Peroxiredoxin-2 nitrosylation facilitates cardiomyogenesis of mouse embryonic stem cells via XBP-1s/PI3K pathway

Wu, Bowen; Yu, Hao; Wang, Yifan; Pan, Zongfu; Zhang, Yihan; Li, Tong; Li, Lü; Zhang, Weichen; Ge, Lijia; Chen, Ying; Ho, Choe Kyong; Zhu, Danyan; Huang, Xin; Lou, Yijia

doi:10.1016/j.freeradbiomed.2016.05.025

Cited by 10 publications

(13 citation statements)

References 60 publications

(73 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Biotin‐switch assay confirmed that both total protein and HIF‐1α nitrosylation is markedly increased upon GSNO exposure, while nitrosylation scanvenger DTT can attenuated the HIF‐1α nitrosylation in a concentration‐dependent manner. Since DTT prevent protein nitrosylation via directly reducing −SNO motif in culture medium [Bouïs et al, ; Wu et al, ], present study reveals that S ‐nitrosylation reaction stabilizes HIF‐1α protein level followed by aldolase A and GLUT1 upregulation. HIF‐1α S ‐nitrosylation associated aldolase A activity enhancement is the upstream signaling of mitochondria injury in ECs by GSNO exposure.…”

Section: Discussionmentioning

confidence: 66%

“…Given that GSNO could activate PI3 K/Akt in relatively low concentration [Carver et al, ; Wu et al, ], but inhibit the pathway in high concentration [Giri et al, ]. We explored whether PI3 K/Akt activity was involved in GSNO‐induced glycolytic pathway enhancement.…”

Section: Resultsmentioning

confidence: 99%

“…Under the relative higher concentration, GSNO can protect the neurovascular unit and reduces secondary injury in rat [Sakakima et al, ; Khan et al, ,]. Temporary GSNO exposure could promote embryonic stem cell‐derived cardiomyogenesis by peroxiredoxin‐2 S ‐nitrosylation, implying its potential in regenerative medicine [Wu et al, ]. Although inhalation treatment of beagle dogs and rats with highest achieved doses GSNO displays the safety [Colagiovanni et al, ], the lack of its bioavailability seems not enough to support other delivery way.…”

mentioning

confidence: 99%

See 2 more Smart Citations

Enhanced Aerobic Glycolysis by S-Nitrosoglutathione via HIF-1α Associated GLUT1/Aldolase A Axis in Human Endothelial Cells

et al. 2017

Self Cite

View full text Add to dashboard Cite

S-nitrosoglutathione (GSNO)-induced apoptosis is associated with reactive oxygen species and loss of mitochondrial Omi/HtrA2 in human endothelial cells (ECs). But its upstream regulation is still not elucidated. Here, we demonstrate that hypoxia induced factor-1α (HIF-1α)-linked aerobic glycolysis is associated with mitochondrial abnormality by treatment of human EC-derived EA.hy926 cells with GSNO (500 µM) for 6 h. GSNO exposure increased the levels of Aldolase A and glucose transporter-1 (GLUT1) mRNAs and proteins. And selectively enhanced aldolase A activity to form glyceraldehyde 3-phosphate, dihydroxyacetone phosphate, which subsequently increased intracellular levels of methylglyoxal and reactive oxygen species in parallel. Using the biotin switch assay, we found that GSNO increased the S-nitrosylating levels of total protein and HIF-1α. Knockdown of HIF-1α with siRNA attenuated its target aldolase A and GLUT1 expression but not VEGF. In contrast, nitrosylation scanvenger dithiothreitol could decrease all the protein levels. It suggested that aerobic glycolytic flux was more dependent on HIF-1α level, and that HIF-1α S-nitrosylation was crucial for its target expression under the normoxic condition. Moreover, GSNO-induced PI3 K (phosphoinositide 3-kinase)/Akt phosphorylation might contribute to HIF-1α stabilization and nucleus translocation, thereby aiding aldolase A and GLUT1 mRNAs upregulation. Taken together, higher concentration GSNO promotes glycolytic flux enhancement and methylglyoxal formation via HIF-1α S-nitrosylation. These findings reveal the mechanism of enhanced glycolysis-associated mitochondrial dysfunction in ECs by GSNO exposure under normoxic and non-hyperglycemic condition. And offer the early potential targets for vascular pathophysiological evaluation. J. Cell. Biochem. 118: 2443-2453, 2017. © 2017 Wiley Periodicals, Inc.

show abstract

Section: Discussionmentioning

confidence: 66%

Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

Enhanced Aerobic Glycolysis by S-Nitrosoglutathione via HIF-1α Associated GLUT1/Aldolase A Axis in Human Endothelial Cells

et al. 2017

Self Cite

View full text Add to dashboard Cite

show abstract

“…PRDX2 plays an important role in the proliferation and differentiation of many kinds of stem cells. Nitrosylation of PRDX2 can promote cardiac formation of mouse embryonic stem cells through X-box binding protein-1s/phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) signaling pathway (30); PRDX2 has also been shown to regulate the differentiation of embryonic stem cells into neurons (31). Compared with primary stem cells, the regulation of stem cell stemness by PRDX2 comes more from the study of cancer stem cells (6,32).…”

Section: Discussionmentioning

confidence: 99%

Deletion of Peroxiredoxin II Inhibits the Growth of Mouse Primary Mesenchymal Stem Cells Through Induction of the G₀/G₁ Cell-cycle Arrest and Activation of AKT/GSK3β/β-Catenin Signaling

