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Guo R.-W.,Kunming General Hospital of Chengdu Military Area | Yang L.-X.,Kunming General Hospital of Chengdu Military Area | Li M.-Q.,Chengdu Medical College | Pan X.-H.,Kunming General Hospital of Chengdu Military Area | And 2 more authors.
Cardiovascular Research | Year: 2012

Aim Despite the fact that angiotensin (Ang) II is a critical regulator of the proliferation and migration of vascular smooth muscle cells (VSMCs), the effect of Ang II on VSMC proliferation has remained unclear. In this study, we determined whether Stim1-and Orai1-mediated store-operated calcium (Ca 2+) entry (SOCE) plays a critical role in Ang II-induced VSMC proliferation and Ang II-accelerated neointimal growth after balloon injury of rat carotid arteries. Methods and results Knockdown of Stim1 and Orai1, putative calcium sensors/modulators, suppressed Ang II-mediated Ca 2+ entry and cell proliferation in synthetic VSMCs. Stim1 and Orai1 short interfering RNAs (siRNAs) decreased neointimal growth induced by Ang II in balloon-injured rat carotid arteries. Ang II signicantly increased the expression of Stim1 and Orai1 in neointima. In addition, our results showed that receptor subtype-1 (AT1) significantly contributed to Ang II-induced Ca 2+ entry and proliferation of synthetic VSMCs. However, we found that transient receptor potential canonical 1 (Trpc1) had no effect on Ang II-induced SOCE or cell proliferation of synthetic VSMCs. Conclusion sWe show for the first time that Stim1-and Orai1-mediated SOCE may be critical for Ang II-induced VSMC proliferation. This provides important information with respect to targeting cardiovascular diseases under the enhanced reninAng system. © 2011 The Author.


Zhang C.-H.,Kunming General Hospital of Chengdu Military Area | Ma W.-Q.,Kunming General Hospital of Chengdu Military Area | Yang Y.-L.,Kunming General Hospital of Chengdu Military Area | Wang H.-M.,Kunming General Hospital of Chengdu Military Area | And 2 more authors.
BMC Anesthesiology | Year: 2015

Background: To determine the median effective concentration of sufentanil as an analgesic during wake-up tests after sevoflurane anesthesia during surgery for adolescent idiopathic scoliosis (AIS). Methods: This is a randomised controlled trial. Sixty patients aged 13-18 years scheduled for AIS surgery were randomized into six groups of 10 patients each to receive target effect-site concentrations of sufentanil of 0.19, 0.1809, 0.1723, 0.1641, 0.1563, and 0.1489 ng/ml (target concentration ratio, 1.05). Wake-up time was recorded. Median EC50 and 95% confidence interval (CI) for sufentanil target-controlled infusion (TCI) were determined using Kärber's method. The primary outcome was median EC50 for sufentanil TCI as an analgesic during the wake-up test after sevoflurane anesthesia during surgery for AIS. Results: The EC50 and 95% CI of sufentanil TCI were 0.1682 ng/ml and 0.1641 ~ 0.1724 ng/ml, respectively. Conclusions: The EC50 of sufentanil TCI was 0.1682 ng/ml (95% CI: 0.1641 ~ 0.1724 ng/ml) during sevoflurane anesthesia in adolescents undergoing surgery for idiopathic scoliosis with intraoperative wake-up tests. © 2015 Zhang et al.; licensee BioMed Central.


