Megakaryopoiesis and thrombopoiesis are complicated processes among the hematopoietic cell lineages [11]. of its progress to refractory form, accurate choice of a biomarker is essential for evaluating prognosis and detection of resistant forms. The overall decrease in CXCR4 gene expression before treatment, the overall decrease in CXCR4 gene expression after treatment, the overall levels of CXCR4 genes expression after treatment than before treatment CXCR4 Gene Expression After Treatment Compared with the Control Group CXCR4 gene expression after treatment was evaluated in ITP patients relative to normal subjects, which was decreased in 22 patients and increased in 2 patients (value0.7130.324 Open in a separate window Discussion ITP is a heterogeneous disorder with reduced platelet count due to accelerated immune destruction of platelets as well as defective platelet production by megakaryocytes [9]. The cause of ITP is not clear but involvement of multiple defects in immune system has been widely accepted in the development of the disease [10]. Survival, proliferation, differentiation and function of normal hematopoietic cells is negatively or positively regulated by various cytokines. Megakaryopoiesis and thrombopoiesis are complicated processes among the hematopoietic cell lineages [11]. While substantial progress has been made in understanding the mechanisms of thrombopoiesis regulation, signaling pathways initiating and regulating this process have not been well established [12]. Cytokines and chemokines play an important role in megakaryopoiesis, and exert their regulatory mechanisms in proliferation, differentiation and release of platelets [13]. Chemokines are a family of proinflammatory molecules that can be used as activators of platelet function [14, 15]. Several chemokines (CCL5, CCL17, CXCL4 and CXCL8) stored in high levels in platelet alpha granules, are released during platelet activation and act as autocrine factors, which represents the important role of chemokines in homeostasis and inflammation [16]. Chemokines and their receptors contribute to pathogenesis of these diseases by forming a complex network [3]. Moreover, there are several reports of expression of chemokine receptors on platelets, including CCR5, CXCR1, CXCR2 and CXCR4 receptors [17]. CXCR4 receptor and its ligand, Stromal cell-derived factor-1 (SDF1), are expressed Verucerfont on all cells of megakaryocytic lineage, showing increased expression with maturation [18]. Studies have shown that CXCR4 inhibition blocks normal megakaryopoiesis and thrombopoiesis, indicating the critical role of CXCR4 in these processes [19]. Several studies have examined the role of this chemokine receptor in various diseases, including systemic lupus erythematosus, HIV and hematologic malignancies such as acute myeloid leukemia (AML), acute lymphoid leukemia (ALL), essential thrombocythemia (ET) and aplastic anemia. In all these studies, the importance of this chemokine in disease prognosis has been emphasized [20C22]. In the study of Ahn et al. [23], it was found that Verucerfont CXCR4 expression in AML patients is associated with poor prognosis. Despite many studies on the role of CXCR4 in various diseases, the effect of platelet disorders on regulation of chemokines has been rarely studied. Reduced expression of CXCR4 on platelets has been described in essential thrombocythemia patients [24]. Although CXCR4 is expressed on platelets and binds SDF1 with high affinity, no platelet activation or aggregation response is observed due to this binding [25]. Therefore, there are few evidences of biological CXCR4 expression on platelets. Several inflammatory factors have been studied in ITP but chemokines have been rarely considered in this disease. Given the important role of chemokines in megakaryopoiesis, more attention should be paid to the role and contribution of these molecules to ITP pathogenesis. In our study, reduced CXCR4 gene expression was observed in samples of newly diagnosed Verucerfont ITP patients before and after treatment compared to the control Verucerfont group, which was is contrary to the results of the two previous studies. In the study of Rabbit Polyclonal to APLF Jiaan et al., it was found that CXCR4 level on.