Long Noncoding RNA Expression Signatures of Abdominal Aortic Aneurysm Revealed by Microarray / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>This study is aimed at observing the role of long noncoding RNAs (lncRNAs) in the pathogenesis of abdominal aortic aneurysm (AAA).</p><p><b>METHODS</b>LncRNA and mRNA expression signatures of AAA tissues and normal abdominal aortic tissues (NT) were analyzed by microarray and further verified by Real-time quantitative reverse-transcription PCR (qRT-PCR). The lncRNAs-mRNAs targeting relationships were identified using computational analysis. The effect of lnc-ARG on 5-lipoxygenase (ALOX5) expression was tested in HeLa cells.</p><p><b>RESULTS</b>Differential expressions of 3,688 lncRNAs and 3,007 mRNAs were identified between AAA and NT tissues. Moreover, 1,284 differentially expressed long intergenic noncoding RNAs and 206 differentially expressed enhancer-like lncRNAs adjacent to protein-coding genes were discerned by bioinformatics analysis. Some differentially expressed lncRNAs and mRNAs between AAA and normal tissue samples were further verified using qRT-PCR. A co-expression network of coding and noncoding genes was constructed based on the correlation analysis between the differentially expressed lncRNAs and mRNAs. In addition, the lnc-ARG located within the upstream of ALOX5 was sorted as a noncoding transcript by analyzing the protein-coding potential using computational analysis. Furthermore, we found that lnc-ARG can decrease the mRNA level of ALOX5 and reactive oxygen species production in HeLa cells.</p><p><b>CONCLUSION</b>This study revealed new lncRNA candidates are related to the pathogenesis of AAA.</p>

Comparison of open and endovascular repair for abdominal aortic aneurysm mid-term outcomes: a single center randomized controlled trial / 中华外科杂志

<p><b>OBJECTIVE</b>To compare the effects of open and endovascular repair for abdominal aortic aneurysm.</p><p><b>METHODS</b>Between January 2009 and January 2011, 84 patients were randomized to endovascular aneurysm repair (EVAR) or open repair. There were 48 patients in EVAR group, 42 cases were male (87.5%), 6 cases were female (12.5%), aged from 50 to 83 years with a mean of 70.8 years. There were 36 patients in open repair group, 31 cases were male (86.1%), 5 cases were female (13.9%), aged from 50 to 80 years with a meal of 67.4 years. The results of perioperative period and follow-up were analyzed.</p><p><b>RESULTS</b>Between the two groups, there was significant difference on operative time (t = 9.863, P = 0.000), blood loss (t = 4.647, P = 0.000), blood transfusion (t = 3.334, P = 0.002), hospital stay (t = 2.327, P = 0.022), and medical expense (t = 2.314, P = 0.023). There was no significant difference for perioperative complications (χ(2) = 0.480, P = 0.488). There was no significant difference for complications (χ(2) = 0.664, P = 0.415) and mortality (P = 0.429) during 3 months follow-up. There was no significant difference for complications during 6 months follow-up (χ(2) = 0.128, P = 0.720).</p><p><b>CONCLUSIONS</b>Operative time, blood loss and transfusion, hospital stay in EVAR group are less than which in open repair group, the medical expense of EVAR was higher than open repair. There is no significant difference for complications during 6 months follow-up between 2 groups. Long-term follow-up and more patents are needed to analyze survival rate and long-term complications.</p>

