A role for the renin-angiotensin system in hematopoiesis.

Haematologica (Impact Factor: 5.87). 07/2009; 94(6):745-7. DOI: 10.3324/haematol.2009.006965
Source: PubMed
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    ABSTRACT: Renal transplantation has become one of the most common surgical procedures performed to replace a diseased kidney with a healthy kidney from a donor. It can help patients with kidney failure live decades longer. However, renal transplantation also faces a risk of developing various blood disorders. The blood disorders typically associated with renal transplantation can be divided into two main categories: (1) Common disorders including post-transplant anemia (PTA), post-transplant lymphoproliferative disorder (PTLD), post-transplant erythrocytosis (PTE), and post-transplant cytopenias (PTC, leukopenia/neutropenia, thrombocytopenia, and pancytopenia); and (2) Uncommon but serious disorders including hemophagocytic syndrome (HPS), thrombotic microangiopathy (TMA), therapy-related myelodysplasia (t-MDS), and therapy-related acute myeloid leukemia (t-AML). Although many etiological factors involve the development of post-transplant blood disorders, immunosuppressive agents, and viral infections could be the two major contributors to most blood disorders and cause hematological abnormalities and immunodeficiency by suppressing hematopoietic function of bone marrow. Hematological abnormalities and immunodeficiency will result in severe clinical outcomes in renal transplant recipients. Understanding how blood disorders develop will help cure these life-threatening complications. A potential therapeutic strategy against post-transplant blood disorders should focus on tapering immunosuppression or replacing myelotoxic immunosuppressive drugs with lower toxic alternatives, recognizing and treating promptly the etiological virus, bacteria, or protozoan, restoring both hematopoietic function of bone marrow and normal blood counts, and improving kidney graft survival.
    Frontiers in Cell and Developmental Biology 01/2015; 3:18. DOI:10.3389/fcell.2015.00018
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    ABSTRACT: Introduction: Thrombocytopenia is an abnormally low number of platelets in the blood resulting from either too few platelets being produced or existing platelets being destroyed. Severe thrombocytopenia leads to excessive bleeding and can be the result of numerous medical conditions or a side effect of medications or treatments. Although platelet transfusions are typically administered to correct thrombocytopenia, transfusions represent a temporary and unsustainable solution. As there is a limited supply of platelet units available for transfusion, along with the significant financial cost and risk of infection, investigation to uncover mechanisms that boost platelet production may have important clinical and therapeutic implications. Treatment with angiotensin 1 - 7 (A(1 - 7)) has been shown in a preclinical and clinical evaluations to have a positive effect on platelet recovery. Areas covered: The authors provide an overview of the current treatment options available for platelet recovery and highlight the need for alternatives. Following on, the authors discuss the use of A(1 - 7) as a potential therapeutic option for platelet recovery, including its safety and efficacy. Expert opinion: Current evidence provides a good basis for continued research and evaluation of the benefits of A(1 - 7) treatment in stimulating platelet recovery following myelosuppression. A(1 - 7) therapy has the potential to make a significant contribution to healthcare by providing standalone and additive treatments to address unmet medical needs and life-threatening diseases by utilizing the regenerative arm of the renin-angiotensin system.
    Expert Opinion on Investigational Drugs 02/2014; DOI:10.1517/13543784.2014.891015 · 5.43 Impact Factor
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    ABSTRACT: Objective: The prominent functions of the local renin-angiotensin system (RAS) in primitive hematopoiesis further support the hypothesis that local autocrine bone marrow RAS could also be active in neoplastic hematopoiesis. The aim of this study is to examine critical RAS elements in normal CD34+ hematopoietic stem cells and multiple myeloma (MM)-related progenitor cells. Materials and Methods: The study group comprised the total bone marrow cells (CBM) of 10 hematologically normal people, the CD34+ stem cell samples (CD34+CBM) of 9 healthy donors for allogeneic peripheral stem cell transplantation, and the CD34+ stem cell samples (CD34+MM) of 9 MM patients undergoing autologous peripheral stem cell transplantation. We searched for the gene expression of the major RAS components in healthy hematopoietic cells and myeloma cells by quantitative real-time polymerase chain reaction analysis. Results: RENIN, angiotensinogen (ANGTS), and angiotensin converting enzyme-I (ACE I) mRNA expression levels of CBM were significantly higher than those in myeloma patients (p=0.03, p=0.002, and p=0.0008, respectively). Moreover, RENIN and ANGTS mRNA expression levels were significantly higher in CD34+ stem cell samples of healthy allogeneic donors compared to those in myeloma patients (p=0.001 and p=0.01). However, ACE I expression levels were similar in CD34+CBM and CD34+MM hematopoietic cells (p=0.89). Conclusion: Although found to be lower than in the CBM and CD34+CBM hematopoietic cells, the local RAS components were also expressed in CD34+MM hematopoietic cells. This point should be kept in mind while focusing on the immunobiology of MM and the processing of autologous cells during the formation of transplantation treatment protocols.
    Turkish Journal of Haematology 06/2014; 31(2):136-42. DOI:10.4274/tjh.2013.0011 · 0.34 Impact Factor


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Jun 1, 2014