Han

Jin

et al. 2019

In Vivo

View full text Add to dashboard Cite

Background/Aim: Dermal mesenchymal stem cells (DMSCs) are pluripotent stem cells found in the skin which maintain the thickness of the dermal layer and participate in skin wound healing. Materials and Methods: The MTT assay was performed to detect cell proliferation and cell-cycle progression and cell-surface markers were assessed by flow cytometry. The levels of proteins in related signaling pathways were detected by western blotting assay and the translocation of β-catenin into the nucleus were detected by immunofluorescence. Red oil O staining was performed to examine the differentiational ability of DMSCs. Results: Knockout of PRDX2 inhibited DMSC cell growth, and cell-cycle arrest at G 0 /G 1 phase; p16, p21 and cyclin D1 expression levels in Prdx2 knockout DMSCs were significantly increased. Furthermore, AKT phosphorylation were significantly increased in Prdx2 knockout DMSCs, GSK3β activity were inhibited, result in β-Catenin accumulated in the nucleus. Conclusion: In conclusion, these results demonstrated that PRDX2 plays a pivotal role in regulating the proliferation of DMSCs, and this is closely related to the AKT/glycogen synthase kinase 3 beta/β-catenin signaling pathway. Skin has a strong capacity for repair and regeneration due to the fact that it contains various stem cells, such as epidermal stem cells, skin-derived precursors and dermal mesenchymal stem cells (DMSCs) (1, 2). DMSCs play two major roles, one is as a direct source of fibroblasts, and the other is to secrete a variety of cytokines which promote fibroblasts to produce collagen and elastin (3). Therefore, the function of DMSCs plays decisive role in skin development and wound repair (4). Peroxiredoxin 2 (PRDX2) is wildly distributed in various tissues and cells, and functions as a scavenger of reactive oxygen species (ROS) (5, 6). Our previous study showed that 133 This article is freely accessible online.

show abstract

“…Importantly, a high glucose concentration had been shown to promote cardiac differentiation of ESCs via mitochondrial ROS generation [ 59 ]. Temporally reduced antioxidant activity of peroxiredoxin-2 via nitrosylation can cause transient endogenous ROS accumulation and promote ESC-derived cardiomyogenesis [ 60 ]. During cardiac differentiation of human ESCs, PGC-1 α -dependent mitochondrial biogenesis was associated with increased ROS levels in the CM population [ 61 ].…”

Section: Ros Mediate Cardiac Differentiation Of Pscsmentioning

confidence: 99%

Roles of Reactive Oxygen Species in Cardiac Differentiation, Reprogramming, and Regenerative Therapies

Liang

Chen

et al. 2020

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

Reactive oxygen species (ROS) have been implicated in mechanisms of heart development and regenerative therapies such as the use of pluripotent stem cells. The roles of ROS mediating cell fate are dependent on the intensity of stimuli, cellular context, and metabolic status. ROS mainly act through several targets (such as kinases and transcription factors) and have diverse roles in different stages of cardiac differentiation, proliferation, and maturation. Therefore, further detailed investigation and characterization of redox signaling will help the understanding of the molecular mechanisms of ROS during different cellular processes and enable the design of targeted strategies to foster cardiac regeneration and functional recovery. In this review, we focus on the roles of ROS in cardiac differentiation as well as transdifferentiation (direct reprogramming). The potential mechanisms are discussed in regard to ROS generation pathways and regulation of downstream targets. Further methodological optimization is required for translational research in order to robustly enhance the generation efficiency of cardiac myocytes through metabolic modulations. Additionally, we highlight the deleterious effect of the host’s ROS on graft (donor) cells in a paracrine manner during stem cell-based implantation. This knowledge is important for the development of antioxidant strategies to enhance cell survival and engraftment of tissue engineering-based technologies. Thus, proper timing and level of ROS generation after a myocardial injury need to be tailored to ensure the maximal efficacy of regenerative therapies and avoid undesired damage.

show abstract

Peroxiredoxin-2 nitrosylation facilitates cardiomyogenesis of mouse embryonic stem cells via XBP-1s/PI3K pathway

Cited by 10 publications

References 60 publications

Enhanced Aerobic Glycolysis by S-Nitrosoglutathione via HIF-1α Associated GLUT1/Aldolase A Axis in Human Endothelial Cells

Enhanced Aerobic Glycolysis by S-Nitrosoglutathione via HIF-1α Associated GLUT1/Aldolase A Axis in Human Endothelial Cells

Deletion of Peroxiredoxin II Inhibits the Growth of Mouse Primary Mesenchymal Stem Cells Through Induction of the G₀/G₁ Cell-cycle Arrest and Activation of AKT/GSK3β/β-Catenin Signaling

Roles of Reactive Oxygen Species in Cardiac Differentiation, Reprogramming, and Regenerative Therapies

Contact Info

Product

Resources

About

Peroxiredoxin-2 nitrosylation facilitates cardiomyogenesis of mouse embryonic stem cells via XBP-1s/PI3K pathway

Cited by 10 publications

References 60 publications

Enhanced Aerobic Glycolysis by S-Nitrosoglutathione via HIF-1α Associated GLUT1/Aldolase A Axis in Human Endothelial Cells

Enhanced Aerobic Glycolysis by S-Nitrosoglutathione via HIF-1α Associated GLUT1/Aldolase A Axis in Human Endothelial Cells

Deletion of Peroxiredoxin II Inhibits the Growth of Mouse Primary Mesenchymal Stem Cells Through Induction of the G0/G1 Cell-cycle Arrest and Activation of AKT/GSK3β/β-Catenin Signaling

Roles of Reactive Oxygen Species in Cardiac Differentiation, Reprogramming, and Regenerative Therapies

Contact Info

Product

Resources

About

Deletion of Peroxiredoxin II Inhibits the Growth of Mouse Primary Mesenchymal Stem Cells Through Induction of the G₀/G₁ Cell-cycle Arrest and Activation of AKT/GSK3β/β-Catenin Signaling