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	1. 17β-Estradiol Protects the Sprague-Dawley Rats Retinal from Light-Induced Damage via Anti-oxidation
	Wang Shaolan,Wang Baoying,Feng Yan,Mo Mingshu,Du Fangying,Li Hongbo,Yu Xiaorui
	Basic Medicine 27 June 2014
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	Abstract:Oxidative stress is thought to be a major cause of light induced retinal neurodegeneration. The protective role of 17β-estradiol (βE2) in neurodegenerative disorders is well known, however, the underlying mechanism remains unclear. Here, we applied light induced retinal damage model to explore the mechanism by which βE2 exerts its neuroprotection. Adult male and female- ovariectomized (OVX) rats were exposed to 8000 lx white light for 12h to induce retinal light damage. Electroretinogram (ERG) assay and hematoxylin and eosin (H&E) staining show that exposure to light for 12h resulted in functional damage to the rat retina, histological changes and retinal neurons loss, while intravitreal injection (IVI) with βE2 significantly rescued impaired retina function in both female and male rats. By detecting malonylodialdehyde (MDA) production (a biomarker for oxidative stress) indicated an increasing retinal oxidative stress following exposure to light, and βE2 reduced the light induced oxidative stress. qRT-PCR indicated that antioxidant enzymes SOD and Gpx mRNA level were diminished in female-OVX rats but up-regulated in male rats after exposing to light, suggesting a gender differences in regulating the genes of these antioxidant enzymes in response to light. However, administration of βE2 recovered or enhanced the SOD and Gpx expression upon light stimulation. In spite of the CAT expression was not sensitive to light, βE2 also increased the gene expressions both in female-OVX and male rats. Further study indicated the antioxidant proteins Trx and Nrf2 were also involved in βE2 mediated anti-oxidation, while cytoprotective HO-1 exerts a key role in endogenous defense mechanisms against light but not via βE2. Taken together, we provide evidence that βE2 protected the retinal from light damage via anti-oxidative effect, the underline mechanism involved in regulation of the genes of antioxidant enzymes (SOD, CAT, Gpx) and proteins (Trx and Nrf2). Our study will provide the theory evidence for estrogen replacement therapy in postmenopausal women for reducing the risk of Age-related macular degeneration.
	TO cite this article:Wang Shaolan,Wang Baoying,Feng Yan, et al. 17β-Estradiol Protects the Sprague-Dawley Rats Retinal from Light-Induced Damage via Anti-oxidation[OL].[27 June 2014] http://en.paper.edu.cn/en_releasepaper/content/4602681


	2. Gene Expression Profile of Hedgehog Signaling Pathway Inhibition in Human Carcinoma Cells
	TANG Xiaoli,DENG Libin,ZHANG Weilong,GAO Meng,HUANG Dengliang,LUO Shiwen,LU Quqin
	Basic Medicine 10 March 2014
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	Abstract:Background: Aberrant activation of the Hedgehog (Hh) signaling pathway frequency occurs in human cancers, and increased evidence implicates the considerable role of GANT61 (Gli-ANTagonist, a kind of Hh signaling inhibitor) in anticancer therapy. However, it is still lacking the systematic scanning for the common mechanism of various cancer cells in respond to Hh-inhibition. Methodology/Principal Findings: Gene expression profiling of Hh inhibited HT-29 and MKN45 cells was determined by Illumina? Sentrix? BeadChip arrays. From the 17,329 expressed genes across genome, we identified 668 and 269 differentially expressed genes (DEGs, p < 0.01) in comparison pairs of HT-29 and MKN45, respectively. Interesting, large number of common DEGs (77 genes) were seen in both two comparison pairs, which was clearly more than the predicted number (10, p < 10?4). Further interpretation of gene ontology was based on over-representation analysis. Two nested categories of GO biological processes ("cell death", and "response to stimulus") were detected as candidates with the enrichments of DEGs in both two cell lines. In addition, cDNA microarray profiling of extra cancer cells (ES2 and H4) verified the change of expression in six common DEGs related to "cell death" (CDKN1A, DDIT3, IER3, IL8, MFGE8, and PPP1R15A) following GANT61 treatment. Conclusions/Significance: Our research indicates that inhibition of Hh has considerable effect on genes from pathway of "cell death" in various carcinoma cells. And, the aberrant of "response to DNA damage" related genes (such as DDIT3) may play a critical role in GANT61-induced cell death. In summary, this dataset provide insight into the molecular mechanisms of GANT61-induced antitumor activity, and the list of novel GLI-targets in cancer cells.
	TO cite this article:TANG Xiaoli,DENG Libin,ZHANG Weilong, et al. Gene Expression Profile of Hedgehog Signaling Pathway Inhibition in Human Carcinoma Cells[OL].[10 March 2014] http://en.paper.edu.cn/en_releasepaper/content/4589220


	3. A FoxO1-Bim pathway is involved in HDAC inhibitor depsipeptide induced apoptosis
	Yang Yang,Ying Zhao,Jing Yang,Wei-guo Zhu
	Basic Medicine 17 March 2009
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	Abstract:Histone deacetylase (HDAC) inhibitors have been shown to induce cell cycle arrest and apoptosis in cancer cells. However, the mechanisms of HDAC inhibitor induced apoptosis are not completely understood. In this study, a novel HDAC inhibitor, depsipeptide was found to induce p53-independent apoptosis in human lung cancer cells. Further study showed that Bim, a BH3-only pro-apoptotic protein, was significantly up-regulated by depsipeptide in cancer cells, indicating Bim may play a role in this depsipeptide induced apoptosis. In additional experiments, Bim’s function in depsipeptide-induced apoptosis was confirmed by knock down of Bim with RNAi. Furthermore, depsipeptide-induced expression of Bim was found to be dependent on forkhead transcription factor 1 (FoxO1) by FoxO1 siRNA. These data show for the first time that HDAC inhibitor may induce apoptosis through the FoxO1-Bim pathway.
	TO cite this article:Yang Yang,Ying Zhao,Jing Yang, et al. A FoxO1-Bim pathway is involved in HDAC inhibitor depsipeptide induced apoptosis[OL].[17 March 2009] http://en.paper.edu.cn/en_releasepaper/content/30413

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