Jiang C.,Kunming General Hospital of Chengdu Military Area | Jiang C.,PLA Fourth Military Medical University | Niu J.,PLA Fourth Military Medical University | Li M.,PLA Fourth Military Medical University | And 3 more authors.
PLoS ONE | Year: 2014

Objective: Increasing evidence suggests that, when used in combination, tumor necrosis factor-α (TNF-α) synergizes with traditional chemotherapeutic drugs to exert a heightened antitumor effect. The present study investigated the antitumor efficacy of recombinant mutated human TNF-α specifically targeted to the tumor vasculature (RGD-rmhTNF-α) combined with the chemotherapeutic agent doxorubicin in 2 murine allografted tumor models. Methods: Mice bearing hepatoma or sarcoma allografted tumors were treated with various doses of RGD-rmhTNF-α alone or in combination with doxorubicin (2 mg/kg). We then evaluated tumor growth and tumor vessel permeability as well as intratumoral levels of RGD-rmhTNF-α and doxorubicin. Results: RGD-rmhTNF-α treatment enhanced the permeability of the tumor vessels and increased intratumoral doxorubicin levels. In addition, intratumoral RGD-rmhTNF-α levels were significantly higher than that of rmhTNF-α. In both of the tested tumor models, administering RGD-rmhTNF-α in combination with doxorubicin resulted in an enhanced antitumor response compared to either treatment alone. Double-agent combination treatment of doxorubicin with 50,000 IU/kg RGD-rmhTNF-α induced stronger antitumor effects on H22 allografted tumor-bearing mice than the single doxorubicin agent alone. Moreover, doxorubicin with 10,000 IU/kg RGD-rmhTNF-α synergized to inhibit tumor growth in S180 allografted tumor-bearing mice. Conclusions: These results suggest that targeted delivery of low doses of RGD-rmhTNF-α into the tumor vasculature increases the antitumor efficacy of chemotherapeutic drugs. © 2014 Jiang et al.


Yang Y.,Chongqing Medical University | Yang L.,Kunming General Hospital of Chengdu Military Area | Liang X.,Kunming General Hospital of Chengdu Military Area | Zhu G.,Kunming General Hospital of Chengdu Military Area
Cellular Physiology and Biochemistry | Year: 2015

Aims: Accumulating evidence suggests that atherosclerotic progression depends on persistent and chronic inflammation in the arterial walls. MicroRNA-155 is reportedly involved in cardiovascular disease and has been implicated as a pro-inflammation regulator. Although some researchers have focused on microRNA-155 as an atherosclerosis regulator, the mechanisms by which microRNA-155 functions as a putative pro-atherosclerosis microRNA are largely unknown. This study aims to analyze microRNA-155's effects on atherosclerotic inflammation and to explore its mechanism. Methods: MicroRNA-155's effects on atherosclerotic inflammation were observed along with the expression and activity levels of SOCS1, STAT3 and NF-κB though microRNA-155 inhibition or overexpression. Results: Highly expressions of microRNA-155 in oxLDL-stimulated macrophages and atherosclerosis mice were inversely correlated with SOCS1 expression. Ectopic microRNA-155 overexpression significantly promoted inflammatory cytokine and chemokine production and atherosclerosis progression. We then observed microRNA-155's functional role in the atherosclerotic pathophysiological process in vivo and in vitro. The observation revealed that by enhancing STAT3 and NF-κB signaling and facilitating immune inflammation by targeting SOCS1, microRNA-155 plays a promotable role in atherosclerosis progression. Conclusions: microRNA-155 works as a promoter in the atherosclerotic procession. Its mechanism may include enhancing inflammatory response in atherosclerosis by increasing STAT3 and NF-κB signaling via targeting SOCS1. © 2015 S. Karger AG, Basel.


Yang L.-X.,Kunming General Hospital of Chengdu Military Area | Liu G.,Kunming General Hospital of Chengdu Military Area | Zhu G.-F.,Kunming General Hospital of Chengdu Military Area | Liu H.,Kunming General Hospital of Chengdu Military Area | And 3 more authors.
JRAAS - Journal of the Renin-Angiotensin-Aldosterone System | Year: 2014

