Abstract:BACKGROUND: Evidence implied that calponin h2 (CNh2), an actin-binding protein, may be an antiproliferative gene. However, the expression of CNh2 in anti Thy1.1 glomerulonephritis (ATG) has not yet become clear. In this study, we sought to assess the relationship between CNh2 and transforming growth factor beta 1(TGF-β1) expression in vitro and in vivo. METHODS: In vivo study, ATG rats were generated and expression of CNh2 and TGF-β1 were assessed by immunohistochemistry, reverse transcription polymerase chain reaction (RT-PCR) and western blot, respectively. In vitro study, cultured mesangial cells(MsC) were stimulated with 2.08mmol/L argrinine or 200mmol/L ethanol for 48 hour, then expression of CNh2 and TGF-β1 were evaluated at the mRNA and protein level. RESULTS: CNh2 expression enhanced from day 3 to day 14, whereas TGF-β1 expression greatly increased from day 7 to day 28 in ATG (P<0.05). Up-regulation of TGF-β1expression and down-regulation of CNh2 expression were observed in MsC incubated with argrinine, whereas increased TGF-β1 expression and decreased CNh2 expression were shown in MsC treated with ethanol. CONCLUSIONS: CNh2 expression was enhanced in the early stage of ATG. With the progression of ATG, CNh2 expression decreased accompanied by an evident increase in TGF-β1 expression. CNh2 may function as a negative feedback regulator of TGF-β1 expression in rat MsC.

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	1. Expression of calponin h2 in anti-Thy-1.1 nephritis: negative correlation with TGF beta1 expression
	LI Hui
	Basic Medicine 08 February 2012
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	Abstract:BACKGROUND: Evidence implied that calponin h2 (CNh2), an actin-binding protein, may be an antiproliferative gene. However, the expression of CNh2 in anti Thy1.1 glomerulonephritis (ATG) has not yet become clear. In this study, we sought to assess the relationship between CNh2 and transforming growth factor beta 1(TGF-β1) expression in vitro and in vivo. METHODS: In vivo study, ATG rats were generated and expression of CNh2 and TGF-β1 were assessed by immunohistochemistry, reverse transcription polymerase chain reaction (RT-PCR) and western blot, respectively. In vitro study, cultured mesangial cells(MsC) were stimulated with 2.08mmol/L argrinine or 200mmol/L ethanol for 48 hour, then expression of CNh2 and TGF-β1 were evaluated at the mRNA and protein level. RESULTS: CNh2 expression enhanced from day 3 to day 14, whereas TGF-β1 expression greatly increased from day 7 to day 28 in ATG (P<0.05). Up-regulation of TGF-β1expression and down-regulation of CNh2 expression were observed in MsC incubated with argrinine, whereas increased TGF-β1 expression and decreased CNh2 expression were shown in MsC treated with ethanol. CONCLUSIONS: CNh2 expression was enhanced in the early stage of ATG. With the progression of ATG, CNh2 expression decreased accompanied by an evident increase in TGF-β1 expression. CNh2 may function as a negative feedback regulator of TGF-β1 expression in rat MsC.
	TO cite this article:LI Hui. Expression of calponin h2 in anti-Thy-1.1 nephritis: negative correlation with TGF beta1 expression[OL].[ 8 February 2012] http://en.paper.edu.cn/en_releasepaper/content/4465455


	2. VEGF is involved in the increase of dermal microvessel permeability induced by tryptase
	Bai Qianming,Wang Xinhong,Xu Yali,Yin Lianhua,Li Xiaobo
	Basic Medicine 31 January 2012
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	Abstract:Mast cells abundantly reside near the dermal vessels and release tryptase in the condition of cutaneous hypersensitivity and allergy, which is meanifested by rapid edema due to increased vascular permeability. However, the mechanism of mast cell tryptase promoting permeability remains to be defined. In this study, we investigated the effect of tryptase/human mast cells (HMC-1) supernatant on the permeability of human dermal microvascular endothelial cells (HDMECs) and studied whether vascular endothelial growth factor (VEGF) is involved in this effect or not. HMC-1 cells released tryptase pro-degranulating agent a23187 dose-dependently and HMC-1 cells density-dependently. Both tryptase and HMC-1 supernatant can promote permeability of HDMECs dramatically dose-dependently, which was resisted by tryptase inhibitor APC366 (a specific tryptase inhibitor) and partially reversed by a VEGF neutralizing antibody. Tryptase added to HDMECs caused a significant increase of mRNA and protein levels of VEGF, VEGF receptors (Flt-1 and Flk-1) by Real-time RT-PCR assay and Western-blot respectively. Our results suggest that mast cells tryptase can up-regulate the expression of VEGF and VEGF receptors. The VEGF neutralizing antibody can block the dermal microvessel hypermeability induced by tryptase. Thus, VEGF is involved in the increase of tryptse-induced dermal microvessel hypermeability and edema.
	TO cite this article:Bai Qianming,Wang Xinhong,Xu Yali, et al. VEGF is involved in the increase of dermal microvessel permeability induced by tryptase[OL].[31 January 2012] http://en.paper.edu.cn/en_releasepaper/content/4464501

