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Distinct Kinin-Induced Functions Are Altered in Circulating Cells of Young Type 1 Diabetic Patients

By Nicolle Kränkel, Stephen Paul Armstrong, Craig Alexander McArdle, Colin Dayan and Paolo Madeddu
Topics: Research Article
Publisher: Public Library of Science
OAI identifier: oai:pubmedcentral.nih.gov:2887352
Provided by: PubMed Central

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  1. (2007). Avogaro A
  2. (2008). Bone marrow-derived circulating endothelial precursors do not contribute to vascular endothelium and are not needed for tumor growth.
  3. (2009). Bradykinin-induced dilation of human coronary arterioles requires NADPH oxidase-derived reactive oxygen species.
  4. (2008). Circulating endothelial/skeletal progenitor cells for bone regeneration and healing.
  5. (2009). CXCR4 expression determines functional activity of bone marrow-derived mononuclear cells for therapeutic neovascularization in acute ischemia.
  6. (2009). Diabetes impairs the vascular recruitment of normal stem cells by oxidant damage, reversed by increases in pAMPK, heme oxygenase-1, and adiponectin.
  7. (2009). Diabetic retinopathy is associated with bone marrow neuropathy and a depressed peripheral clock.
  8. (2008). Differential vascular functions of Nox family NADPH oxidases.
  9. (2008). Effects of bradykinin postconditioning on endogenous antioxidant enzyme activity after transient forebrain ischemia in rat.
  10. (2007). Endothelial nitric oxide synthase uncoupling impairs endothelial progenitor cell mobilization and function in diabetes.
  11. (2008). Enhanced functional response of CD133+ circulating progenitor cells in patients early after acute myocardial infarction.
  12. (2008). Ex vivo priming of endothelial progenitor cells with SDF-1 before transplantation could increase their proangiogenic potential.
  13. (2008). Fractalkine Deficiency Markedly Reduces Macrophage Accumulation and Atherosclerotic Lesion Formation
  14. (2001). Impaired collateral vessel development in diabetes: potential cellular mechanisms and therapeutic implications.
  15. (2009). Increased expression of CXCR4 and integrin alphaM in hypoxia-preconditioned cells contributes to improved cell retention and angiogenic potency.
  16. (2005). International union of pharmacology. XLV. Classification of the kinin receptor family: from molecular mechanisms to pathophysiological consequences.
  17. (2004). Mobilization of CD34/CXCR4+, CD34/CD117+, c-met+ stem cells, and mononuclear cells expressing early cardiac, muscle, and endothelial markers into peripheral blood in patients with acute myocardial infarction.
  18. (2009). Molecular control of blood flow and angiogenesis: role of nitric oxide.
  19. (2006). Nitric oxide cytoskeletal-induced alterations reverse the endothelial progenitor cell migratory defect associated with diabetes.
  20. (1997). Nitric oxide inactivates NADPH oxidase in pig neutrophils by inhibiting its assembling process.
  21. (2007). Nitric oxide suppresses NADPH oxidase-dependent superoxide production by S-nitrosylation in human endothelial cells. Cardiovasc Res.75:
  22. (2009). NOX and inflammation in the vascular adventitia.
  23. (2006). Number and function of endothelial progenitor cells as a marker of severity for diabetic vasculopathy.
  24. (2007). Oxidant stress impairs in vivo reendothelialization capacity of endothelial progenitor cells from patients with type 2 diabetes mellitus: restoration by the peroxisome proliferator-activated receptor-gamma agonist rosiglitazone.
  25. (2008). Participation of kallikrein-kinin system in different pathologies.
  26. (2008). Role of kinin B2 receptor signaling in the recruitment of circulating progenitor cells with neovascularization potential.
  27. (2008). Spatiotemporal regulation of ERK2 by dual-specificity phosphatases.
  28. (2002). Targeting kinin B(1) receptor for therapeutic neovascularization.
  29. (2009). The definition of EPCs and other bone marrow cells contributing to neoangiogenesis and tumor growth: Is there common ground for understanding the roles of numerous marrow-derived cells in the neoangiogenic process?
  30. (2005). Transgenic activation of the kallikrein-kinin system inhibits intramyocardial inflammation, endothelial dysfunction and oxidative stress in experimental diabetic cardiomyopathy.