Abstract
Bone marrow (BM) neural tissues are important components of bone marrow microenvironment and play important roles in normal hematopoiesis. Neuropathy of BM can cause immunological alteration in hematopoietic microenvironment. It also can induce the impairment of normal hematopoiesis and promote the development of hematologic diseases. In the present study, we determined the expression levels and clinical significances of nerve-related molecules [nestin, tyrosine hydroxylase (TH), Glial Fibrillary Acidic protein (GFAP) and S100B] and T helper-related molecules (IL-17, Foxp3) in BM of AML patients and controls by immunohistochemical analysis and RT-PCR. Our results showed that the positive rates and expression levels of nestin, TH, GFAP and IL-17 were significantly decreased while Foxp3 and the ratio of Foxp3/IL-17 were statistically elevated in BM of AML patients. We found that there were significantly positive correlations between nestin with TH and IL-17 in BM of AML patients. We also observed significantly negative correlations between nestin with TH and Foxp3/IL-17 ratio. Moreover, the expression of nestin was positively correlated with the overall survival of AML patients. Our study suggests that neuropathy together with imbalanced T helper immunology in bone marrow might play important roles in AML.
Highlights
Acute myeloid leukemia (AML) is characterized by malignant clone of hematopoietic stem cells and accumulation of immature myeloblasts in bone marrow
The positive rate of tyrosine hydroxylase (TH) in Bone marrow (BM) of AML patients (3/60, 5.00%) was statistically lower than that in controls (14/35, 40.00%; P=0.000), and we found that most of TH expression was located in megakaryocyte
Bone marrow neural tissues are important components of bone marrow microenvironment, which is composed of sympathetic nervous system (SNS) fibers, nonmyelinating Schwann cells and nestin-expressing perivascular cells containing all bone marrow mesenchymal stem and progenitor cell (MSPC) [14]
Summary
Acute myeloid leukemia (AML) is characterized by malignant clone of hematopoietic stem cells and accumulation of immature myeloblasts in bone marrow. Though the therapeutic strategy has made great progress, there are still many AML patients that fail to achieve complete remission (CR) and relapse at last. It is of importance to clarify the pathogenesis of AML and explore novel therapeutic strategy. Bone marrow microenvironment, playing an important role in the development of leukemia, comprises a rich network of hematopoietic stem cells (HSCs), mesenchymal stem cells (MSCs), osteoblasts, adipocytes, sinusoidal vessels, perivascular reticular cells and bone marrow neural tissue. Bone marrow neural tissue, playing key role in hematopoiesis and immunity, is composed of sympathetic nervous system (SNS) fiber, ensheathing Schwann cells, supporting Schwann cells and nestin+ MSCs [1,2,3]
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