Background: MicroRNA-155 (miR-155) is a multifunctional signal microRNA that participates in a variety of cardiovascular diseases and is involved in physiological and pathological processes in different cell types. Objective: The objective of this article is to examine the effect of miR-155 on angiotensin II (Ang II)-induced primary mice vascular smooth muscle cell (VSMC) proliferation. Methods: Primary cultured VSMCs from the aorta of C57/BL6 mice were incubated with Ang II and miR-155. Cells were counted using CCK-8 and EdU, and flow cytometric analysis of cell cycle progression was performed. Angiotensin II 1 type receptor (AT1R) gene and protein expression were measured by real-time polymerase chain reaction and Western blotting. Results: 1) Ang II increased the viability of VSMCs in a dose- and time-dependent manner. 2) miR-155 opposed the Ang II-induced increase in VSMC viability. 3) miR-155 inhibited Ang II-induced proliferation of VSMCs. 4) miR-155 increased the number of VSMCs in the G1 phase compared to G2 and M cell cycle phases. 5) miR-155 decreased ATR1 gene and protein expression. Conclusion: miR-155 downregulation of Ang II-induced VSMC viability identifies it as an important regulator of cell proliferation. © 2014 The Author(s).


Zhu G.-F.,Kunming General Hospital of Chengdu Military Area | Yang L.-X.,Kunming General Hospital of Chengdu Military Area | Guo R.-W.,Kunming General Hospital of Chengdu Military Area | Liu H.,Kunming General Hospital of Chengdu Military Area | And 3 more authors.
Coronary Artery Disease | Year: 2014

OBJECTIVES: This study aimed to investigate the association between microRNA-155 (miR-155) and the severity and extent of coronary stenotic lesions. PATIENTS AND METHODS: We measured the miR-155 expression by real-time PCR in 110 consecutive patients undergoing coronary angiography for suspected coronary artery disease. The severity and extent of coronary stenotic lesions were evaluated on the basis of coronary angiography findings by the Gensini score. RESULTS: The miR-155 expression was significantly lower in 56 patients with coronary heart disease than those in 54 controls (P<0.01). The level of miR-155 in peripheral blood mononuclear cells or plasma was lower in patients with unstable angina pectoris and acute myocardial infarction than in patients with chest pain syndrome, whereas no statistically significant differences were observed between patients with stable angina pectoris and chest pain syndrome. Spearman's correlation analysis showed that the expression of miR-155 in plasma correlated positively with the expression in peripheral blood mononuclear cells. The levels of miR-155 in the patients with diseased vessels of two and three or more were significantly lower than in those with diseased vessel of zero and one. The levels of miR-155 were not significantly different among groups with diseased vessels of zero and one. miR-155 were associated negatively with Gensini scores (r=-0.663, P<0.001). The miR-155 expression was correlated significantly to age (r=-0.227), hypertension (r=-0.440), total cholesterol (r=0.239), high-density lipoprotein cholesterol (r=0.280), low-density lipoprotein cholesterol (r=-0.315), tobacco use (r=-0.363), angiotensin- converting enzyme inhibitor (r=-0.250), statins (r=-0.368), and high-sensitivity C-reactive protein (r=-0.515). CONCLUSION: miR-155 expression is associated inversely with complicated proatherogenic metabolic risk factors, and the severity of coronary stenotic lesions calculated by Gensini scores.© 2014 Wolters Kluwer Health.


Yang Y.,Chongqing Medical University | Yang L.,Chongqing Medical University | Yang L.,Kunming General Hospital of Chengdu Military Area
Inflammation | Year: 2016

This study aims to provide experimental proof that Rab6a is an efficient target of microRNA-155 in regulating pro-inflammatory tumor necrosis factor (TNF) secretion stimulated by lipopolysaccharide (LPS) in macrophages. We identified Rab6a as a new target of microRNA-155 (miR-155) and found that overexpression of miR-155 decreased Rab6a expression at both protein and mRNA levels, which resulted in a significant reduction of TNF secretion induced by lipopolysaccharide stimulation. We have demonstrated that miR-155 can negatively regulate inflammatory TNF secretion in lipopolysaccharide stimulated macrophages, partly by targeting Rab6a, thereby providing new insights into the role of miR-155 in cytokine secretion in inflammatory macrophages. © 2015, Springer Science+Business Media New York.


