Over-expression of Oct4 and Sox2 transcription factors enhances differentiation of human umbilical cord blood cells in vivo

被引：10

作者：

Guseva, Daria ^{[1
,2
]}

Rizvanov, Albert A. ^{[3
]}

Salafutdinov, Ilnur I. ^{[3
]}

Kudryashova, Nezhdana V. ^{[3
]}

Palotas, Andras ^{[3
,4
,5
]}

Islamov, Rustem R. ^{[1
]}

机构：

[1] Kazan State Med Univ, Kazan, Republic Of Tat, Russia

[2] Hannover Med Sch, Hannover, Germany

[3] Kazan Fed Univ, Kazan, Republic Of Tat, Russia

[4] Asklepios Med, Private Med Practice, H-6722 Szeged, Hungary

[5] Asklepios Med, Res Ctr, H-6722 Szeged, Hungary

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2014年 / 451卷 / 04期

基金：

俄罗斯科学基金会;

关键词：

Amyotrophic lateral sclerosis; Differentiation; Umbilical cord blood mono-nuclear cell; Pluripotency; Transcription factor; PLURIPOTENT STEM-CELLS; AMYOTROPHIC-LATERAL-SCLEROSIS; SELF-RENEWAL; MOUSE MODEL; FIBROBLASTS; GENERATION; NEURONS; NANOG;

D O I：

10.1016/j.bbrc.2014.07.132

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Gene and cell-based therapies comprise innovative aspects of regenerative medicine. Even though stem cells represent a highly potential therapeutic strategy, their wide-spread exploitation is marred by ethical concerns, potential for malignant transformation and a plethora of other technical issues, largely restricting their use to experimental studies. Utilizing genetically modified human umbilical cord blood mono-nuclear cells (hUCB-MCs), this communication reports enhanced differentiation of transplants in a mouse model of amyotrophic lateral sclerosis (ALS). Over-expressing Oct4 and Sox2 induced production of neural marker PGP9.5, as well as transformation of hUCB-MCs into micro-glial and endothelial lines in ALS spinal cords. In addition to producing new nerve cells, providing degenerated areas with trophic factors and neo-vascularisation might prevent and even reverse progressive loss of moto-neurons and skeletal muscle paralysis. (C) 2014 Elsevier Inc. All rights reserved.

引用

页码：503 / 509

页数：7

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