作者机构：
[Huang, Fulian; Zhou, Shouhong; Tian, Shaowen; Yang, Yufeng; Deng, Haifeng; Li, Zhenbang] Univ S China, Coll Med, Dept Physiol, Hengyang 421001, Hunan, Peoples R China.;[Li, Peng] Univ S China, Coll Life Sci & Technol, Dept Biol, Hengyang 421001, Hunan, Peoples R China.
通讯机构：
[Tian, Shaowen] U;Univ S China, Coll Med, Dept Physiol, Hengyang 421001, Hunan, Peoples R China.
关键词：
Nicotine;Learning and memory;Contextual fear memory;Reconsolidation;Rats
摘要：
There is increasing evidence that nicotine is involved in learning and memory. However, there remains no study that has explored the relationship between nicotine and memory reconsolidation. At present study, we tested the effects of nicotine on the reconsolidation of contextual fear memory in rats. Behavior procedure involved four training phases: habituation (Day 0), fear conditioning (Day 1), reactivation (Day 2) and test (Day 3). Rats were injected saline or nicotine (0.25, 0.5 and 1.0mg/kg) immediately after reactivation. Percent of time spent freezing was used to measure conditioned fear response. Results showed that compared with saline rats, rats with nicotine at 1.0mg/kg presented a significant increase of freezing response on Day 3. Nicotine at 1.0mg/kg was ineffective when injected 6h after reactivation. Further results showed that the enhancement of freezing response induced by nicotine at 1.0mg/kg was dependent on fear memory reconsolidation, and was not attributed to an enhancement of the nonspecific freezing response 24h after nicotine administration. The results suggest that nicotine administration immediately after reactivation enhances contextual fear memory reconsolidation. Our present finding extends previous research on the nicotinic effects on learning and memory.
作者：
Yan, Limei;Hao, Hong;Elton, Terry S.;Liu, Zhenguo*;Ou, Hesheng
期刊：
Molecular and Cellular Biochemistry,2011年357(1-2):9-19 ISSN：0300-8177
通讯作者：
Liu, Zhenguo
作者机构：
[Yan, Limei] Univ S China, Biochem Res Ctr, Hengyang 421001, Hunan, Peoples R China.;[Liu, Zhenguo; Hao, Hong; Elton, Terry S.; Ou, Hesheng] Ohio State Univ, Med Ctr, Davis Heart & Lung Res Inst, Columbus, OH 43210 USA.;[Liu, Zhenguo; Hao, Hong; Elton, Terry S.; Ou, Hesheng] Ohio State Univ, Med Ctr, Div Cardiovasc Med, Columbus, OH 43210 USA.;[Ou, Hesheng] Guangxi Med Univ, Coll Pharm, Nanning 530021, Peoples R China.;[Liu, Zhenguo] Ohio State Univ, Med Ctr, Davis Heart & Lung Res Inst, DHLRI Suite 200,473 W 12th Ave, Columbus, OH 43210 USA.
通讯机构：
[Liu, Zhenguo] O;Ohio State Univ, Med Ctr, Davis Heart & Lung Res Inst, DHLRI Suite 200,473 W 12th Ave, Columbus, OH 43210 USA.
摘要：
Intronic microRNA (miRNAs) suppressed the expression of endothelial nitric oxide synthase (eNOS) gene in endothelial cells (ECs). This study was to investigate the role of signal transducer and activator of transcription 3 (STAT3) in the regulation of eNOS expression and vascular EC proliferation by the intronic 27-nucleotide (nt) miRNA derived from the 27-base pair repeats in intron 4 of eNOS gene. A detectable level of the 27-nt miRNA was present in the control ECs. Overexpression of the 27-nt miRNA dramatically suppressed the expression of eNOS and STAT3 at both transcription and translation levels in ECs in association with significant inhibition of EC proliferation. Mutation of the 27-nt miRNA at the 3'-terminal region resulted in substantial reduction of the inhibitory effect of miRNA on eNOS and STAT3 expression, and EC proliferation. Overexpression of active STAT3 significantly reversed the inhibitory effect of the 27-nt miRNA on eNOS expression and EC proliferation. In summary, we demonstrated that the 27-nt intronic miRNA functioned as a negative regulator for the expression of its host gene eNOS and cell proliferation in ECs. The sequence in 3'-terminal region played a key role in the function of the 27-nt miRNA. The regulatory effect of the intronic miRNA on eNOS gene expression was associated with miRNA polymorphisms, and mediated through inhibition of STAT3 signaling in ECs.
关键词：
Human telomerase reverse transcriptase;Lung adenocarcinoma;RNAi;Telomerase;siRNA
摘要：
Human telomerase reverse transcriptase (hTERT) is the catalytic subunit and the activity determinant factor of the telomerase enzyme which maintains the length of human chromosomes. In recent years it has become an attractive molecular target for cancer gene therapy. In the present study, we show that hTERT siRNA effectively suppressed the expression of hTERT mRNA and hTERT protein levels, reduced telomerase activity, and induced apoptosis of A549 lung adenocarcinoma cells (P<0.05). In vivo, tumors treated with the hTERT siRNA were of reduced sizes, indicating that the hTERT siRNA also reduced the tumorigenic potential of lung adenocarcinoma cells (P<0.05). These results demonstrate that hTERT siRNA can cause effective suppression of telomerase and lead to apoptosis in A549 lung adenocarcinoma cells. hTERT siRNA may, therefore, be a strong candidate for highly selective therapy for chemoprevention and treatment of lung adenocarcinoma.
作者机构：
[戴文建] Hunan Environment and Biology Polytechnique College, Hengyang 421005, Hunan Province, China;[柳威; 杨莉] Institute of Pharmacy and Pharmacology, University of South China, Hengyang 420001, Hunan Province, China;[毛小环] Hunan Environment and Biology Polytechnique College, Hengyang 421005, Hunan Province, China, Institute of Pharmacy and Pharmacology, University of South China, Hengyang 420001, Hunan Province, China
通讯机构：
[Mao, X.-h.] H;Hunan Environment and Biology Polytechnique College, Hengyang 421005, Hunan Province, China