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	3. Attenuation of neointima hyperplasia without thrombosis by a small molecule inhibitor of the store-operated channels in rabbits
	WANG Tengfei,YANG Liang,LI Jing,YU Yan,CAI Xiangyu,WANG Youjun,ZHENG Xi-long,GILL Donald L.,TANG Xiang D.
	Basic Medicine 22 January 2012
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	Abstract:Objective: Stromal interacting molecule 1 (STIM1) is associated with neointima hyperplasia by mediating store-operated Ca2+ entry (SOCE) in multiple cell types. We tested whether the small molecule SOCE inhibitor could prevent neointima formation and vascular stenosis using 2-aminoethyl diphenylborate (2-APB) as a prototype drug. Methods: VSMCs were isolated from rat aortas or rabbit common carotid arteries using the tissue explant protocol and phenotypic modulation was induced by 5% fetal bovine serum (FBS). VSMC proliferation was determined using the propidium iodine/ bromodeoxyuridine double-staining method. Neointimal hyperplasia was induced in rabbit carotid arteries by air-drying injury, and 2-APB was dissolved in PLF-127 gel and coated to the extravascular surface with rapamycin as a vis-à-vis control. Results: SOCE in the VSMCs was inhibited by 2-APB accompanied by cell cycle arrest in the G1 phase. In air drying-induced rabbit carotid artery injury models, extravascular application of 2-APB effectively blunted neointima formation with a potency comparable to rapamycin. 2-APB also attenuated leukocyte infiltration by perturbing the degranulation process preserving integrity of the internal and external elastic lamina. Likewise, the SOCE inhibitor prevented platelet activation but very likely in part by an indirect mechanism involving leukocyte inactivation. More interestingly, 2-APB did not seem to induce thrombosis, a fetal complication of public concern with the use of sirolimus-eluting stents. Conclusion: Small molecule SOCE inhibitors like 2-APB could blunt neointima hyperplasia without inducing thrombosis, and thus may serve as potentially new therapeutic agents for the prevention of restenosis and proliferative vascular disorders including hypertension, coronary heart disease and diabetes. (Corresponding authors: stang@ nankai.edu.cn or stellarli@ nankai .edu.cn)
	TO cite this article:WANG Tengfei,YANG Liang,LI Jing, et al. Attenuation of neointima hyperplasia without thrombosis by a small molecule inhibitor of the store-operated channels in rabbits[OL].[22 January 2012] http://en.paper.edu.cn/en_releasepaper/content/4463251


	4. TEIF associated centrosomal activity is regulated by EGF/PI3K/Akt signaling
	ZHAO Jing,CHI Yingkai,LIU Haijing,ZOU Yongxin,CUI Suping,JIANG Ping,WANG Huali,ZHANG Hong,MAO Jingzhuo,HOU Lin,ZHANG Bo
	Basic Medicine 11 January 2012
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	Abstract:Centrosome amplification, a characteristic of cancer cells, has been believed a driving force for genetic instability in the development of cancer and received extensively exploration in recent years. In our previous work, we have demonstrated that TEIF（transcriptional elements-interacting factor）distributes at the centrosome and regulates its status in physiological condition, DNA damage response or carcinogenesis. Here, we further expand our knowledge of TEIF to the downstream effector of EGF/PI3K/Akt signaling. The addition of EGF or transfection of active Akt stimulated TEIF expression, resulting in an increase of centrosome splitting and amplification, while the inhibitors of either PI3K or Akt attenuated the changes in TEIF and its associated centrosome status. A consensus motif for Akt phosphorylation (RHRVLT) was revealed in TEIF domain of localizing at the centrosome and identified as the site for phosphorylation of TEIF both in vitro and in vivo experiments, indicating TEIF as a direct substrate to Akt1. Furthermore, in a collection of aggressive breast cancers a positive correlation between the expression of TEIF and centrosome amplification was clarified and also closely concerned to the over-expression of CerbB2 (a member of EGFR family) and the level of phosphorylated Akt (pAkt) in cancer tissues. These findings not only could link EGF/PI3K/Akt oncogenic signaling with centrosome amplification, but also could provide more choices in the development of specific inhibitors for anti-cancer therapeutic agents targeting to EGF/PI3K/Akt signaling.
	TO cite this article:ZHAO Jing,CHI Yingkai,LIU Haijing, et al. TEIF associated centrosomal activity is regulated by EGF/PI3K/Akt signaling[OL].[11 January 2012] http://en.paper.edu.cn/en_releasepaper/content/4461460


