Dopamine （DA） exposure at a dose of 100 pmol/L for 24 hours causes oxidative stress in SH-SY5Y cells with induction of neuronal differentiation by retinoic acid （RA,10 pmol/L,72 hours） followed by phorbol ester 12...Dopamine （DA） exposure at a dose of 100 pmol/L for 24 hours causes oxidative stress in SH-SY5Y cells with induction of neuronal differentiation by retinoic acid （RA,10 pmol/L,72 hours） followed by phorbol ester 12-O-tetradecanoyl-phorbol-13-acetate （TPA,80 nmol/L,72 hours）. However,it remains unclear whether the alteration of phenotype observed in response to oxidative stress is associated with protein regulation in this cellular model for Parkinson＇s disease. The present study detected protein regulation affected by oxidative stress at a proteomic level：selection of differentially altered proteins using two dimensional difference in-gel electrophoresis and identification of these proteins using matrix assisted laser desorption/ionization time-of-flight mass spectrometry. The results demonstrated significant alterations in expression of six proteins in SH-SY5Y cells following the differentiation and fourteen proteins in the differentiated cells following the exposure,exemplified by an increase of tubulin alpha1 in the former but a decrease of tubulin alpha-ubiquitous chain in the latter. These results suggest that two potentially specific but relevant patterns of proteomic change may be produced in SH-SY5Y cells with the induction of differentiation by RA followed by TPA,and in the differentiated cells after DA exposure.展开更多
Increasing evidence in recent years sug-gests homocysteine （Hcy） is involved in the pathogene-sis of Alzheimer’s disease （AD）, and that modifying this risk factor may be an alternative approach to delaying or pre...Increasing evidence in recent years sug-gests homocysteine （Hcy） is involved in the pathogene-sis of Alzheimer’s disease （AD）, and that modifying this risk factor may be an alternative approach to delaying or preventing onset of this disease. However, intervention studies uggest inconsistent effects of folic acid supple-mentation, with or without vitamin B12, on the prevention of incident AD. Studies with Hcy-lowering therapy show benefcial effects of B vitamins inpatients with mild cog-nitive impairment （MCI）, especially in those with high Hcy levels. Further studies are needed to confrm elevated Hcy levels as a potentially treatable risk factor for AD.展开更多
基金the Science and Technology Development Program of Jilin Province, No. 200505200the Distinguished Professor Foundation of Jilin University, No. 450011011204
文摘Dopamine （DA） exposure at a dose of 100 pmol/L for 24 hours causes oxidative stress in SH-SY5Y cells with induction of neuronal differentiation by retinoic acid （RA,10 pmol/L,72 hours） followed by phorbol ester 12-O-tetradecanoyl-phorbol-13-acetate （TPA,80 nmol/L,72 hours）. However,it remains unclear whether the alteration of phenotype observed in response to oxidative stress is associated with protein regulation in this cellular model for Parkinson＇s disease. The present study detected protein regulation affected by oxidative stress at a proteomic level：selection of differentially altered proteins using two dimensional difference in-gel electrophoresis and identification of these proteins using matrix assisted laser desorption/ionization time-of-flight mass spectrometry. The results demonstrated significant alterations in expression of six proteins in SH-SY5Y cells following the differentiation and fourteen proteins in the differentiated cells following the exposure,exemplified by an increase of tubulin alpha1 in the former but a decrease of tubulin alpha-ubiquitous chain in the latter. These results suggest that two potentially specific but relevant patterns of proteomic change may be produced in SH-SY5Y cells with the induction of differentiation by RA followed by TPA,and in the differentiated cells after DA exposure.
文摘Increasing evidence in recent years sug-gests homocysteine （Hcy） is involved in the pathogene-sis of Alzheimer’s disease （AD）, and that modifying this risk factor may be an alternative approach to delaying or preventing onset of this disease. However, intervention studies uggest inconsistent effects of folic acid supple-mentation, with or without vitamin B12, on the prevention of incident AD. Studies with Hcy-lowering therapy show benefcial effects of B vitamins inpatients with mild cog-nitive impairment （MCI）, especially in those with high Hcy levels. Further studies are needed to confrm elevated Hcy levels as a potentially treatable risk factor for AD.
