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Resveratrol reduces brain injury after subarachnoid hemorrhage by inhibiting oxidative stress and endoplasmic reticulum stress
Xie, YK;Zhou, X;Yuan, HT;Qiu, J;Xin, DQ;Chu, XL;Wang, DC;Wang, Z
NEURAL REGENERATION RESEARCH 2019年 14卷10期 页码:1734-1742
NEURONAL APOPTOSIS; RAT-BRAIN; PROTECTS; ANTIOXIDANT; PATHWAY; CELLS; MODEL; NEUROPROTECTION; DYSFUNCTION; ACTIVATOR
Previous studies have shown that resveratrol, a bioactive substance found in many plants, can reduce early brain injury after subarachnoid hemorrhage, but how it acts is still unclear. This study explored the mechanism using the experimental subarachnoid hemorrhage rat model established by injecting autologous blood into the cerebellomedullary cistern. Rat models were treated with an intraperitoneal injection of 60 mg/kg resveratrol 2, 6, 24 and 46 hours after injury. At 48 hours after injury, their neurological function was assessed using a modified Garcia score. Brain edema was measured by the wet-dry method. Neuronal apoptosis in the prefrontal cortex was detected by terminal deoxyribonucleotidyl transferase-mediated biotin-16-dUTP nick-end labeling assay. Levels of reactive oxygen species and malondialdehyde in the prefrontal cortex were determined by colorimetry. CHOP, glucose-regulated protein 78, nuclear factor-erythroid 2-related factor 2 and heme oxygenase-1 mRNA expression levels in the prefrontal cortex were measured by reverse transcription polymerase chain reaction. Tumor necrosis factor-alpha content in the prefrontal cortex was detected by enzyme linked immunosorbent assay. Immunohistochemical staining was used to detect the number of positive cells of nuclear factor-erythroid 2-related factor 2, heme oxygenase 1, glucose-regulated protein 78, CHOP and glial fibrillary acidic protein. Western blot assay was utilized to analyze the expression levels of nuclear factor-erythroid 2-related factor 2, heme oxygenase 1, glucose-regulated protein 78 and CHOP protein expression levels in the prefrontal cortex. The results showed that resveratrol treatment markedly alleviated neurological deficits and brain edema in experimental subarachnoid hemorrhage rats, and reduced neuronal apoptosis in the prefrontal cortex. Resveratrol reduced the levels of reactive oxygen species and malondialdehyde, and increased the expression of nuclear factor-erythroid 2-related factor 2, heme oxygenase-1 mRNA and protein in the prefrontal cortex. Resveratrol decreased glucose-regulated protein 78, CHOP mRNA and protein expression and tumor necrosis factor-alpha level. It also activated astrocytes. The results suggest that resveratrol exerted neuroprotective effect on subarachnoid hemorrhage by reducing oxidative damage, endoplasmic reticulum stress and neuroinflammation.
The impact of unicornuate uterus on perinatal outcomes after IVF/ICSI cycles: a matched retrospective cohort study
Chen, XX;Liu, PH;Sheng, Y;Li, WP;Tang, R;Ding, LL;Qin, YY;Chen, ZJ
JOURNAL OF MATERNAL-FETAL & NEONATAL MEDICINE 2019年 32卷15期 页码:2469-2474
CONGENITAL UTERINE ANOMALIES; REPRODUCTIVE OUTCOMES; CLINICAL-IMPLICATIONS; PREGNANCY OUTCOMES; TWIN PREGNANCY; MULLERIAN ANOMALIES; WOMEN; PREVALENCE
Objective: To evaluate the impact of unicornuate uterus on perinatal outcomes after in vitro fertilization and/or intracytoplasmic sperm injection (IVF/ICSI) cycles. Methods: We performed a retrospective cohort study including 160 women with unicornuate uterus and 1:1 matched controls with normally shaped uterus. They received IVF/ICSI treatment during January 2009 and December 2011. The perinatal outcomes were followed up till December 2014. Results: There were no significant differences in pregnancy rate, clinical pregnancy rate or live birth rate (53.6 versus 52.7, 41.4 versus 43.5, 33.8% versus 31.8%) between unicornuate uterus group and controls. Their biochemical pregnancy rate (22.8 versus 17.5%) and miscarriage rate (16.0 versus 18.8%) were similar. No significant differences were identified in preterm birth rate (18.3 versus 11.8%), birthweight (3.24 +/- 0.60 versus 3.33 +/- 0.54 kg) or birth length (50.47 +/- 2.33 versus 50.06 +/- 2.40 cm) among the singletons. However, lower gestational age (35.56 +/- 2.68 versus 36.71 +/- 1.73, p = .019), higher preterm birth rate (55.0 versus 34.4%, p = .038), lower birthweight (2.33 +/- 0.58 versus 2.69 +/- 0.38 kg, p = .001), lower birth length (45.33 +/- 2.46 versus 48.88 +/- 2.06 cm, p = .000), as well as higher rate of very low birthweight (13.2% versus 0, p = .007) were found for the twins from unicornuate uterus group. Conclusions: The results indicated unimpaired pregnancy and perinatal outcomes for women with unicornuate uterus conceiving one fetus. However, close attention should be paid to twin pregnancy in unicornuate uterus owing to increased risks of prematurity and low birthweight. Selected single embryo transfer is recommended for women with unicornuate uterus undergoing IVF/ICSI cycles.
