Xian Ping Yi
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Xian Ping Yi has a total of 12 co-authors. Here are the top co-authors by number of shared publications:
Faqian Li
University of Rochester Medical Center
1 shared publication- Faqian Li
Sanford Research/USD, Cardiovascular Research Institute, Sanford School of Medicine of The University of South Dakota and Sanford Health, Sioux Falls, SD 57105
1 shared publication Ling Zhong
1 shared publicationPing Chen
Jiangmen Central Hospital
1 shared publicationQiaoli Zheng
Department of Pathology, Sun Yat-sen University the Fifth Affiliated Hospital, 52 Meihua E. Road, Zhuhai, 519000, Guangdong, People's Republic of China
1 shared publicationWan-Wei Cao
1 shared publication
Latest Publications
- 17 April 2013
- Published by Springer Nature in Journal of Molecular Histology
- Vol. 44 (5) , 565-573
Expression and redistribution of β-catenin in the cardiac myocytes of left ventricle of spontaneously hypertensive rat
Beta-catenin is not only an adhering junction protein, but also the central player of the canonical Wnt signalling pathway. In order to investigate the roles of β-catenin in the mechanism of myocardial hypertrophy, we determined the expression and distribution of β-catenin in the cardiomyocytes of spontaneously hypertensive heart failure (SHHF) rats and age-matched Wistar-Kyoto (WKY) rats. We identified the reducing of β-catenin expression in the membrane protein fraction but increasing in the nuclear protein in the 6 and 12 month-old SHHF rats as compared with the age-matched WKY rats by Western blotting. Immunolabeling of β-catenin colocalized with cadherin at the intercalated disc sites and showed nuclear accumulation in myocytes of SHHF rats. We also revealed that the association between glycogen synthase kinase-3β and β-catenin had weakened in the 6 month-old SHHF rats as compared with the age-matched WKY rats by immunoprecipitation. These findings suggested that nuclear translocation of β-catenin might play important roles in regulating signal transduction in the decompensated hypertrophy stage.
- 17 April 2013
- Published by Springer Nature in Journal of Molecular Histology
- Vol. 44 (5) , 565-573
Expression and redistribution of β-catenin in the cardiac myocytes of left ventricle of spontaneously hypertensive rat
Beta-catenin is not only an adhering junction protein, but also the central player of the canonical Wnt signalling pathway. In order to investigate the roles of β-catenin in the mechanism of myocardial hypertrophy, we determined the expression and distribution of β-catenin in the cardiomyocytes of spontaneously hypertensive heart failure (SHHF) rats and age-matched Wistar-Kyoto (WKY) rats. We identified the reducing of β-catenin expression in the membrane protein fraction but increasing in the nuclear protein in the 6 and 12 month-old SHHF rats as compared with the age-matched WKY rats by Western blotting. Immunolabeling of β-catenin colocalized with cadherin at the intercalated disc sites and showed nuclear accumulation in myocytes of SHHF rats. We also revealed that the association between glycogen synthase kinase-3β and β-catenin had weakened in the 6 month-old SHHF rats as compared with the age-matched WKY rats by immunoprecipitation. These findings suggested that nuclear translocation of β-catenin might play important roles in regulating signal transduction in the decompensated hypertrophy stage.
- 1 October 2007
- Vol. 36 (10) , 677-80
[Expression of focal adhesion kinase in cardiac myocytes of hypertrophic ventricle].
To investigate the role of focal adhesion kinase (FAK) in the pathogenesis of cardiac hypertrophy induced by hypertension. Using immunofluorescent labeling, confocal microscopy and Western blotting, the expression and subcellular localization of FAK in the cardiac myocytes of left ventricle were determined in 2, 6, 12, and 18 month-old rats with spontaneously hypertensive heart failure (SHHF) along with age-matched control Wistar-Kyoto (WKY) rats. There was no significant difference of FAK expression between 2 month-old SHHF and WKY rats (50.5+/-6.9 vs. 49.8+/-5.0, n=6, P>0.05). In contrast with the control groups, the expression of FAK significantly increased in 6, 12 and 18 month-old SHHF rats (130.6+/-3.0 vs. 47.3+/-1.3, 144.7+/-5.4 vs. 46.4+/-3.1, 141.4+/-9.8 vs. 48.5+/-2.2, each groups n=6, P<0.05) with FAK protein primarily cumulated in the intercalated disks and nuclei. FAK may play a role in the cell signaling transduction leading to cardiac hypertrophy, presumably through regulations of hypertrophic gene transcription and RNA processing.
- 1 October 2007
- Vol. 36 (10) , 677-80
[Expression of focal adhesion kinase in cardiac myocytes of hypertrophic ventricle].
To investigate the role of focal adhesion kinase (FAK) in the pathogenesis of cardiac hypertrophy induced by hypertension. Using immunofluorescent labeling, confocal microscopy and Western blotting, the expression and subcellular localization of FAK in the cardiac myocytes of left ventricle were determined in 2, 6, 12, and 18 month-old rats with spontaneously hypertensive heart failure (SHHF) along with age-matched control Wistar-Kyoto (WKY) rats. There was no significant difference of FAK expression between 2 month-old SHHF and WKY rats (50.5+/-6.9 vs. 49.8+/-5.0, n=6, P>0.05). In contrast with the control groups, the expression of FAK significantly increased in 6, 12 and 18 month-old SHHF rats (130.6+/-3.0 vs. 47.3+/-1.3, 144.7+/-5.4 vs. 46.4+/-3.1, 141.4+/-9.8 vs. 48.5+/-2.2, each groups n=6, P<0.05) with FAK protein primarily cumulated in the intercalated disks and nuclei. FAK may play a role in the cell signaling transduction leading to cardiac hypertrophy, presumably through regulations of hypertrophic gene transcription and RNA processing.