著者

Xin Liu Hua Wang Guang Li Hui-Zhe Huang Yi-Quan Wang

出版者

日本遺伝学会

雑誌

Genes & Genetic Systems (ISSN:13417568)

巻号頁・発行日

vol.88, no.4, pp.261-269, 2013 (Released:2014-01-25)

参考文献数

25

被引用文献数

2 8

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Vertebrate Pax1 gene is a member of Pax gene family and encodes a transcription factor associated with crucial roles in the development of pharyngeal pouch, scletrotome and limb bud. In zebrafish, the genome contains two Pax1 paralogs, DrPax1a and DrPax1b, which share high sequence similarity with other Pax1 genes. To elucidate the function of zebrafish DrPax1b gene, we first examined the gene expression pattern and found that it was mainly expressed in the endodermal pharyngeal pouch, caudal somites, notochord, and fin bud. Then, we performed knockdown experiments using antisense morpholino oligonucleotides, which lead to the defects in the vertebral column, tail, pharyngeal skeleton, and pectoral fin. Additionally, we also found that the mouse MmPax1 mRNA, but not the amphioxus AmphiPax1/9 mRNA, could rescue the MO-induced defects. Furthermore, sequence alignment revealed that the N-terminal region of vertebrate Pax1 and amphioxus Pax1/9 were highly conserved, whereas their C-terminal regions were relatively divergent. However, the chimeric Am(N)Dr(C)Pax1, Mm(N)Dr(C)Pax1 and Dr(N)Mm(C)Pax1 mRNA could partially rescue the defects, while the Dr(N)Am(C)Pax1 mRNA could not. In conclusion, our data demonstrate a conserved function of DrPax1b in the development of the vertebral column, pectoral fin and pharyngeal skeleton formation in zebrafish and also provide critical insight into the functional evolution of Pax1 gene by changing its C-terminal sequence.

著者

Zhen-Guang Li Zhan-Cai Yu Yong-Peng Yu Dao-Zhen Wang Wei-Ping Ju Qi-Zhuan Wu

出版者

Japan Brain Science society

雑誌

脳科学誌 (ISSN:13415301)

巻号頁・発行日

vol.37, pp.35-46, 2011 (Released:2017-06-01)

参考文献数

32

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Lysophosphatidic acid (LPA) is released from activated platelets. Statins are the commonly used anti-atherosclerotic drug. The purpose of this study is to observe whether atorvastatin could decrease the plasma LPA levels in ischemic stroke patients. A total of 386 subjects, including the 247 ischemic stroke cases and 139 healthy controls, were enrolled in this study. The 247 ischemic stroke cases were divided into Group A (n=109) and Group B (n=138) who had and had not received atorvastatin treatment before a stroke respectively. The plasma LPA levels of all the subjects were measured using chromatography. There was significant diffidence in the LPA levels between cases and controls (3.22±1.51μmol/L vs. 1.83±1.07μmol/L, p<0.01). The plasma LPA level in Group A was lower than that of Group B (2.66±1.23umol/L vs. 3.83±1.14umol/L, p<0.01). Atorvastatin (20mg/d) significantly reduced LPA levels in ischemic stroke patients (n=138) compared with that before atorvastatin administration (1.96±0.87μmol/L vs. 3.83±1.14μmol/L, p<0.01). However, the LPA levels re-elevated after atorvastatin withdrawl for one month. Atorvastatin could decrease the plasma LPA levels in patients with ischemic stroke, which providing a better understanding of how statins protect against ischemic stroke. It is plausible to speculate that statins might have an effect of anti platelet activation.