Delivery during extracorporeal membrane oxygenation (ECMO) support of pregnant woman with severe respiratory distress syndrome caused by influenza: a case report and review of the literature
Liu, CL;Sun, WQ;Wang, CT;Liu, FL;Zhou, MX
JOURNAL OF MATERNAL-FETAL & NEONATAL MEDICINE 2019年 32卷15期 页码:2570-2574
H1N1 INFLUENZA; CESAREAN-SECTION; INFECTION; DEATH
Objective: To report a case of labour induction during extracorporeal membrane oxygenation (ECMO) support in a patient with acute respiratory distress syndrome (ARDS) caused by influenza and review of the literature. Methods: Case report and the literature search of all English articles on delivery while on ECMO in patients with ARDS caused by influenza. Results: A 25-year-old pregnant woman was initiated with ECMO due to severe ARDS caused by influenza A (H1N1) virus. When the patient had symptoms of colporrhagia and uterine contractions, the medical team decided to start labour induction while on ECMO. There were in total five case reports identified. Maternal oxygenation was improved after delivery and ECMO was successfully discontinued. Conclusions: Maternal oxygenation was improved after delivery, which may be beneficial to reduce the duration of ECMO. Caesarean section (CS) may be the most used mode and labour induction could be another option. The procedure should be performed by an experienced ECMO team, cooperating with the obstetrician, anaesthesiologist, and ICU doctors.
27-Hydroxycholesterol enhanced osteoclastogenesis in lung adenocarcinoma microenvironment
Zhang, LS;Liu, M;Liu, JL;Li, XK;Yang, M;Su, BH;Lin, YL
JOURNAL OF CELLULAR PHYSIOLOGY 2019年 234卷8期 页码:12692-12700
NECROSIS-FACTOR-ALPHA; BONE METASTASIS; KAPPA-B; CANCER; CELLS; EXPRESSION; TRANSCRIPTION; OSTEOBLASTS; CONTRIBUTES; SUPPRESSION
27-Hydroxycholesterol (27-HC) has been implicated in the pathological process of estrogen receptor positive breast cancer. However, the role of 27-HC in lung adenocarcinoma is still unclear. Because bone metastasis is a main reason for the high mortality of lung adenocarcinoma, this study aimed to investigate the effect of 27-HC on osteoclastogenesis in lung adenocarcinoma microenvironment. The results showed that the conditioned media (CM) from lung adenocarcinoma cells cocultured with macrophages promoted osteoclast differentiation, which was enhanced by 27-HC. Further investigation showed that CM inhibited miR-139 expression and promoted c-Fos expression. Luciferase reporter assay identified c-Fos as a direct target of miR-139. CM also induced the expression and nuclear translocation of NFATc1 and STAT3 phosphorylation, which was enlarged by 27-HC but was attenuated by miR-139. Coimmunoprecipitation assay demonstrated that 27-HC increased the interaction between NFATc1 and phosphorylated STAT3, which was restricted by miR-139. Chromatin immunoprecipitation assay showed that pSTAT3 could bind to the promoter of c-Fos, c-Fos could bind to the promoter of NFATc1, and both pSTAT3 and NFATc1 could bind to the promoter of Oscar, which were enlarged by 27-HC but were blocked by miR-139. Knockdown of c-Fos mimicked the effect of miR-139. These results suggested that CM, especially containing 27-HC, promoted osteoclastogenesis by inhibiting miR-139 expression and activating the STAT3/c-Fos/NFATc1 pathway.
