Publication

Role of the Ang2-Tie2 Axis in Vascular Damage Driven by High Glucose or Nucleoside Diphosphate Kinase B Deficiency

Chatterjee, A., Eshwaran, R., Huang, H., Zhao, D., Schmidt, M., Wieland, T. & Feng, Y., 2020, In : International Journal of Molecular Sciences. 21, 10

Research output: Contribution to journalArticleAcademicpeer-review

APA

Chatterjee, A., Eshwaran, R., Huang, H., Zhao, D., Schmidt, M., Wieland, T., & Feng, Y. (2020). Role of the Ang2-Tie2 Axis in Vascular Damage Driven by High Glucose or Nucleoside Diphosphate Kinase B Deficiency. International Journal of Molecular Sciences, 21(10). https://doi.org/10.3390/ijms21103713

Author

Chatterjee, Anupriya ; Eshwaran, Rachana ; Huang, Hongpeng ; Zhao, Di ; Schmidt, Martina ; Wieland, Thomas ; Feng, Yuxi. / Role of the Ang2-Tie2 Axis in Vascular Damage Driven by High Glucose or Nucleoside Diphosphate Kinase B Deficiency. In: International Journal of Molecular Sciences. 2020 ; Vol. 21, No. 10.

Harvard

Chatterjee, A, Eshwaran, R, Huang, H, Zhao, D, Schmidt, M, Wieland, T & Feng, Y 2020, 'Role of the Ang2-Tie2 Axis in Vascular Damage Driven by High Glucose or Nucleoside Diphosphate Kinase B Deficiency', International Journal of Molecular Sciences, vol. 21, no. 10. https://doi.org/10.3390/ijms21103713

Standard

Role of the Ang2-Tie2 Axis in Vascular Damage Driven by High Glucose or Nucleoside Diphosphate Kinase B Deficiency. / Chatterjee, Anupriya; Eshwaran, Rachana; Huang, Hongpeng; Zhao, Di; Schmidt, Martina; Wieland, Thomas; Feng, Yuxi.

In: International Journal of Molecular Sciences, Vol. 21, No. 10, 2020.

Research output: Contribution to journalArticleAcademicpeer-review

Vancouver

Chatterjee A, Eshwaran R, Huang H, Zhao D, Schmidt M, Wieland T et al. Role of the Ang2-Tie2 Axis in Vascular Damage Driven by High Glucose or Nucleoside Diphosphate Kinase B Deficiency. International Journal of Molecular Sciences. 2020;21(10). https://doi.org/10.3390/ijms21103713


BibTeX

@article{ea55555a522f4a8683a62246f58eea83,
title = "Role of the Ang2-Tie2 Axis in Vascular Damage Driven by High Glucose or Nucleoside Diphosphate Kinase B Deficiency",
abstract = "Ablation of nucleoside diphosphate kinase B (NDPK-B) in mice causes a breakdown of the neurovascular unit in the retina, mimicking diabetic retinopathy. The NDPK-B deficiency-induced vascular damage is mediated by excessive angiopoietin 2 (Ang2). Herein, the potential involvement of its receptor, Tie2, was investigated. NDPK-B-deficient mouse retinas showed an upregulation of Tie2, specifically in the deep capillary layer. A similar upregulation of Tie2 was observed in cultured endothelial cells (ECs) from different origins upon NDPK-B depletion, whereas high glucose (HG) treatment did not alter Tie2 expression. Immunofluorescence staining and subcellular fractionation showed that the majority of Tie2 upregulation occurred at the plasma membrane. Similar to HG, however, NDPK-B depletion reduced Tie2 tyrosine phosphorylation. Compared to HG, a stronger increase of Ang2 was observed in NDPK-B depleted ECs. Treatment of ECs with soluble Tie2 or siRNA-mediated Tie2 knockdown attenuated NDPK-B depletion- but not HG-induced Ang2 upregulation. Like NDPK-B depletion, overexpression of recombinant Ang2 in ECs enhanced Ang2 secretion and concomitantly promoted the upregulation of Tie2. Thus, we identified a new mechanism showing that after reaching a threshold level of secretion, Ang2 sustains its own expression and secretion by a Tie2-dependent positive feedback loop.",
author = "Anupriya Chatterjee and Rachana Eshwaran and Hongpeng Huang and Di Zhao and Martina Schmidt and Thomas Wieland and Yuxi Feng",
year = "2020",
doi = "10.3390/ijms21103713",
language = "English",
volume = "21",
journal = "International Journal of Molecular Sciences",
issn = "1422-0067",
publisher = "MDPI AG",
number = "10",

