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Ma R.,The Peoples Hospital of Sanya | Zhang W.,The Peoples Hospital of Sanya | Wang T.,The Peoples Hospital of Sanya | He X.,The Peoples Hospital of Sanya | And 3 more authors.
Journal of International Medical Research | Year: 2014

Objectives: To investigate expression of pentraxin 3, long (PTX3) in patients with acute coronary syndrome (ACS) and its correlation with matrix metalloproteinase-9 (MMP-9) and C-reactive protein (CRP) levels. Methods: Patients with ACS were randomly assigned to the ACS group (subdivided into unstable angina pectoris [UAP] and acute myocardial infarction [AMI]). Healthy participants and patients with stable angina pectoris (SAP) were enrolled as controls. Mononuclear cell PTX3 expression, and serum MMP-9 and CRP levels, were measured by enzyme-linked immunosorbent assay. Results: The ACS group comprised 200 patients (80 in the UAP subgroup; 120 in the AMI subgroup). The control group comprised 130 participants (80 healthy volunteers and 50 patients with SAP). PTX3 expression was significantly higher in the ACS group compared with controls (3.64±0.49 versus 1.85±0.65 ng/ml), and significantly higher in the AMI compared with the UAP subgroup (5.44±0.47 versus 3.39±0.59 ng/ml). Serum MMP-9 and CRP levels were significantly higher in the ACS group compared with controls (48.55±14.22 versus 23.14±0.62 ng/ml; 4.88±1.76 versus 1.26±0.19 ng/ml, respectively), and significantly higher in the AMI compared with the UAP subgroup (58.13±7.24 versus 31.77±3.61 ng/ml; 5.80±1.46 versus 3.27±0.83 ng/ ml, respectively). PTX3 expression, and MMP-9 and CRP levels in the SAP subgroup, were not significantly different from the healthy participants. PTX3 expression positively correlated with MMP-9 and CRP levels. © The Author(s) 2014 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav.

Zhu J.,The Peoples Hospital of Sanya | Chen S.,Wright State University | Wang J.,Wright State University | Zhang C.,Wright State University | And 6 more authors.
Journal of Cardiothoracic Surgery | Year: 2013

Background: The spleen is an active lymphoid organ. The effect of splenectomy on the immune response remains unclear. This study investigated whether splenectomy can induce immune tolerance and has a beneficial role in cardiac allograft.Methods: Wistar rats were used for heart donors. The Sprague-Dawley (SD) rats designated as the recipients of heart transplantation (HT) were randomly assigned into four groups: sham, splenectomy, HT, splenectomy + HT. The survival of transplanted hearts was assessed by daily checking of abdominal palpation. At various time points after transplantation, the transplanted hearts were collected and histologically examined; the level of CD4 +CD25 + T regulatory lymphocytes (Tregs) and rate of lymphocyte apoptosis (annexin-v+ PI+ cells) in the blood were analyzed by using flow cytometric method.Results: 1) Splenectomy significantly prolonged the mean survival time of heart allografts (7 ± 1.1 days and 27 ± 1.5 days for HT and splenectomy + HT, respectively; n = 12-14/group, HT vs. splenectomy + HT, p < 0.001); 2) Splenectomy delayed pathological changes (inflammatory cell infiltration, myocardial damage) of the transplanted hearts in splenectomy + HT rats; 3) The level of CD4 +CD25 + Tregs in the blood of splenectomized rats was significantly increased within 7 days (2.4 ± 0.5%, 4.9 ± 1.3% and 5.3 ± 1.0% for sham, splenectomy and splenectomy + HT, respectively; n = 15/group, sham vs. splenectomy or splenectomy + HT, p < 0.05) after splenectomy surgery and gradually decreased to baseline level; 4) Splenectomy increased the rate of lymphocyte apoptosis (day 7: 0.3 ± 0.05%, 3.9 ± 0.9% and 4.1 ± 0.9% for sham, splenectomy and splenectomy + HT, respectively; n = 15/group, sham vs. splenectomy or splenectomy + HT, p < 0.05) in a pattern similar to the change of the CD4 +CD25 + Tregs in the blood.Conclusions: Splenectomy inhibits the development of pathology and prolongs the survival time of cardiac allograft. The responsible mechanism is associated with induction of immune tolerance via elevating CD4 +CD25 + Tregs and increasing lymphocyte apoptosis. © 2013 Zhu et al.; licensee BioMed Central Ltd.

PubMed | Guangdong Medical College, Wright State University, Hainan Medical University and the Peoples Hospital of Sanya
Type: Journal Article | Journal: PloS one | Year: 2014

Cell-released microvesicles (MVs) represent a novel way of cell-to-cell communication. Previous evidence indicates that endothelial progenitor cells (EPCs)-derived MVs can modulate endothelial cell survival and proliferation. In this study, we evaluated whether EPC-MVs protect cardiomyocytes (CMs) against angiotensin II (Ang II)-induced hypertrophy and apoptosis. The H9c2 CMs were exposed to Ang II in the presence or absence of EPC-MVs. Cell viability, apoptosis, surface area and -myosin heavy chain (-MHC) expression were analyzed. Meanwhile, reactive oxygen species (ROS), serine/threonine kinase (Akt), endothelial nitric oxide synthase (eNOS), and their phosphorylated proteins (p-Akt, p-eNOS) were measured. Phosphatidylinositol-3-kinase (PI3K) and NOS inhibitors were used for pathway verification. The role of MV-carried RNAs in mediating these effects was also explored. Results showed 1) EPC-MVs were able to protect CMs against Ang II-induced changes in cell viability, apoptosis, surface area, -MHC expression and ROS over-production; 2) The effects were accompanied with the up-regulation of Akt/p-Akt and its downstream eNOS/p-eNOS, and were abolished by PI3K inhibition or partially blocked by NOS inhibition; 3) Depletion of RNAs from EPC-MVs partially or totally eliminated the effects of EPC-MVs. Our data indicate that EPC-MVs protect CMs from hypertrophy and apoptosis through activating the PI3K/Akt/eNOS pathway via the RNAs carried by EPC-MVs.

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