LINC00520 targeting miR-27b-3p regulates OSMR expression level to promote acute kidney injury development through the PI3K/AKT signaling pathway
Tian, XH;Ji, YQ;Liang, YF;Zhang, J;Guan, LN;Wang, CT
JOURNAL OF CELLULAR PHYSIOLOGY 2019年 234卷8期 页码:14221-14233
ONCOSTATIN M RECEPTOR; EPIDEMIOLOGY; MORTALITY; PROTECTS; MICRORNA; CELLS; RISK; AKI
BackgroundAcute kidney injury (AKI) shows several kinds of disorders, which acutely harm the kidney. However, the current medical methods have limited therapeutic effects. The present study aimed to find out the molecular mechanism of AKI pathogenesis, which may provide new insights for future therapy.;-;MethodsBioinformatic analysis was conducted using the R language (AT&T BellLaboratories, University of Auckland, New Zealand) to acquire the differentially expressed long noncoding RNAs (lncRNAs) and messenger RNAs (mRNAs) in AKI. The expression levels of RNAs and related proteins in tissues and cells were detected by quantitative real-time PCR (qRT-PCR) and western blot. Dual-luciferase reporter gene assays were performed to verify the target relationship between microRNA (miRNA) and lncRNA as well as miRNA and mRNA. Flow cytometry and tunnel assay were used to detect the cell apoptotic rate in AKI.;-;ResultsLINC00520, miR-27b-3p, and OSMR form an axis to regulate AKI. Knockdown of LINC00520 reduced acute renal injury both in vitro and in vivo. LINC00520 activated the PI3K/AKT pathway to aggravate renal ischemia/reperfusion injury, while upregulation of miR-27b-3p or downregulation of OSMR could accelerate the recovery of AKI.;-;ConclusionOverexpression of LINC00520 contributes to the aggravation of AKI by targeting miR-27b-3p/OSMR.
Assessment of disease activity in Takayasu arteritis: A quantitative study with computed tomography angiography
Chen, BJ;Wang, XM;Yin, WH;Gao, Y;Hou, ZH;An, YQ;Li, ZN;Ren, XS;Zhao, S;Das, P;Lu, B
INTERNATIONAL JOURNAL OF CARDIOLOGY 2019年 289卷 页码:144-149
IMAGING SPECTRUM; MURAL CHANGES; CT; DIAGNOSIS; AORTA
Background: Identifying disease activity in Takayasu arteritis (TAK) is challenging. This study aimed to investigate the value of quantitative characterization with computed tomography angiography in the assessment of disease activity in patients with TAK.;-;Methods: We retrospectively analysed the data on 162 aortic CT angiography from 140 TAK patients. Patients were categorized based on disease activity according to the National Institutes of Health criteria into two groups: active disease group (n = 65) and inactive disease group (n = 97).;-;Results: Patients with active TAK had a thickerwall compared with patients with inactive TAK (5.2 +/- 2.4 mm vs. 2.5 +/- 0.8 mm, p < 0.001). The relative post-contrast enhancement ratio of the thickened wall was higher in active TAK than in inactive TAK (1.5 +/- 0.3 vs. 1.1 +/- 0.2, p < 0.001). Given a thickness cutoff of 3.3 mm, sensitivity for active-phase TAK was 83.1%, specificity 89.7%, positive predictive value 84.4%, and negative predictive value 88.8%. With a relative post-contrast enhancement ratio cutoff of 1.2, sensitivity for active-phase TAK was 89.2%, specificity 76.3%, positive predictive value 71.6%, and negative predictive value 91.3%. In receiver-operating characteristic curves comparison, maximal wall thickness and relative post-contrast enhancement ratio were superior to C-reactive protein and erythrocyte sedimentation rate for determining active phase disease (p < 0.05).;-;Conclusions: Quantitative characterization with CT angiography was a useful tool to assess disease activity in TAK patients. Maximal wall thickness and relative post-contrast enhancement ratio have a high sensitivity and specificity for detecting TAK activity. (c) 2019 Elsevier B.V. All rights reserved.
