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Genetic deletion of the GATA1‐regulated protein α‐synuclein reduces oxidative stress and nitric oxide synthase levels in mature erythrocytes
Author(s) -
Renella Raffaele,
Schlehe Julia S.,
Selkoe Dennis J.,
Williams David A.,
LaVoie Matthew J.
Publication year - 2014
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/ajh.23796
Subject(s) - erythropoiesis , oxidative stress , biology , haematopoiesis , nitric oxide , nitric oxide synthase , reactive oxygen species , endocrinology , medicine , microbiology and biotechnology , immunology , stem cell , anemia
α‐Synuclein is highly expressed in neural tissue and during erythropoiesis, where the key erythroid regulator GATA1 has been found to modulate its expression. While specific α‐synuclein ( SNCA ) mutations are known to cause autosomal dominant familial Parkinson's disease, its wild‐type function remains under debate. To investigate the role of α‐synuclein in murine hematopoiesis and erythropoiesis, we utilized Snca knock‐out mice and analyzed erythroid compartments for maturation defects, in vivo erythrocyte survival, and erythrocyte‐based reactive oxygen species (ROS) and nitric oxide synthase (NOS) levels. Our findings show that while bone marrow and spleen erythropoiesis and peripheral blood erythrocyte survival in Snca −/− mice was comparable to controls, the levels of ROS and of NOS‐2 were significantly decreased in mature erythrocytes in these animals. These results indicate a role for α‐synuclein in regulating oxidative stress in erythrocytes in vivo and could open new avenues for the investigation of its function in non‐neural tissue. Am. J. Hematol. 89:974–977, 2014. © 2014 Wiley Periodicals, Inc.