Myoglobin over-expression attenuates angiogenic response in hindlimb ischemia in mice / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Myoglobin is expressed exclusively in striated skeletal muscles and has been implicated in nitric oxide scavenging. Accumulating data suggest a critical role for nitric oxide in both the endogenous and therapeutic angiogenic response to ischemia. A clear role for myoglobin in ischemic skeletal muscle is uncertain. We hypothesized that myoglobin overexpression has an adverse impact on the angiogenic response to ischemia.</p><p><b>METHODS</b>Muscle-specific myoglobin over-expressing transgenic mice (MbTG, n = 11), wild type littermates (WT, n = 23) underwent unilateral femoral artery ligation and excision. Laser doppler perfusion imaging was used to monitor changes in hindlimb perfusion before surgery and weekly after surgery up to 28 days. Tissue ischemia was assessed by a necrosis incidence. Upon termination of the experiment (28 days after surgery), skeletal muscles (gastrocnemius, and tibialis anterior) were harvested, the distal part of the muscle was frozen and embedded for histology study, the proximal part was used either to detect vascular endothelial growth factor (VEGF) level with enzyme-linked immunosorbent assays (ELISA) or to determine the proliferation (proliferating cell nuclear antigen (PCNA)) and apoptosis (Bax, and Bcl-2) condition in ischemic muscle by Western blotting. Capillaries were stained with endothelial phosphate alkaline staining and vascular density was expressed in capillaries/fiber.</p><p><b>RESULTS</b>The recovery of perfusion in MbTG mice was similar to that of WT mice on day 7 (0.485 +/- 0.095 vs 0.500 +/- 0.084) but was significantly less on day 14 (0.536 +/- 0.086 vs 0.623 +/- 0.077, P < 0.05), day 21 (0.588 +/- 0.082 vs 0.684 +/- 0.068, P < 0.01) and day 28 (0.606 +/- 0.079 vs 0.733 +/- 0.093, P < 0.01). The necrosis incidence was higher in MbTG than in WT (54.5% vs 21.6%). Vascular density was less in MbTG compared with that in WT (gastrocnemius 0.19 +/- 0.08 vs 0.30 +/- 0.08, P < 0.05; tibialis anterior 0.22 +/- 0.11 vs 0.33 +/- 0.04, P < 0.05). With ischemic injury, the VEGF level was increased in both MbTG and WT (45.2% and 20.4%, respectively). Western blotting showed that after hindlimb ischemia the proliferation was similar in both MbTG and WT, however, apoptosis was increased in MbTG relative to WT, shown as more expression of Bax and less expression of Bcl-2.</p><p><b>CONCLUSION</b>An increase in expression of myoglobin protein in skeletal muscle reduces the endogenous perfusion recovery following surgically induced hind-limb ischemia.</p>

Reinstate the damaged VEGF signaling pathway with VEGF-activating transcription factor / 中国医学科学杂志(英文版)

<p><b>OBJECTIVE</b>To investigate the role of vascular endothelial growth factor-activating transcriptional factor (VEGF-ATF) on the VEGF signaling pathway in diabetes mellitus.</p><p><b>METHODS</b>Totally, 20 C57BL/6 mice fed with high fat diet was induced into diabetes mellitus. Ten diabetes mellitus mice received a lower limb muscle injection with VEGF-ATF plasmid, and another ten were as control. VEGF-ATF is an engineered transcription factor designed to increase VEGF expression. Three days later, mice were sacrificed and the injected gastrocnemius was used for analysis. VEGF mRNA and protein expressions were examined by real-time PCR and ELISA respectively. VEGF receptor 2 mRNA expression was tested with RT-PCR. Phosphorylated Akt, Akt, endothelial nitric oxide synthase (eNOS), and phosphorylated eNOS were assessed by western blot.</p><p><b>RESULTS</b>At 3 days post-injection, in mice with diabetes mellitus, VEGF gene transfer increased VEGF mRNA copies and VEGF protein expression in injected muscles compared with control; and reinstated the impaired VEGF signaling pathway with increasing the ratios of phosphorylated Akt/Akt and phosphorylated eNOS/eNOS. However, it did not affect the expression of VEGF receptor 2 mRNA.</p><p><b>CONCLUSION</b>Gene transfer with VEGF-ATF is able to reinstate the impaired VEGF downstream pathway, and potentially promote therapeutic angiogenesis in mice with diabetes mellitus.</p>