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Insulin-like growth factor-1 mediate...

Yang, Shuo.

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Insulin-like growth factor-1 mediated protection against hyperglycemia-induced reactive oxygen species in renal and neuronal cell models.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Insulin-like growth factor-1 mediated protection against hyperglycemia-induced reactive oxygen species in renal and neuronal cell models./
作者:	Yang, Shuo.
面頁冊數:	189 p.
附註:	Adviser: Shohreh Amini.
Contained By:	Dissertation Abstracts International68-12B.
標題:	Biology, Cell. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3293269
ISBN:	9780549372011

Insulin-like growth factor-1 mediated protection against hyperglycemia-induced reactive oxygen species in renal and neuronal cell models.
Yang, Shuo.

Insulin-like growth factor-1 mediated protection against hyperglycemia-induced reactive oxygen species in renal and neuronal cell models. - 189 p.

Adviser: Shohreh Amini.

Thesis (Ph.D.)--Temple University, 2007.

Furthermore, I have pointed to the transition of TNFalpha neuroprotective and neurotoxic dual functions in neurons by testing shifting point of ROS accumulation.

ISBN: 9780549372011Subjects--Topical Terms:

1017686
Biology, Cell.

Insulin-like growth factor-1 mediated protection against hyperglycemia-induced reactive oxygen species in renal and neuronal cell models.
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100 1 $a Yang, Shuo. $3 1270509
245 1 0 $a Insulin-like growth factor-1 mediated protection against hyperglycemia-induced reactive oxygen species in renal and neuronal cell models.
300 $a 189 p.
500 $a Adviser: Shohreh Amini.
500 $a Source: Dissertation Abstracts International, Volume: 68-12, Section: B, page: 7764.
502 $a Thesis (Ph.D.)--Temple University, 2007.
520 $a Furthermore, I have pointed to the transition of TNFalpha neuroprotective and neurotoxic dual functions in neurons by testing shifting point of ROS accumulation.
520 $a I have primarily proven that IGF-1 attenuation of HG-induced ROS accumulation might be dependent on WTp66Shc.
520 $a Diabetes, caused by insulin deficiency/resistance, has multiple complications, including nephropathy and neuropathy. Highly active antiretroviral therapy for human immunodeficiency virus (HIV) disease also causes type 2 diabetes. HIV-associated dementia (HAD) is a central nervous system (CNS) disorder in HIV-patients. Hyperglycemia and HIV-induced tumor necrosis factor-alpha (TNFalpha) may work together to cause neurodegeneration.
520 $a Hyperglycemia-induced reactive oxygen species (ROS) cause (renal) mesangial and neuronal cell apoptosis. In mesangial cells, I have verified that insulin-like growth factor-1 (IGF-1) mediated protection from high glucose (HG)-induced damage through ROS reduction, DNA damage attenuation and facilitation of homologous recombination-directed repair (HRR) of DNA double strand break. Furthermore, IGF-1 promotes Rad51, a key enzyme of HRR, recruiting to damaged DNA foci. In neurons, I have demonstrated that IGF-1 attenuates HG-induced ROS accumulation, loss of neuronal processes and apoptosis. IGF-1 also reduces both HG and TNFalpha mediated ROS accumulation and apoptosis.
520 $a The redox and pro-apoptotic function of p66Shc, an adaptor associated with cell aging/death and transcription factor FOXO3a, have been investigated under HG. I have shown that silencing wild type (WT) p66Shc with mutant of p66Shc or with siRNA against p66Shc reduces HG-induced ROS accumulation. This p66Shc inhibition on 36-Ser residue in mesangial cells also reduces HG-induced ROS-dependent phosphorylation of Akt and FOXO3a, known to facilitate FOXO3a nuclear localization and FOXO3a transcriptional activation of superoxide dismutase (SOD). In neurons, IGF-1 increases FOXO3a nuclear presence under HG, attenuating HG-induced ROS accumulation. Moreover, it has initially been demonstrated that FOXO3a activity may be associated with SOD expression in human CNS with HIV-encephalopathy. In my models, I have firstly demonstrated that WTp66Shc is critical for oxidative stress and DNA damage/apoptosis.
520 $a Both IGF-1 treatment and down-regulation of WTp66shc function could offer potential therapeutic strategy against renal/neuronal injuries associated with the impaired glucose metabolism. Further investigation of the transition of TNFalpha dual functions may lead to identification of potential therapeutic strategy for HAD.
590 $a School code: 0225.
650 4 $a Biology, Cell. $3 1017686
650 4 $a Biology, Neuroscience. $3 1017680
690 $a 0317
690 $a 0379
710 2 $a Temple University. $3 959342
773 0 $t Dissertation Abstracts International $g 68-12B.
790 $a 0225
790 1 0 $a Amini, Shohreh, $e advisor
791 $a Ph.D.
792 $a 2007
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3293269