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Hou Q.,Longgang District Central Hospital | Lin J.,Southern Medical University | Huang W.,Sun Yat Sen University | Li M.,Sun Yat Sen University | And 2 more authors.
PLoS ONE | Year: 2015

C1q/TNF-related protein-3 (CTRP3) is a novel adipokine with roles in multiple cellular processes. However, little is known about its function in prostate cells. This study investigated the effects and mechanisms of CTRP3 in prostate cells. We first generated and purified CTRP3 protein in HEK 293T cells. Proliferation of RWPE-1 prostate cells was evaluated by MTT analyses under treatment with different concentrations of CTRP3 for various exposure times. The results revealed maximum enhancement of proliferation with 10 μg/mL CTRP3 for 72 h. Cell apoptosis and cell cycle were determined by TUNEL staining and flow cytometry analysis. TUNEL assay showed decreased TUNEL-positive cells in RWPE-1 prostate cells treated with CTRP3, and flow cytometry showed significantly decreased apoptotic cells upon CTRP3 treatment (treated cells, 8.34±1.175 vs. controls, 20.163±0.35) (P < 0.01). Moreover, flow cytometry analysis also showed a significant decrease of cells in the G1 phase and an increase of cells in the S and G2 phase upon CTRP3 treatment (treated cells, 42.85±1.40 vs. control, 52.77±0.90; 28.41±0.57 vs. 23.49±1.13; 27.08±1.97 vs. 22.20±1.32, respectively) (all P < 0.05). Two-dimensional gel electrophoresis and mass spectrometry identified differentially expressed proteins, including cytokeratin-19, GLRX3 and DDAH1, which were upregulated in CTRP3 treated cells, and cytokeratin-17 and 14-3-3 sigma, which were downregulated. GLRX3, DDAH1 and 14-3-3 sigma were confirmed using western blot analysis. A PKC inhibitor, staurosporine, was used to inhibit PKC activity in CTRP3 treated RWPE-1 cells. Staurosporine completely abolished the CTRP3-induced increased phosphorylation of intracellular PKC substrates and CTRP3-stimulated effect by RWPE-1 cells. Our results provide the first evidence for a physiological role of the novel adipokine, CTRP3, in prostate cells. Our findings suggest that CTRP3 could improve proliferation and anti-apoptosis of prostate cells through protein kinase C signaling pathways. © 2015 Hou et al.


Huang Z.,Longgang District Central Hospital | Gao C.,Linyi Peoples Hospital | Ji B.,Linyi Peoples Hospital | Chi X.,Guangdong Medical College | Wang H.L.,Longgang District Central Hospital
Molecular Medicine Reports | Year: 2016

Hepatocellular carcinoma (HCC) is one of the most lifethreatening diseases in the world. Members of the GTPase of the immunityassociated protein (GIMAP) family are important in regulating apoptosis in cancer cells. However, the basic mechanism of GIMAP in HCC remains to be fully elucidated. The present study was performed to investigate the dysregulation of GIMAP family members in HCC. The techniques of polymerase chain reaction analysis, immunohistochemistry and ELISA were used to analyze the expression of GIMAP5 and GIMAP6 in HCC tissues, in matched noncancerous tissue samples, and in blood samples obtained from patients with HCC and healthy subjects. It was found that the mRNA expression levels of GIMAP5 and GIMAP6 were significantly downregulated in the HCC tumor samples, compared with the levels of expression in the matched nontumor tissue samples. Similarly, the mRNA expression levels of GIMAP5 and GIMAP6 were also significantly downregulated in the blood samples from patients with HCC, compared with the expression levels in the blood from healthy subjects. At the protein level, it was found that the GIMAP5 and GIMAP6 proteins were expressed at lower levels in the tumor tissue samples, compared with the matched normal tissue samples, and their expression levels were also lower in the blood samples from patients with HCC, compared with the blood samples from the healthy subjects. These data, demonstrating the downregulation of the mRNA and protein expression levels of GIMAP5 and GIMAP6 in the tumor tissues and blood of patients with HCC, suggested the involvement of GIMAP5 and GIMAP6 in the pathogenesis of HCC, and indicate their possible use as diagnostic markers for HCC.