Kuang C.-Y.,Chongqing Medical University | Yu Y.,Chongqing Medical University | Guo R.-W.,Kunming General Hospital of Chengdu Military Area | Qian D.-H.,Chongqing Medical University | And 4 more authors.
Biochemical and Biophysical Research Communications | Year: 2010

Knockdown of stromal interaction molecule 1 (STIM1) significantly suppresses neointima hyperplasia after vascular injury. Endothelial progenitor cells (EPCs) are the major source of cells that respond to endothelium repair and contribute to re-endothelialization by reducing neointima formation after vascular injury. We hypothesized that the effect of STIM1 on neointima hyperplasia inhibition is mediated through its effect on the biological properties of EPCs. In this study, we investigated the effects of STIM1 on the proliferation and migration of EPCs and examined the effect of STIM1 knockdown using cultured rat bone marrow-derived EPCs. STIM1 was expressed in EPCs, and knockdown of STIM1 by adenoviral delivery of small interfering RNA (siRNA) significantly suppressed the proliferation and migration of EPCs. Furthermore, STIM1 knockdown decreased store-operated channel entry 48. h after transfection. Replenishment with recombinant human STIM1 reversed the effects of STIM1 knockdown. Our data suggest that the store-operated transient receptor potential canonical 1 channel is involved in regulating the biological properties of EPCs through STIM1. STIM1 is a potent regulator of cell proliferation and migration in rat EPCs and may play an important role in the biological properties of EPCs. © 2010 Elsevier Inc.


PubMed | Kunming General Hospital of Chengdu Military Area and Kunming Medical University
Type: | Journal: Mediators of inflammation | Year: 2016

Inflammation response plays a critical role in all phases of atherosclerosis (AS). Increased evidence has demonstrated that miR-155 mediates inflammatory mediators in macrophages to promote plaque formation and rupture. However, the precise mechanism of miR-155 remains unclear in AS. Here, we also found that miR-155 and PDCD4 were elevated in the aortic tissue of atherosclerotic mice and ox-LDL treated RAW264.7 cells. Further studies showed that miR-155 not only directly inhibited SOCS1 expression, but also increased the expression of p-STAT and PDCD4, as well as the production of proinflammation mediators IL-6 and TNF-


PubMed | Kunming General Hospital of Chengdu Military Area and Chongqing Medical University
Type: Journal Article | Journal: International journal of molecular medicine | Year: 2016

Endothelial progenitor cells (EPCs) play a key role in repairing the injured vascular endothelium by differentiating into mature endothelial cells (ECs) or secreting cytokines in a paracrine manner to promote proliferation of existing ECs. However, the mechanisms underlying the proliferation of EPCs were not fully understood. In order to investigate the mechanisms of EPC proliferation, we isolated EPCs from mononuclear cells of mouse spleens. By manipulating E2-2 expression in vitro, we observed that E2-2 negatively regulated the proliferation of EPCs. Moreover, we noted that E2-2 negatively regulated the autophagy of EPCs by studying the expression of LC3II and p62. We also demonstrated that an autophagy inhibitor chloroquine (CQ) decreased the proliferation of EPCs in a concentration-dependent manner. Interestingly, CQ reversed the increase in cell proliferation and autophagy in the E2-2 knockdown group. Furthermore, we detected the expression of autophagyrelated protein ATG7 in EPCs which had been transfected with small interfering (siRNA)E2-2 and siRNAautophagy related 7 (ATG7) or were untransfected. Our study revealed that E2-2 regulated EPC autophagy via mediating ATG7 expression. We conclude that E2-2 inhibited EPC proliferation via suppressing their autophagy, and E2-2 regulated EPC autophagy by mediating the expression of ATG7.

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