	5. Pretreatment of ginsenoside-Rd reduces ischemia-reperfusion injury in isolated rat hearts by increasing coronary flow
	SONG Chun,WANG Liping,WANG Qilong,GAO Mingtang
	Basic Medicine 06 January 2012
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	Abstract:Objective: To evaluate the myocardial effects of ginsenoside-Rd in isolated rat hearts and to investigate the potential protective mechanism of ischemia-reperfusion injury. Methods: All rat hearts were isolated and perfused with modified Krebs-Heinseleit buffer (KHB) using the Langendorff preparation. For ischemia-reperfusion trial groups, hearts were treated with ginsenoside-Rd for 10 minutes after 20 minutes’ equilibrium, followed by 30 minutes’ global ischemia and 120 minutes’ reperfusion. For working heart trial groups, hearts were perfused with KHB containing ginsenoside-Rd for 40 minutes after 20 minutes’ equilibrium. Both of these two randomized controlled trials were performed using verapamil as positive control. Coronary flow (CF), heart rate (HR), left ventricular end diastolic pressure (LVEDP), left ventricular systolic pressure (LVSP), left ventricular developed pressure (LVDP), and rate pressure product (RPP) were collected to analyze the myocardial effects of ginsenoside-Rd. Results: Ginsenoside-Rd significantly increased the CF in both I/R trial and working heart trial (P<0.05). In I/R trial, it also helped lower the LVEDP and increase the RPP (P<0.05). However, in working heart trial, it showed no significant difference on the HR and LVDP (P>0.05).Conclusion: Pretreatment of ginsenoside-Rd of a middle dose could play a protective role in isolated rat ischemia-reperfusion hearts, by increasing the coronary flow rather than influencing cardiac functional properties previously.
	TO cite this article:SONG Chun,WANG Liping,WANG Qilong, et al. Pretreatment of ginsenoside-Rd reduces ischemia-reperfusion injury in isolated rat hearts by increasing coronary flow[OL].[ 6 January 2012] http://en.paper.edu.cn/en_releasepaper/content/4458840


	6. A small interfering RNA targeting NF-kappaB p65 alone or combined with 5-FU inhibits the growth of esophageal squmous cell carcinoma in nude mice
	TIAN Fang,FAN Tianli,JIANG Yanan,ZHANG Xiaoyan,WANG Xinhua
	Basic Medicine 07 November 2011
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	Abstract:NF-κB signaling pathway plays an important role in carcinogenesis. Although constitutive NF-κB activation has been reported in many human tumors, the effect of NF-κB signaling pathway in esophageal squamous cell carcinoma (ESCC) is still poorly understood. To explore the role of NF-κB signaling pathway in ESCC, RNA interference (RNAi) was used to knockdown NF-κB p65 protein level in the ESCC cells and in nude mice. 5-FU was used to investigated whether knockdown NF-κB p65 can potentiate 5-FU's antitumor effect. Animal results indicated that the tumor growth was inhibited in p65 siRNA and p65 siRNA + 5-FU groups compared with control group. Immunohistochemistry, RT-PCR and TUNEL assay showed that p65 siRNA downregulated the expression of p65 and enhanced the sensitivity of EC9706 cells to 5-FU treatment in vivo. Overall, our work indicated that downregulation of p65 can increase the tumor apoptosis and potentiates the effects of 5-FU by suppressing NF-κB signaling pathway. Thus, p65 is an interesting target for ESCC treatment.
	TO cite this article:TIAN Fang,FAN Tianli,JIANG Yanan, et al. A small interfering RNA targeting NF-kappaB p65 alone or combined with 5-FU inhibits the growth of esophageal squmous cell carcinoma in nude mice[J].


	7. The effects of REIC overexpression on biological phenotypes of gastric carcinoma AGS cell line
	Xu Xiaoyan,Xia Pu,Zheng Huachuan
	Basic Medicine 06 November 2011
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	Abstract:REIC is down-regulated in immortalized cell lines compared with the parental normal counterparts. It may inhibit colony formation, tumor growth, and induce the apoptosis. Here, gastric carcinoma AGS cell line transfected with REIC-expressing plasmid was subjected to the examination of phenotypes. REIC overexpression resulted in a low karyoplasmic ratio and proliferation, G1 arrest, high apoptosis, low migration, and invasion in AGS cells. These results suggest that REIC expression may be a promising objective and effective marker to predict pathobiological behaviors of gastric carcinoma.
	TO cite this article:Xu Xiaoyan,Xia Pu,Zheng Huachuan. The effects of REIC overexpression on biological phenotypes of gastric carcinoma AGS cell line[OL].[ 6 November 2011] http://en.paper.edu.cn/en_releasepaper/content/4448663