PubMed | Southern Medical University, Longgang District Central Hospital, Peking University and Sun Yat Sen University
Type: Journal Article | Journal: PloS one | Year: 2015

C1q/TNF-related protein-3 (CTRP3) is a novel adipokine with roles in multiple cellular processes. However, little is known about its function in prostate cells. This study investigated the effects and mechanisms of CTRP3 in prostate cells. We first generated and purified CTRP3 protein in HEK 293T cells. Proliferation of RWPE-1 prostate cells was evaluated by MTT analyses under treatment with different concentrations of CTRP3 for various exposure times. The results revealed maximum enhancement of proliferation with 10 g/mL CTRP3 for 72 h. Cell apoptosis and cell cycle were determined by TUNEL staining and flow cytometry analysis. TUNEL assay showed decreased TUNEL-positive cells in RWPE-1 prostate cells treated with CTRP3, and flow cytometry showed significantly decreased apoptotic cells upon CTRP3 treatment (treated cells, 8.341.175 vs. controls, 20.1630.35) (P < 0.01). Moreover, flow cytometry analysis also showed a significant decrease of cells in the G1 phase and an increase of cells in the S and G2 phase upon CTRP3 treatment (treated cells, 42.851.40 vs. control, 52.770.90; 28.410.57 vs. 23.491.13; 27.081.97 vs. 22.201.32, respectively) (all P < 0.05). Two-dimensional gel electrophoresis and mass spectrometry identified differentially expressed proteins, including cytokeratin-19, GLRX3 and DDAH1, which were upregulated in CTRP3 treated cells, and cytokeratin-17 and 14-3-3 sigma, which were downregulated. GLRX3, DDAH1 and 14-3-3 sigma were confirmed using western blot analysis. A PKC inhibitor, staurosporine, was used to inhibit PKC activity in CTRP3 treated RWPE-1 cells. Staurosporine completely abolished the CTRP3-induced increased phosphorylation of intracellular PKC substrates and CTRP3-stimulated effect by RWPE-1 cells. Our results provide the first evidence for a physiological role of the novel adipokine, CTRP3, in prostate cells. Our findings suggest that CTRP3 could improve proliferation and anti-apoptosis of prostate cells through protein kinase C signaling pathways.


Ye B.,Guangdong Medical College | Ye B.,Longgang District Central Hospital | Lin Z.-Y.,Longgang District Central Hospital | Xie L.-L.,Longgang District Central Hospital | And 2 more authors.
Chinese Journal of Tissue Engineering Research | Year: 2014

Background: Currently a large number of animal experiments and clinical studies have confirmed that, both immediate implants and delayed implants achieve successful osseointegration, but whether immediate implants can reduce or prevent physiological bone resorption of extracted teeth crypt alveolar crest has been the focus of debates among scholars. Objective: To evaluate the recent changes of immediate implant bone in anterior maxilla by the use of cone-beam CT. Methods: Eighteen patients with 18 maxillary anterior teeth that can not be reserved were treated with immediate implantation, and were included in the study. On the surgery day, postoperative 6 months and 1 year, the patients were detected with cone-beam CT. The bone wall thickness at the lingual side of alveolar crest at 4 mm, 6 mm, 8 mm away from the implant shoulder was measured. The bone height at the lingual-buccal side of missing teeth alveolar crest was also recorded. Results And Conclusion: At 6 months after surgery, the bone height at the lingual-buccal side of missing teeth alveolar crest was (1.83±0.05) mm and (1.50±0.04) mm, the bone resorption at the lingual side of alveolar crest at 4 mm, 6 mm, 8 mm away from the implant shoulder was (1.72±0.30) mm, (1.65±0.26) mm, (1.55±0.25) mm, respectively. At 1 year, the bone height at the lingual-buccal side of missing teeth alveolar crest was (0.85± 0.04) mm and (0.78±0.05) mm, the bone resorption at the lingual side of alveolar crest at 4 mm, 6 mm, 8 mm away from the implant shoulder was (0.52±0.20) mm, (0.45±0.16) mm, (0.32±0.15) mm, respectively. Immediate implant may induce horizontal resorption at the lingual side bone wall, but has no impact on the osseointegration of the implant, and the bone resorption is stable 1 year later.


