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Long Q, Luo Q, Wang K, et al. Mash1-dependent Notch Signaling Pathway Regulates GABAergic Neuron-Like Differentiation from Bone Marrow-Derived Mesenchymal Stem Cells. Aging Dis. 2017;8(3):301-313doi: 10.14336/AD.2016.1018.
Long, Q., Luo, Q., Wang, K., Bates, A., & Shetty, A. K. (2017). Mash1-dependent Notch Signaling Pathway Regulates GABAergic Neuron-Like Differentiation from Bone Marrow-Derived Mesenchymal Stem Cells. Aging and disease, 8(3), 301-313. https://doi.org/10.14336/AD.2016.1018
Long, Qianfa, et al. "Mash1-dependent Notch Signaling Pathway Regulates GABAergic Neuron-Like Differentiation from Bone Marrow-Derived Mesenchymal Stem Cells." Aging and disease vol. 8,3 (2017): 301-313. doi: https://doi.org/10.14336/AD.2016.1018
Long Q, Luo Q, Wang K, Bates A, Shetty AK. Mash1-dependent Notch Signaling Pathway Regulates GABAergic Neuron-Like Differentiation from Bone Marrow-Derived Mesenchymal Stem Cells. Aging Dis. 2017 May 02;8(3):301-313. doi: 10.14336/AD.2016.1018. eCollection 2017 May. PMID: 28580186; PMCID: PMC5440110.
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Aging Dis. 2017 May 02;8(3):301-313. doi: 10.14336/AD.2016.1018. eCollection 2017 May.

Mash1-dependent Notch Signaling Pathway Regulates GABAergic Neuron-Like Differentiation from Bone Marrow-Derived Mesenchymal Stem Cells.

Aging and disease

Qianfa Long, Qiang Luo, Kai Wang, Adrian Bates, Ashok K Shetty

Affiliations

  1. 1Department of Neurosurgery, Xi'an Central Hospital, Xi'an Jiao Tong University School of Medicine, Xi'an 710003, China.
  2. 2Institute for Regenerative Medicine, Texas A&M Health Science Center College of Medicine at Scott & White, Temple and College Station, Texas, 76502, USA.
  3. 3Department of Neurosurgery, Qingdao 401 Hospital of PLA, Qingdao 266071, China.
  4. 4Research Service, Olin E. Teague Veterans' Medical Center, CTVHCS, Temple, Texas, USA.

PMID: 28580186 PMCID: PMC5440110 DOI: 10.14336/AD.2016.1018

Abstract

GABAergic neuronal cell grafting has promise for treating a multitude of neurological disorders including epilepsy, age-related memory dysfunction, Alzheimer's disease and schizophrenia. However, identification of an unlimited source of GABAergic cells is critical for advancing such therapies. Our previous study implied that reprogramming of bone marrow-derived mesenchymal stem cells (BMSCs) through overexpression of the Achaete-scute homolog 1 (Ascl1, also called Mash1) could generate GABAergic neuron-like cells. Here, we investigated mechanisms underlying the conversion of BMSCs into GABAergic cells. We inhibited γ-secretase (an enzyme that activates Notch signaling) with N-[N-(3,5-difluorophenacetyl)-L-alanyl]-S-phenylglycine t-butyl ester (DAPT) or manipulated the expression of Notch signaling components such as the

Keywords: GABAergic neuron-like cells; Notch signaling pathway; bone marrow-derived mesenchymal stem cells; hairy and enhancer of split-1; mammalian achaete scute homolog-1

Conflict of interest statement

Conflict of interest All authors declare that they have no conflict of interest in this article. We confirm that we have read the Journal’s policy on issues involved in ethical publication and affirm

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