Q Chen

Nanjing Medical University, Nan-ching, Jiangsu Sheng, China

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Publications (3)18.77 Total impact

  • X Cheng · Y Yang · Z Fan · L Yu · H Bai · B Zhou · X Wu · H Xu · M Fang · A Shen · Q Chen · Y Xu
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    ABSTRACT: Malignant tumors are exemplified by excessive proliferation and aggressive migration/invasion contributing to increased mortality of cancer patients. Matrix metalloproteinase 9 (MMP9) expression is positively correlated with lung cancer malignancy. The mechanism underlying an elevated MMP9 expression is not clearly defined. We demonstrate here that the transcriptional modulator megakaryocytic leukemia 1 (MKL1) was activated by hypoxia and transforming growth factor (TGF-β), two prominent pro-malignancy factors, in cultured lung cancer cells. MKL1 levels were also increased in more invasive types of lung cancer in humans. Depletion of MKL1 in lung cancer cells attenuated migration and invasion both in vitro and in vivo. Overexpression of MKL1 potentiated the induction of MMP9 transcription by hypoxia and TGF-β, whereas MKL1 silencing diminished MMP9 expression. Of interest, MKL1 knockdown eliminated histone H3K4 methylation surrounding the MMP9 promoter. Further analyses revealed that MKL1 recruited ASH2, a component of the H3K4 methyltransferase complex, to activate MMP9 transcription. Depletion of ASH2 ameliorated cancer cell migration and invasion in an MMP9-dependent manner. Together our data indicate that MKL1 potentiates lung cancer cell migration and invasion by epigenetically activating MMP9 transcription.Oncogene advance online publication, 9 March 2015; doi:10.1038/onc.2015.14.
    Oncogene 03/2015; DOI:10.1038/onc.2015.14 · 8.56 Impact Factor
  • Y Xu · Lingling Qian · Guijuan Zong · K Ma · X Zhu · H Zhang · N Li · Q Yang · H Bai · J Ben · X Li · Q Chen
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    ABSTRACT: Class A scavenger receptor (SR-A) is primarily expressed in microglia/macrophages and plays an important role in immune responses. However, whether SR-A can influence microglia/macrophage polarization in cerebral ischemic injury is not known. To this end we monitored the phenotypic alteration of microglia/macrophages in an animal model of cerebral ischemia injury. SR-A was up-regulated in mouse brains 24h after permanent occlusion of middle cerebral artery (MCAO). SR-A-deficient mice displayed reduced infarct size and improved neurological function compared with wild-type mice littermate controls. Furthermore, a decrease in inflammatory F4/80(+)CD11b(+)CD45(high)CD11c(+) microglia/macrophages and attenuated nuclear factor-kappaB (NF-κB) activation was found in ischemic brains in the SR-A null mice. This was accompanied by alleviation of classically activated M1 macrophage markers and preservation of alternatively activated M2 macrophage markers. These data suggest that SR-A contributes to cerebral ischemic injury by pivoting the phenotype of microglia/macrophages to a skewed M1 polarization.
    Neuroscience 05/2012; 218:35-48. DOI:10.1016/j.neuroscience.2012.05.036 · 3.33 Impact Factor
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    S S Zhu · Y Ren · M Zhang · J Q Cao · Q Yang · XY Li · H Bai · L Jiang · Q Jiang · Z G He · Q Chen
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    ABSTRACT: We aimed to evaluate the effect of the mutant Wld(S) (slow Wallerian degeneration; also known as Wld) gene in experimental diabetes on early experimental peripheral diabetic neuropathy and diabetic retinopathy. The experiments were performed in four groups of mice: wild-type (WT), streptozotocin (STZ)-induced diabetic WT, C57BL/Wld(S) and STZ-induced diabetic C57BL/Wld(S). In each group, intraperitoneal glucose and insulin tolerance tests were performed; blood glucose, glycated haemoglobin and serum insulin were monitored. These mice were also subjected to the following behavioural tests: grasping test, hot-plate test and von Frey aesthesiometer test. For some animals, sciatic-tibial motor nerve conduction velocity, tail sensory nerve conduction velocity and eye pattern electroretinogram were measured. At the end of the experiments, islets were isolated to detect glucose-stimulated insulin secretion, ATP content and extent of apoptosis. The NAD/NADH ratio in islets and retinas was evaluated. Surviving retinal ganglion cells were estimated by immunohistochemistry. We found that the Wld(S) gene is expressed in islets and protects beta cells against multiple low doses of STZ by increasing the NAD/NADH ratio, maintaining the ATP concentration, and reducing apoptosis. Consistently, significantly higher insulin concentrations, lower blood glucose concentrations, and better glucose tolerance were observed in Wld(S) mice compared with WT mice after STZ treatment. Furthermore, Wld(S) alleviated abnormal sensory responses, nerve conduction, retina dysfunction and reduction of surviving retinal ganglion cells in STZ-induced diabetic models. We provide the first evidence that expression of the Wld(S) gene decreases beta cell destruction and preserves islet function in STZ-induced diabetes, thus revealing a novel protective strategy for diabetic models.
    Diabetologia 09/2011; 54(9):2440-50. DOI:10.1007/s00125-011-2226-1 · 6.88 Impact Factor

Publication Stats

31 Citations
18.77 Total Impact Points

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Institutions

  • 2011–2015
    • Nanjing Medical University
      • • Department of Pathophysiology
      • • Atherosclerosis Research Center
      Nan-ching, Jiangsu Sheng, China