}

RIS

TY - JOUR

T1 - Role of the Ang2-Tie2 Axis in Vascular Damage Driven by High Glucose or Nucleoside Diphosphate Kinase B Deficiency

AU - Chatterjee, Anupriya

AU - Eshwaran, Rachana

AU - Huang, Hongpeng

AU - Zhao, Di

AU - Schmidt, Martina

AU - Wieland, Thomas

AU - Feng, Yuxi

PY - 2020

Y1 - 2020

N2 - Ablation of nucleoside diphosphate kinase B (NDPK-B) in mice causes a breakdown of the neurovascular unit in the retina, mimicking diabetic retinopathy. The NDPK-B deficiency-induced vascular damage is mediated by excessive angiopoietin 2 (Ang2). Herein, the potential involvement of its receptor, Tie2, was investigated. NDPK-B-deficient mouse retinas showed an upregulation of Tie2, specifically in the deep capillary layer. A similar upregulation of Tie2 was observed in cultured endothelial cells (ECs) from different origins upon NDPK-B depletion, whereas high glucose (HG) treatment did not alter Tie2 expression. Immunofluorescence staining and subcellular fractionation showed that the majority of Tie2 upregulation occurred at the plasma membrane. Similar to HG, however, NDPK-B depletion reduced Tie2 tyrosine phosphorylation. Compared to HG, a stronger increase of Ang2 was observed in NDPK-B depleted ECs. Treatment of ECs with soluble Tie2 or siRNA-mediated Tie2 knockdown attenuated NDPK-B depletion- but not HG-induced Ang2 upregulation. Like NDPK-B depletion, overexpression of recombinant Ang2 in ECs enhanced Ang2 secretion and concomitantly promoted the upregulation of Tie2. Thus, we identified a new mechanism showing that after reaching a threshold level of secretion, Ang2 sustains its own expression and secretion by a Tie2-dependent positive feedback loop.

AB - Ablation of nucleoside diphosphate kinase B (NDPK-B) in mice causes a breakdown of the neurovascular unit in the retina, mimicking diabetic retinopathy. The NDPK-B deficiency-induced vascular damage is mediated by excessive angiopoietin 2 (Ang2). Herein, the potential involvement of its receptor, Tie2, was investigated. NDPK-B-deficient mouse retinas showed an upregulation of Tie2, specifically in the deep capillary layer. A similar upregulation of Tie2 was observed in cultured endothelial cells (ECs) from different origins upon NDPK-B depletion, whereas high glucose (HG) treatment did not alter Tie2 expression. Immunofluorescence staining and subcellular fractionation showed that the majority of Tie2 upregulation occurred at the plasma membrane. Similar to HG, however, NDPK-B depletion reduced Tie2 tyrosine phosphorylation. Compared to HG, a stronger increase of Ang2 was observed in NDPK-B depleted ECs. Treatment of ECs with soluble Tie2 or siRNA-mediated Tie2 knockdown attenuated NDPK-B depletion- but not HG-induced Ang2 upregulation. Like NDPK-B depletion, overexpression of recombinant Ang2 in ECs enhanced Ang2 secretion and concomitantly promoted the upregulation of Tie2. Thus, we identified a new mechanism showing that after reaching a threshold level of secretion, Ang2 sustains its own expression and secretion by a Tie2-dependent positive feedback loop.

U2 - 10.3390/ijms21103713

DO - 10.3390/ijms21103713

M3 - Article

C2 - 32466219

VL - 21

JO - International Journal of Molecular Sciences

JF - International Journal of Molecular Sciences

SN - 1422-0067

IS - 10

ER -

ID: 129583526