كاهشبيان پروتئين هاى ميتوكندريايى در پروتئوم سيستم عصبى مركزى مدل حيوانى ب بيمارى مالتيپل اسكلروزيس

Abolhassan Shahzadeh Fazeli; Mohammad Hossein Sanati; Davood Nasrabadi; Alireza Pouya; Hossein Baharvand; Ghasem Hosseini Salekdeh

كاهشبيان پروتئين هاى ميتوكندريايى در پروتئوم سيستم عصبى مركزى مدل حيوانى ب بيمارى مالتيپل اسكلروزيس

Translated title of the contribution: Central nervous system proteomics in animal model of multiple sclerosis revealed down-regulation of mithochondrial proteins

Abolhassan Shahzadeh Fazeli, Mohammad Hossein Sanati, Davood Nasrabadi, Alireza Pouya, Hossein Baharvand, Ghasem Hosseini Salekdeh

Research output: Contribution to journal › Article › peer-review

3 Citations (Scopus)

Abstract

Objective: Detection of central nervous system (CNS) molecular defects in an animal model of multiple sclerosis.

Materials and Methods: Experimental autoimmune encephalomyelitis (EAE) was induced by a myelin oligodendrocyte glycoprotein. Protein expression profiles in the central nervous system between healthy clinical scores 1 and 3 of EAE were studied using a two dimensional electrophoresis based proteomics approach coupled with MALDI TOF/TOF mass spectrometry.

Results: We identified 8 mitochondrial proteins that were differentially expressed in CNS, all of them down-regulated in scores 1 and/or 3. Of these, 5 proteins belong to the mitochondrial respiratory chain including: NADH dehydrogenase (ubiquinone) Fe-S protein 8, cytochrome c oxidase Va, cytochrome c oxidase Vb, ATP5B, NADH dehydrogenase (ubiquinone) flavoprotein 2. We also observed down-regulation of three other mitochondrial proteins including: glutaredoxin 5, estradiol 17 beta-dehydrogenase 8 and isocitrate dehydrogenase.

Conclusion: Down-regulation of mitochondrial proteins supported the hypothesis that hypoxia-like tissue injury in multiple sclerosis (MS) lesions may be due to mitochondrial impairment.

Translated title of the contribution	Central nervous system proteomics in animal model of multiple sclerosis revealed down-regulation of mithochondrial proteins
Original language	Arabic
Pages (from-to)	236-243
Number of pages	8
Journal	Yakhteh
Volume	11
Issue number	2
Publication status	Published - 2009
Externally published	Yes

Keywords

mitochondria
proteomics
EAE
multiple sclerosis

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https://celljournal.org/journal/article/abstract/2799

Cite this

@article{cc929e16763a45419dc2ff99c716f4e0,

title = "كاهشبيان پروتئين هاى ميتوكندريايى در پروتئوم سيستم عصبى مركزى مدل حيوانى ب بيمارى مالتيپل اسكلروزيس",

abstract = "Objective: Detection of central nervous system (CNS) molecular defects in an animal model of multiple sclerosis. Materials and Methods: Experimental autoimmune encephalomyelitis (EAE) was induced by a myelin oligodendrocyte glycoprotein. Protein expression profiles in the central nervous system between healthy clinical scores 1 and 3 of EAE were studied using a two dimensional electrophoresis based proteomics approach coupled with MALDI TOF/TOF mass spectrometry. Results: We identified 8 mitochondrial proteins that were differentially expressed in CNS, all of them down-regulated in scores 1 and/or 3. Of these, 5 proteins belong to the mitochondrial respiratory chain including: NADH dehydrogenase (ubiquinone) Fe-S protein 8, cytochrome c oxidase Va, cytochrome c oxidase Vb, ATP5B, NADH dehydrogenase (ubiquinone) flavoprotein 2. We also observed down-regulation of three other mitochondrial proteins including: glutaredoxin 5, estradiol 17 beta-dehydrogenase 8 and isocitrate dehydrogenase. Conclusion: Down-regulation of mitochondrial proteins supported the hypothesis that hypoxia-like tissue injury in multiple sclerosis (MS) lesions may be due to mitochondrial impairment.",

keywords = "mitochondria, proteomics, EAE, multiple sclerosis",

author = "Fazeli, {Abolhassan Shahzadeh} and Sanati, {Mohammad Hossein} and Davood Nasrabadi and Alireza Pouya and Hossein Baharvand and Salekdeh, {Ghasem Hosseini}",