Knockdown of long noncoding RNA-taurine-upregulated gene 1 inhibits tumor angiogenesis in ovarian cancer by regulating leucine-rich alpha-2-glycoprotein-1
Fan, MJ;Li, CY;He, PJ;Fu, YB;Li, MJ;Zhao, XB
ANTI-CANCER DRUGS 2019年 30卷6期 页码:562-570
LRG1 PROMOTES ANGIOGENESIS; PROLIFERATION; CARCINOMA; BEVACIZUMAB; MIGRATION; SURVIVAL; INVASION; PROGRESS; SURGERY
To investigate the role of long noncoding RNA taurineupregulated gene 1 (TUG1) on ovarian cancer-induced angiogenesis and to explore possible signaling pathways. Ovarian cancer cell line SKOV3 or CAOV3 was transfected with short hairpin-TUG1 to suppress TUG1 expression. Supernatant from cultured cancer cells was used as a condition medium to incubate endothelial cell line human umbilical vein endothelial cells, whose proliferation rate was quantified by 3-(4,5-dimethylthiazol-2-yl)2,5- diphenyltetrazolium bromide assay. Migration and invasion of endothelial cells were examined by wound healing and Transwell assays, followed by in-vitro angiogenesis assay. One of the secretory factors mediating angiogenesis, leucine-rich a-2-glycoprotein-1 (LRG1), was measured in ovarian cancer cells. Signaling pathway mediating angiogenesis was further detected by western blotting. TUG1 was down-regulated in ovarian cancer cells by short hairpin RNA. Conditional medium originating from TUG1-knockdown cancer cells led to suppressed proliferation, migration, or invasion of endothelial cell line human umbilical vein endothelial cells. LRG1 expression and secretion was suppressed in ovarian cancer cells after TUG1 knockdown. Moreover, recombinant LRG1 rescued TUG1 knockdown-induced angiogenesis inhibition, and LRG1 probably mediated angiogenesis by tumor growth factor-ss signaling pathway in endothelial cells. Long noncoding RNA-TUG1 mediates angiogenesis of endothelial cells by regulating LRG1 secretion from ovarian cancer cells partially through tumor growth factor-ss pathway. Our results indicate the potency of TUG1 as a biomarker and therapeutic target for tumor-induced angiogenesis.
KMT2D inhibits the growth and metastasis of bladder Cancer cells by maintaining the tumor suppressor genes
Sun, P;Wu, T;Sun, XL;Cui, ZL;Zhang, HY;Xia, QH;Zhang, D
BIOMEDICINE & PHARMACOTHERAPY 2019年 115卷
MUTATIONAL LANDSCAPE; HISTONE MODIFICATION; SOMATIC MUTATIONS; H3K4 METHYLATION; FGFR3; PROGRESSION; LYMPHOMA; PROMOTES; PIK3CA; PROLIFERATION
KMT2D, a kind of histone H3 lysine 4 (H3K4) methyltransferase, its abnormal expression confirmed to be associated with diverse tumors, but is lack of defined role in bladder cancer (BC). KMT2D mutation was analyzed using several databases. Immunohistochemistry and clinicopathological analysis of KMT2D in 51 paired of BC tissues and corresponding normal tissues were used to evaluate the relationship between KMT2D and BC. The effects of silencing or over-expressing KMT2D on HTB-9 and T24 cell viability, migration and invasion were performed using MTT, wound scratch and Transwell, respectively. Also, bladder cancer mouse model was established by hypodermic injection of the BC cells. Associated expressions of methylation genes, oncogenes and tumor suppressors were assessed by western blot and quantitative real-time PCR. KMT2D was frequent mutation in various tumors, including BC. It was negative expression in BC tissues and cells, also implicated with tumor stages and lymph node metastasis. In silencing KMT2D HTB-9 and T24 cells, cell viability, migration and invasion were notably promoted. Meanwhile, knockdown of KMT2D benefited to solid tumor formation in vivo. However, over-expressing KMT2D represented contrary results. Especially, KMT2D over-expression induced the activity of H3K4 monomethylation (me1), and effectively enhanced PTEN and p53 expressions as well as repressed STAG2 expression. Meanwhile, KMT2D had no obvious effect on Survivin. This work suggested an anti-tumor role for KMT2D in vitro and in vivo, as well as provided a possible tumor inhibition mechanism in which KMT2D enhanced H3K4me1 activity to support the expressions of tumor suppressors.