Xu Z.,Hebei University | Li Y.,Hebei University | Zhao X.,Hebei University | Liu Z.-Q.,Longgang District Central Hospital
British Journal of Hospital Medicine | Year: 2014

Allergic diseases and cardiovascular diseases are increasing in prevalence. There is an association between allergic diseases and cardiovascular diseases, as they share similar inflammatory processes. This article focuses on current understanding of the detrimental influences of allergic diseases on cardiovascular diseases.


Gao Y.,Longgang District Central Hospital | Wu X.,Longgang District Peoples Hospital | Zhou L.,Longgang District Central Hospital | Jiang A.,Longgang District Central Hospital | And 3 more authors.
Applied Mechanics and Materials | Year: 2012

Objective: The aim of the study was to explore most effective way to control infection during implant treatment. Methods: The study was carried out in two implant operating surgeries (Surgery A, Surgery B), which were set up air disinfectant machine and ultraviolet disinfection respectively. For baseline measurements, the number of bacterials in the air of the two surgeries was counted at 5min, 15min, 30min, 45min and 60min before sanitizing. To compare sanitizing effect of static air disinfection, air samples from these surgeries were collected for bacterial cultivation after sanitizing for 5min, 15min, 30min, 45min and 60min, and the the sterilization rate was calculated. To compare dynamic air disinfection, the two surgeries were sterilized before implant surgery, and the air samples were collected at 5min, 15min, 30min, 45min, 60min after implant operation. Results: There were no significant differences between air disinfectant machine and ultraviolet disinfection in static air disinfection (p<0.05). However, air disinfectant machine was more effective in dynamic air disinfection. Conclusion: Air disinfectant machine is the most effective way for the prevention of nosocomial infections.


PubMed | Nanjing Medical University, China Pharmaceutical University, Longgang District Central Hospital, Nanjing University and Soochow University of China
Type: | Journal: Oncotarget | Year: 2016

Although recent evidence shows that long noncoding RNAs (lncRNAs) are involved in the regulation of gene expression and cancer progression, the understanding of the role of lncRNAs in lung cancer metastasis is still limited. To identify novel lncRNAs in non-small cell lung cancer (NSCLC), we profile NSCLC tumor and matched normal samples using GeneChip Human Gene 2.0 ST Array, which provides the most accurate, sensitive, and comprehensive measurement of protein coding and lncRNA transcripts. We identified a panel of key factors dysregulated in lung cancer. Among them, the expression of FOXF1-AS1 was significantly downregulated in lung cancer. Stable overexpression of FOXF1-AS1 inhibits lung cancer cell migration and invasion by regulating EMT. Meanwhile, loss of FOXF1-AS1 mediates stem-like properties of lung cancer cells. Interestingly, we found that FOXF1-AS1 physically associates with PRC2 components EZH2 and loss of FOXF1-AS1 mediates cell migration and stem-like properties require EZH2. Loss of FOXF1-AS1 is also correlated with downregulation of FOXF1 in lung cancer. These results suggested that FOXF1-AS1 might regulate EMT, stemness and metastasis of NSCLC cells via EZH2, indicating it as a therapeutic target for future treatment of NSCLC.


