PMID- 20129651 OWN - NLM STAT- MEDLINE DCOM- 20110624 LR - 20161125 IS - 1618-0372 (Electronic) IS - 0065-1281 (Linking) VI - 113 IP - 3 DP - 2011 May TI - Relationship between down-regulation of HIC1 and PTEN genes and dysfunction of pancreatic islet cells in diabetic rats. PG - 340-8 LID - 10.1016/j.acthis.2010.01.005 [doi] AB - The aim of the study was to investigate the protein expression of hypermethylated in cancer 1 (HIC1 ) and phosphatase and tensin homologue (PTEN) genes and to study their mRNA expressions in normal and diabetic pancreatic islet cells in rats in order to try and identify the functions of these genes in the development and advancement of diabetes. We further aimed to analyze the expression of mammalian target of rapamycin (mTOR), which is regulated by PTEN and to investigate the possible mechanism of PTEN affecting the function of diabetic islet cells. The expressions of HIC1, PTEN and mTOR genes were examined in the pancreatic islets of 20 normal male Wistar rats and 47 diabetic male Wistar rats by immunohistochemistry, Western blot, RT-PCR and real-time RT-PCR. Results showed that expressions of HIC1 and PTEN in protein and mRNA levels were lower in pancreatic islets of diabetic rats than in normal rats. Expressions of mTOR in protein and mRNA levels were higher in pancreatic islets of diabetic rats than in the normal rats. Marked apoptosis of pancreatic islet cells was observed in 29 cases (29/47, 61.7%) in diabetic rats, but not in the remaining 18 (18/47, 38.3%) diabetic rats. The down-regulation of HIC1 and PTEN and up-regulation of mTOR in protein and mRNA level are positively correlated with functional impairment of islet cells in diabetic rats. From this study we conclude that HIC1, PTEN and mTOR cannot be recognized as the key influencing factors promoting pancreatic islet cells apoptosis of diabetic rats; however, lower expressions of HIC1 and PTEN and higher expression of mTOR may affect the function of the pancreatic islet cells in diabetic rats. CI - Copyright (c) 2010 Elsevier GmbH. All rights reserved. FAU - Liu, Hao-ling AU - Liu HL AD - Department of Endocrinology, The First Clinical College of Harbin Medical University, Harbin, PR China. FAU - Yang, Hai-yan AU - Yang HY FAU - Liu, Lian-xin AU - Liu LX FAU - Chen, Yue AU - Chen Y FAU - Kuang, Hong-yu AU - Kuang HY FAU - Zhang, Hui-juan AU - Zhang HJ FAU - Yin, Hui-qing AU - Yin HQ LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20100202 PL - Germany TA - Acta Histochem JT - Acta histochemica JID - 0370320 RN - 0 (HIC1 protein, human) RN - 0 (Kruppel-Like Transcription Factors) RN - EC 3.1.3.67 (PTEN Phosphohydrolase) RN - EC 3.1.3.67 (PTEN protein, human) SB - IM MH - Animals MH - Blotting, Western MH - Diabetes Mellitus, Experimental/*physiopathology MH - *Down-Regulation MH - Immunohistochemistry MH - Islets of Langerhans/*pathology MH - Kruppel-Like Transcription Factors/genetics/*metabolism MH - Male MH - PTEN Phosphohydrolase/genetics/*metabolism MH - Rats MH - Rats, Wistar MH - Reverse Transcriptase Polymerase Chain Reaction EDAT- 2010/02/05 06:00 MHDA- 2011/06/28 06:00 CRDT- 2010/02/05 06:00 PHST- 2009/09/09 00:00 [received] PHST- 2010/01/12 00:00 [revised] PHST- 2010/01/13 00:00 [accepted] PHST- 2010/02/05 06:00 [entrez] PHST- 2010/02/05 06:00 [pubmed] PHST- 2011/06/28 06:00 [medline] AID - S0065-1281(10)00006-1 [pii] AID - 10.1016/j.acthis.2010.01.005 [doi] PST - ppublish SO - Acta Histochem. 2011 May;113(3):340-8. doi: 10.1016/j.acthis.2010.01.005. Epub 2010 Feb 2.