Mesenchymal stem cell derived EVs mediate neuroprotection after spinal cord injury in rats via the microRNA-21-5p/FasL gene axis
Zhou, X;Chu, XL;Yuan, HT;Qiu, J;Zhao, CL;Xin, DQ;Li, TT;Ma, WW;Wang, HF;Wang, Z;Wang, DC
BIOMEDICINE & PHARMACOTHERAPY 2019年 115卷
FUNCTIONAL RECOVERY; MESSENGER-RNAS; STROMAL CELLS; FAS LIGAND; APOPTOSIS; EXOSOMES; INFLAMMATION; EXPRESSION; MICRORNAS; TARGETS
Spinal cord injury (SCI) represents a relatively common type of motor system trauma. While the SCI patient will experience varying degrees of paraplegia and quadriplegia, which severely affects their quality of life, a heavy burden is also placed on the family and society as a whole. The exact pathogenic mechanisms underlying this condition remain unknown and no specific treatments are currently available. Findings from recent studies have shown that mesenchymal stem cells (MSCs), derived from extracellular vesicles (EVs) can reduce apoptosis, inflammation and promote angiogenesis after SCI. However, the mechanisms through which EVs exert these effects have yet to be identified, indicating the necessity for further investigation. In the present study, we report that treatment with MSCs-EVs significantly improved functional recovery and attenuated lesion size and apoptosis in a rat model of SCI. These MSCs-EVs were found to be directed to the spinal injury site and mainly incorporated into neurons within the lesioned site of the spinal cord. Tandem Mass Tags quantitative proteomics was applied to compare protein changes after SCI and MSCs-EVs treatment. A total of 883 differential proteins were identified, many of which being associated with apoptosis and inflammation. Subsequently, miRNA contents of MSCs-EVs were determined using qRT-PCR, with the result that miR-21-5p was one of the most highly expressed miRNA in these MSCs-EVs. Moreover, inhibition of miR-21-5p in MSCs-EVs significantly reversed the beneficial effects of MSCs-EVs on motor function and apoptosis, an effect which was associated with modulating FasL expression. The data suggest that modulation of the MSCs-EVs miR-21-5p/FasL gene axis may serve as a promising strategy for clinical treatment of SCI and other neurological diseases.
IQGAP1 mediates podocyte injury in diabetic kidney disease by regulating nephrin endocytosis
Liu, YP;Su, H;Ma, CQ;Ji, D;Zheng, XL;Wang, P;Zheng, SX;Wang, L;Wang, ZS;Xu, DM
CELLULAR SIGNALLING 2019年 59卷 页码:13-23
PROTEINS; TRAFFICKING; BIOLOGY; BINDING; DOMAIN
Diabetic kidney disease (DKD) is a complication associated with diabetes and is a major public health problem in modern society. Podocyte injury is the central target of the development of DKD, and the loss or dysregulation of nephrin, a key structural and signalling molecule located in the podocyte slit diaphragm (SD), initiates potentially catastrophic downstream events within podocytes. IQGAP1, a scaffold protein containing multiple-binding domains that regulates endocytosis, can interact with nephrin in podocytes. It is hypothesized that IQGAP1 contributes to nephrin endocytosis and may participate in the pathogenesis of DKD. The dramatically increased histo-nephrin granularity score in DKD glomeruli showed a significant positive correlation with increased IQGAP1-nephrin interaction without changes in the total protein content of nephrin and IQGAP1. In cultured human podocytes, hyperglycaemia induced the intracellular translocation of IQGAP1 from the cytosol to the vicinity of the cytomembrane, reinforced the IQGAP1-nephrin interaction, and augmented nephrin endocytosis. Moreover, impaired podocyte function, such as migration, extensibility and permeability, were further aggravated by wild-type IQGAP1 plasmid transfection, and these effects were partially restored by siRNA-mediated IQGAP1 downregulation. Collectively, these findings show that IQGAP1, an intracellular partner of nephrin, is involved in nephrin endocytosis and the functional regulation of podocytes in DKD.
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