Further studies are necessary to elucidate the above and other mechanisms involved in the action of central, especially NAc, TRPV1 antagonism on drug addiction. Allogeneic hematopoietic stem cell transplantation has been considered as one of the effective treatment strategies for hematological malignancies and other benign hematological disorders. For patients who undergo allogeneic HSCT, acute graft-versus-host disease is the most common complication that may lead to target organ damage. In those patients, impaired hematopoiesis has been associated with a poor prognosis. The mechanisms for hematopoietic dysfunction after aGvHD are still not fully understood. It was previously suggested that hematopoietic suppression might be mediated by inhibitory cytokines, such as TNF-a, produced during aGvHD as part of “cytokine storm”, or by a deficient bone marrow microenvironment damaged by conditioning reagents and/or by cytokines. Two types of BM niches were identified in recent years. Endosteal niche is mainly located in the endostium and composed of osteoblast cells; while vascular niche is formed with sinusoidal vascular endothelial cells and perivascular cells. Both endosteal and vascular niches play important roles in regulating self-renewal capacity and maintaining the stability of hematopoietic stem cell pool. Recently, Shono et al reported that, in an MHC-mismatched murine HSCT model, GvHD does not directly affect HSCs but rather targets osteoblast cells, leading to BM endosteal niche failure to ICI 182780 129453-61-8 support hematopoiesis reconstitution after HSCT. It is known that the major targets of aGvHD, liver, skin, and intestinal tract, are characterized by being covered with endothelial cells. We hypothesized that vascular niche, mainly composed of SECs, might be the target of aGvHD. Further, the dysfunction of vascular niche may play an important role in hematopoietic impairment in aGvHD. In this study, we investigated the effect of aGvHD on viability and functions of vascular niche, and its impact on hematopoietic reconstitution in an MHC haploidentical matched aGvHD mouse model. Suppression of hematopoiesis during aGvHD has long been observed in both clinical and experimental studies. In an MHC-mismatched murine GvHD model, Shono, et al reported that the disrupted hematopoiesis was not caused by direct elimination of HSCs in GvHD, but instead, was due to GvHDimpaired osteoblastic cells in the BM niche, which consequently failed to support the reconstitution of hematopoiesis, mainly B lymphopoiesis.