30,59 to promote mtROS production via pSer36-p66Shc, thereby enhancing VEGFR2 activation and angiogenic responses. This may represent a novel positive feed-forward ROS-induced ROS release mechanism orchestrated by the Nox4/Nox2/pS36-p66Shc/mtROS axis, which promotes sustained activation of VEGFR2 angiogenesis signaling program (Fig.…”

Section: Discussionmentioning

confidence: 99%

ROS-induced ROS release orchestrated by Nox4, Nox2, and mitochondria in VEGF signaling and angiogenesis

Kim

Tatsunami

et al. 2017

American Journal of Physiology-Cell Physiology

190

158

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Reactive oxygen species (ROS) derived from NADPH oxidase (NOX) and mitochondria play a critical role in growth factor-induced switch from a quiescent to an angiogenic phenotype in endothelial cells (ECs). However, how highly diffusible ROS produced from different sources can coordinate to stimulate VEGF signaling and drive the angiogenic process remains unknown. Using the cytosol- and mitochondria-targeted redox-sensitive RoGFP biosensors with real-time imaging, here we show that VEGF stimulation in human ECs rapidly increases cytosolic RoGFP oxidation within 1 min, followed by mitochondrial RoGFP oxidation within 5 min, which continues at least for 60 min. Silencing of Nox4 or Nox2 or overexpression of mitochondria-targeted catalase significantly inhibits VEGF-induced tyrosine phosphorylation of VEGF receptor type 2 (VEGFR2-pY), EC migration and proliferation at the similar extent. Exogenous hydrogen peroxide (HO) or overexpression of Nox4, which produces HO, increases mitochondrial ROS (mtROS), which is prevented by Nox2 siRNA, suggesting that Nox2 senses Nox4-derived HO to promote mtROS production. Mechanistically, HO increases S36 phosphorylation of p66Shc, a key mtROS regulator, which is inhibited by siNox2, but not by siNox4. Moreover, Nox2 or Nox4 knockdown or overexpression of S36 phosphorylation-defective mutant p66Shc(S36A) inhibits VEGF-induced mtROS, VEGFR2-pY, EC migration, and proliferation. In summary, Nox4-derived HO in part activates Nox2 to increase mtROS via pSer36-p66Shc, thereby enhancing VEGFR2 signaling and angiogenesis in ECs. This may represent a novel feed-forward mechanism of ROS-induced ROS release orchestrated by the Nox4/Nox2/pSer36-p66Shc/mtROS axis, which drives sustained activation of angiogenesis signaling program.

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“…To further measure the ROS level in live RGPs during mouse cortical development, we collected the VZ tissues at E11.5, E13.5, E15.5 and E17.5, and prepared neurospheres in culture. We stained the neurospheres with CellROX Green, a cell-permeant dye that measures ROS levels and oxidative stress in live cells (Vlaski-Lafarge and Ivanovic, 2015), and found that ROS levels and oxidative stress progressively increased in the neurospheres prepared at different developmental stages (Fig. S1).…”

Section: Progressive Increase In Oxidative Stress In the Developing Mmentioning

confidence: 99%

Oxidative stress regulates progenitor behavior and cortical neurogenesis

et al. 2020

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Orderly division of radial glial progenitors (RGPs) in the developing mammalian cerebral cortex generates deep and superficial layer neurons progressively. However, the mechanisms that control RGP behavior and precise neuronal output remain elusive. Here, we show that the oxidative stress level progressively increases in the developing mouse cortex and regulates RGP behavior and neurogenesis. As development proceeds, numerous gene pathways linked to reactive oxygen species (ROS) and oxidative stress exhibit drastic changes in RGPs. Selective removal of PRDM16, a transcriptional regulator highly expressed in RGPs, elevates ROS level and induces expression of oxidative stressresponsive genes. Coinciding with an enhanced level of oxidative stress, RGP behavior was altered, leading to abnormal deep and superficial layer neuron generation. Simultaneous expression of mitochondrially targeted catalase to reduce cellular ROS levels significantly suppresses cortical defects caused by PRDM16 removal. Together, these findings suggest that oxidative stress actively regulates RGP behavior to ensure proper neurogenesis in the mammalian cortex.

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Reliability of ROS and RNS detection in hematopoietic stem cells − potential issues with probes and target cell population

Cited by 17 publications

References 121 publications

α-Tocopherol Acetate Attenuates Mitochondrial Oxygen Consumption and Maintains Primitive Cells within Mesenchymal Stromal Cell Population

α-Tocopherol Acetate Attenuates Mitochondrial Oxygen Consumption and Maintains Primitive Cells within Mesenchymal Stromal Cell Population

ROS-induced ROS release orchestrated by Nox4, Nox2, and mitochondria in VEGF signaling and angiogenesis

Oxidative stress regulates progenitor behavior and cortical neurogenesis

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