Li K.,Southern Medical University | Xu R.,Longgang District Central Hospital | Zhang H.,Longgang District Central Hospital | Wang Q.,Southern Medical University
Yi chuan = Hereditas / Zhongguo yi chuan xue hui bian ji | Year: 2014

In order to evaluate the missing heritability of bipolar disorder, we queried the GWAS catalog of National Human Genome Research Institute, retrieve all the susceptible gene variation of bipolar disorder, and calculate the heritability explanation degree of each susceptibility variant using the multifactorial liability threshold model. The total heritability explanation degree of bipolar disorder was obtained through summing up the heritability explanation degree of each susceptibility variant. Then, we evaluated the missing heritability of bipolar disorder based on the total heritability explanation degree. The results showed that the total heritability explanation degree of bipolar disorder explained by known susceptible variants was 38.34%, and the other 61.66% of heritability can't be explained by known susceptibility variants, which belong to the missing heritability of bipolar disorder. The total heritability explanation degree of bipolar disorder in this study was significantly increased compared to earlier similar studies abroad. With constant discovery of new bipolar disorder susceptibility variants, the missing heritability of bipolar disorder has been greatly reduced, but the missing heritability of bipolar disorder still exists and occupies a large part of the bipolar disorder heritability, indicating that the molecular genetic mechanisms of bipolar disorder need to be further clarified.


PubMed | Longgang District Central Hospital and Southern Medical University
Type: Journal Article | Journal: Yi chuan = Hereditas | Year: 2014

In order to evaluate the missing heritability of bipolar disorder, we queried the GWAS catalog of National Human Genome Research Institute, retrieve all the susceptible gene variation of bipolar disorder, and calculate the heritability explanation degree of each susceptibility variant using the multifactorial liability threshold model. The total heritability explanation degree of bipolar disorder was obtained through summing up the heritability explanation degree of each susceptibility variant. Then, we evaluated the missing heritability of bipolar disorder based on the total heritability explanation degree. The results showed that the total heritability explanation degree of bipolar disorder explained by known susceptible variants was 38.34%, and the other 61.66% of heritability cant be explained by known susceptibility variants, which belong to the missing heritability of bipolar disorder. The total heritability explanation degree of bipolar disorder in this study was significantly increased compared to earlier similar studies abroad. With constant discovery of new bipolar disorder susceptibility variants, the missing heritability of bipolar disorder has been greatly reduced, but the missing heritability of bipolar disorder still exists and occupies a large part of the bipolar disorder heritability, indicating that the molecular genetic mechanisms of bipolar disorder need to be further clarified.


PubMed | Linyi Peoples Hospital, Longgang District Central Hospital and Guangdong Medical College
Type: Journal Article | Journal: Molecular medicine reports | Year: 2016

Hepatocellular carcinoma (HCC) is one of the most lifethreatening diseases in the world. Members of the GTPase of the immunityassociated protein (GIMAP) family are important in regulating apoptosis in cancer cells. However, the basic mechanism of GIMAP in HCC remains to be fully elucidated. The present study was performed to investigate the dysregulation of GIMAP family members in HCC. The techniques of polymerase chain reaction analysis, immunohistochemistry and ELISA were used to analyze the expression of GIMAP5 and GIMAP6 in HCC tissues, in matched noncancerous tissue samples, and in blood samples obtained from patients with HCC and healthy subjects. It was found that the mRNA expression levels of GIMAP5 and GIMAP6 were significantly downregulated in the HCC tumor samples, compared with the levels of expression in the matched nontumor tissue samples. Similarly, the mRNA expression levels of GIMAP5 and GIMAP6 were also significantly downregulated in the blood samples from patients with HCC, compared with the expression levels in the blood from healthy subjects. At the protein level, it was found that the GIMAP5 and GIMAP6 proteins were expressed at lower levels in the tumor tissue samples, compared with the matched normal tissue samples, and their expression levels were also lower in the blood samples from patients with HCC, compared with the blood samples from the healthy subjects. These data, demonstrating the downregulation of the mRNA and protein expression levels of GIMAP5 and GIMAP6 in the tumor tissues and blood of patients with HCC, suggested the involvement of GIMAP5 and GIMAP6 in the pathogenesis of HCC, and indicate their possible use as diagnostic markers for HCC.

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