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BACKGROUND: The imbalance of Treg/Th17 cells is an important pathogenic factor for immune thrombocytopenic purpura (ITP). We previously reported miR-125a-5p targeted CXCL13 and participated in the process of ITP. In the present study, the role of miR-125a-5p in regulating Treg/Th17 ratio and its potential molecular mechanism were investigated. METHOD: A total of 30 adults with ITP and 30 healthy subjects were included. MEG3 expression in peripheral blood derived CD4+ T cells from ITP patients and healthy subjects were detected by real-time PCR. In vitro experiments, the effects of inhibiting or overexpressing MEG3 on the expression of miR-125a-5p, Foxp3 and ROTγt in CD4+ T cells were investigated. RESULTS: MEG3 expression was increased in CD4+ T cells of patients with ITP. Dexamethasone decreased MEG3 expression level of CD4+ T cells in vitro. MEG3 directly interacted with miR-125a-5p and MEG3 overexpression inhibited miR-125a-5p expression in CD4+ T cells exposed to dexamethasone. MEG3 down-regulation or miR-125a-5p overexpression promoted Foxp3 expression and inhibited RORγt expression. CONCLUSION: MEG3 interacted with miR-125a-5p and inhibited its expression, and MEG3/miR-125a-5p contributed to induce immune imbalance of Treg/Th17 in ITP.

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BACKGROUND: Immune thrombocytopenia (ITP) is an acquired and autoimmune disease of adults and children characterized by decreased platelet production. CXC chemokine ligand-13 (CXCL13) participates in multiple immunological responses. However, it is still unknown the relationship between CXCL13 and ITP. METHODS: Plasma CXCL13 was detected in ITP (n = 30) children. CD4+ T cells was isolated from peripheral blood mononuclear cells (PBMCs) from healthy volunteers. Treated CD4+ T cells with dexamethasone and/or miR-125-5p mimic/inhibitor, to observe the regulation of CXCL13. RESULTS: Compared with controls, ITP children had elevated plasma CXCL13, the concentration of which was reduced after treatment. In vitro, dexamethasone decreased CXCL13 level in in dose- dependent and in time-dependent manner. MiR-125-5p mimic decreased CXCL13 level and miR-125-5p inhibitor increased CXCL13 level in CD4+ T cells. CXCL13 was implied to be target gene of miR-125-5p. MiR-125-5p inhibitor also canceled dexamethasone induced decrease of CXCL13. CONCLUSION: CXCL13 is the target gene of miR-125-5p, which is possibly involved in the pathological process of ITP.

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OBJECTIVE: To investigate the expressions of transforming growth factor-beta(1) and Smad4 in the prostatic tissue of rat models of chronic nonbacterial prostatitis (CNP), and to explore the mechanisms of CNP and its fibrosis. METHODS: Sixty 6-month-old SD rats were randomly allocated into three groups of equal number: normal control, 30 d CNP model and 45 d CNP model, the models made by castration + high-dose intramuscular injection of estradiol benzoate. The expressions of TGF-beta1 and Smad4 in the prostatic tissue were detected by immunohistochemistry and Western blot. RESULTS: Compared with the normal controls, the 30 d and 45 d CNP rat models showed a significantly increased expression of TGF-beta1 and decreased expression of Smad4 (P < 0.05), even more significantly in the 45 d than in the 30 d group. And the expression of TGF-beta1 was negatively correlated with that of Smad4 in the CNP rat models. CONCLUSION: TGF-beta1 and Smad4 may be involved in the pathogenesis of CNP, and prostatic fibrosis may make the condition difficult to cure.

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OBJECTIVE: To carry out a genetic detection and analysis of Von Hippel-Lindau (VHL) gene in Chinese patients with sporadic pheochromocytoma. METHODS: DNA samples were extracted from peripheral blood cells and fresh pheochromocytoma specimens from 41 patients with sporadic pheochromocytoma were assayed by polymerase chain reaction and direct sequencing. The DNA samples of 50 healthy volunteers were extracted from peripheral blood as a control. The PCR products of exon 1, exon 2 and exon 3 were used for molecular analysis of the VHL gene. The genetic detection of family members of VHL gene mutations was also performed. RESULTS: One of mutations was located at nucleotide 572 (G-->C) in exon 2, presenting a codon 120 from arginine (R) to threonine (T). Tow small insertions were locatated at nucleotide 623T (TTTGTtG) in exon 2, leading to a frameshift mutation. There were also three carriers of G572C and three carriers of 623T (TTTGTtG) in family members of the three cases. CONCLUSION: There are some Chinese patients with sporadic pheochromocytoma with tumorigenic VHL gene mutations. It is recommended to use the genetic detection and analysis of VHL gene as a routine examination for patients with sporadic pheoehromoeytoma under the age of 50 years with questionable family history. The genetic detection and analysis of VHL gene may be useful as a marker for the diagnosis of hereditary pheochromocytoma.

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OBJECTIVE: To detect the VHL gene mutations in a Chinese family with nonsyndromic pheochromocytoma. METHODS: Mutations of VHL gene were detected in a Chinese family with nonsyndromic pheochromocytoma. Five patients and fifteen relatives were involved in this study. Peripheral blood was collected and total genomic DNA was prepared for polymerase chain reaction (PCR). PCR products of all the three exons of VHL gene were purified and a direct gene sequence analysis was performed. RESULTS: All the five patients presented a codon 125 from Histidine (H) to Proline (P) change at nucleotide 587 (A --> C) in exon 2. Seven members of fifteen relatives were carriers with the same VHL gene mutation. Two carriers were detected with bilateral adrenal tumors and right renal cyst respectively by ultrasonic inspection. CONCLUSION: The novel VHL gene mutation detected in this kindred may be the causative gene. Genetic test can detect the carriers in an early period. It is recommended as a routine method of genetic test in nonsyndromic pheochromocytoma patients.

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