year = "2009",

language = "Arabic",

volume = "11",

pages = "236--243",

journal = "Yakhteh",

issn = "1561-4921",

publisher = "Royan Institute",

number = "2",

}

كاهشبيان پروتئين هاى ميتوكندريايى در پروتئوم سيستم عصبى مركزى مدل حيوانى ب بيمارى مالتيپل اسكلروزيس. / Fazeli, Abolhassan Shahzadeh; Sanati, Mohammad Hossein; Nasrabadi, Davood et al.
In: Yakhteh, Vol. 11, No. 2, 2009, p. 236-243.

Research output: Contribution to journal › Article › peer-review

TY - JOUR

T1 - كاهشبيان پروتئين هاى ميتوكندريايى در پروتئوم سيستم عصبى مركزى مدل حيوانى ب بيمارى مالتيپل اسكلروزيس

AU - Fazeli, Abolhassan Shahzadeh

AU - Sanati, Mohammad Hossein

AU - Nasrabadi, Davood

AU - Pouya, Alireza

AU - Baharvand, Hossein

AU - Salekdeh, Ghasem Hosseini

PY - 2009

Y1 - 2009

N2 - Objective: Detection of central nervous system (CNS) molecular defects in an animal model of multiple sclerosis. Materials and Methods: Experimental autoimmune encephalomyelitis (EAE) was induced by a myelin oligodendrocyte glycoprotein. Protein expression profiles in the central nervous system between healthy clinical scores 1 and 3 of EAE were studied using a two dimensional electrophoresis based proteomics approach coupled with MALDI TOF/TOF mass spectrometry. Results: We identified 8 mitochondrial proteins that were differentially expressed in CNS, all of them down-regulated in scores 1 and/or 3. Of these, 5 proteins belong to the mitochondrial respiratory chain including: NADH dehydrogenase (ubiquinone) Fe-S protein 8, cytochrome c oxidase Va, cytochrome c oxidase Vb, ATP5B, NADH dehydrogenase (ubiquinone) flavoprotein 2. We also observed down-regulation of three other mitochondrial proteins including: glutaredoxin 5, estradiol 17 beta-dehydrogenase 8 and isocitrate dehydrogenase. Conclusion: Down-regulation of mitochondrial proteins supported the hypothesis that hypoxia-like tissue injury in multiple sclerosis (MS) lesions may be due to mitochondrial impairment.

AB - Objective: Detection of central nervous system (CNS) molecular defects in an animal model of multiple sclerosis. Materials and Methods: Experimental autoimmune encephalomyelitis (EAE) was induced by a myelin oligodendrocyte glycoprotein. Protein expression profiles in the central nervous system between healthy clinical scores 1 and 3 of EAE were studied using a two dimensional electrophoresis based proteomics approach coupled with MALDI TOF/TOF mass spectrometry. Results: We identified 8 mitochondrial proteins that were differentially expressed in CNS, all of them down-regulated in scores 1 and/or 3. Of these, 5 proteins belong to the mitochondrial respiratory chain including: NADH dehydrogenase (ubiquinone) Fe-S protein 8, cytochrome c oxidase Va, cytochrome c oxidase Vb, ATP5B, NADH dehydrogenase (ubiquinone) flavoprotein 2. We also observed down-regulation of three other mitochondrial proteins including: glutaredoxin 5, estradiol 17 beta-dehydrogenase 8 and isocitrate dehydrogenase. Conclusion: Down-regulation of mitochondrial proteins supported the hypothesis that hypoxia-like tissue injury in multiple sclerosis (MS) lesions may be due to mitochondrial impairment.

KW - mitochondria

KW - proteomics

KW - EAE

KW - multiple sclerosis

UR - http://www.scopus.com/inward/record.url?scp=68849121002&partnerID=8YFLogxK

M3 - Article

AN - SCOPUS:68849121002

SN - 1561-4921

VL - 11

SP - 236

EP - 243

JO - Yakhteh

JF - Yakhteh

IS - 2

ER -

كاهشبيان پروتئين هاى ميتوكندريايى در پروتئوم سيستم عصبى مركزى مدل حيوانى ب بيمارى مالتيپل اسكلروزيس

Abstract

Keywords

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