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LCP1 up-regulated by partial pancreatectomy supports cell proliferation and differentiation.

Authors
Choi, Jong-HoLee, Min-YoungRamakrishna SureshKim, YooleeShim, Jeoung-YunHan, Sang-MoonKim, Ji-YoungLee, Dong-HyeonChoi, Young-KilBaek, Kwang-Hyun
Issue Date
Nov-2011
Publisher
ROYAL SOC CHEMISTRY
Citation
MOLECULAR BIOSYSTEMS, v.7, no.11, pp.3104 - 3111
Indexed
SCIE
SCOPUS
Journal Title
MOLECULAR BIOSYSTEMS
Volume
7
Number
11
Start Page
3104
End Page
3111
URI
https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/167143
DOI
10.1039/c1mb05326d
ISSN
1742-206X
Abstract
The pancreas is the critical organ controlling blood glucose levels and has been shown to rapidly regenerate after injury. In this study, 60% partial pancreatectomy (PPX) was performed on rats and the protein expression profile was acquired using 2-dimensional gel electrophoresis (2-DE)/MALDI-TOF analysis. In total, 34 proteins were shown to be up-regulated and 27 proteins were down-regulated after PPX. The up-regulated proteins were found to be involved in inflammation and the down-regulated proteins were involved in energy metabolism. Then, we compared the results from previous 4 different omics studies along with our present data and listed several genes which were found to be reproducibly regulated by PPX. The quantification of differentially regulated genes at transcriptional level by real-time PCR analysis showed that the three genes (Apoa1, Lcp1 and Lipa) were up-regulated and three genes (Gatm, Ivd and Pck2) were down-regulated. Of these, lymphocyte cytosolic protein 1 (LCP1) was highly (folds = 8.40 ± 2.57) up-regulated by PPX and found to augment cell proliferation in PANC-1 and INS-1 cells. Finally, the validation of islet markers on exogenously expressed LCP1 cells showed up-regulation of genes which are responsible for pancreatic regeneration. These data indicate that the LCP1 may play a critical role in the pancreas regeneration.
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Ramakrishna, Suresh
GRADUATE SCHOOL OF BIOMEDICAL SCIENCE AND ENGINEERING (DEPARTMENT OF BIOMEDICAL SCIENCE)
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