	8. The research about REIC expression and its correlation with clinicopathological parameters of gastric carcinomas
	Xu Xiaoyan,Xia Pu,Zheng Huachuan
	Basic Medicine 27 October 2011
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	Abstract:REIC is down-regulated in immortalized cell lines compared with the parental normal counterparts. It may inhibit colony formation, tumor growth, and induce the apoptosis. Here, REIC expression was examined in gastric carcinomas by RT-PCR, Western blot and immunohistochemistry, and compared with clinicopathological parameters of carcinoma. Immunohistochemically, REIC expression was negatively associated with tumor size, lymph node metastasis, dedifferentiation or poor prognosis of carcinoma. These results suggest that REIC expression may be a promising objective and effective marker to predict pathobiological behaviors and prognosis of gastric carcinoma.
	TO cite this article:Xu Xiaoyan,Xia Pu,Zheng Huachuan. The research about REIC expression and its correlation with clinicopathological parameters of gastric carcinomas[OL].[27 October 2011] http://en.paper.edu.cn/en_releasepaper/content/4447599


	9. Hippocampal neuronal nitric oxide synthase contributes to chronic stress-induced hypothalamic-pituitary-adrenal axis hyperactivity
	ZHOU Qigang,ZHU Lijuan,CHEN Chen,LIU Mengying,SUN Weixiang,ZHU Dongya
	Basic Medicine 27 May 2011
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	Abstract:Hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis is a hallmark of major depression. Impairment of hippocampal glucocorticoid receptor (GR), a molecular believed to mediate the negative feedback of hippocampus on HPA axis, has been thought causally related to the hyperactivity of HPA axis in depression. However, the mechanisms for the impairment of hippocampal GR remain unknown. Here, we report that neuronal nitric oxide synthase (nNOS) acts as an important negative regulator of GR in adult hippocampus. More importantly, hippocampal nNOS mediates GR downregulation of stress-induced glucocorticoids, resulting in overexpression of hypothalamic corticotrophin-releasing factor (CRF), a peptide that governs HPA axis, and in glucocorticoids secretion, indicating hyperactivity of HPA axis.
	TO cite this article:ZHOU Qigang,ZHU Lijuan,CHEN Chen, et al. Hippocampal neuronal nitric oxide synthase contributes to chronic stress-induced hypothalamic-pituitary-adrenal axis hyperactivity[OL].[27 May 2011] http://en.paper.edu.cn/en_releasepaper/content/4429267


	10. Therapeutic value of antioxidants for abnormal prolongation of QT interval and the associated arrhythmias in a rabbit model of diabetes
	Zhang Yiqiang,Sun Xuelin,Zhang Ying,Wang Jingxiong,LV Yanjie,Yang Baofeng,Wang Zhiguo
	Basic Medicine 15 April 2011
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	Abstract:Abnormal QT prolongation is the major cardiac electrical disorder and a predictor of mortality in diabetic patients. Our previous studies suggest that dysfunction of delayed rectifier K+ current (IKr) is the main cause for the problem. Here we report the potential therapeutic role and mechanisms of vitamin E in the rabbit model of diabetes. The QT interval and action potential duration were considerably prolonged with frequent occurrence of ventricular tachyarrhythmias in diabetic rabbits. Administration of vitamin E corrected the abnormal QT prolongation and abolished the arrhythmic incidence. IKr was found markedly reduced resulting in slowing of cardiac repolarization thereby QT prolongation in diabetic hearts. The diabetic depression of IKr is primarily ascribed to oxidative damages to the cardiac membrane and proteins, as indicated by the overproduction of reactive oxygen species leading to severe lipid peroxidation and protein oxidation. Moreover, IKr depression is most likely due to the dysfunction of HERG K+ channel, the major subunit underlying native IKr, in response to oxidative stress, for peroxide aniongenerating system produced similar depression of HERG channels. Vitamin E restored the depressed IKr and HERG by its antioxidant actions which likely underlie its beneficial effects on diabetic QT prolongation and the associated arrhythmias. The data indicate that an antioxidant is sufficient for reversing the IKr/IHERG dysfunction and the consequent electrical disorders in diabetic hearts. Our study also conceptually simplifies the complex nature of diabetic electrical disorders to primarily oxidative stress, and should stimulate interest in antioxidants as a therapeutic strategy for diabetic QT prolongation.
	TO cite this article:Zhang Yiqiang,Sun Xuelin,Zhang Ying, et al. Therapeutic value of antioxidants for abnormal prolongation of QT interval and the associated arrhythmias in a rabbit model of diabetes[OL].[15 April 2011] http://en.paper.edu.cn/en_releasepaper/content/4421002

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