Your browser doesn't support javascript.
loading
Diversity of Ion Channels in Human Bone Marrow Mesenchymal Stem Cells from Amyotrophic Lateral Sclerosis Patients
The Korean Journal of Physiology and Pharmacology ; : 337-342, 2008.
Artículo en Inglés | WPRIM | ID: wpr-728666
ABSTRACT
Human bone marrow mesenchymal stem cells (hBM-MSCs) represent a potentially valuable cell type for clinical therapeutic applications. The present study was designed to evaluate the effect of long-term culturing (up to 10th passages) of hBM-MSCs from eight individual amyotrophic lateral sclerosis (ALS) patients, focusing on functional ion channels. All hBM-MSCs contain several MSCs markers with no significant differences, whereas the distribution of functional ion channels was shown to be different between cells. Four types of K+ currents, including noise-like Ca+2-activated K+ current (IKCa), a transient outward K+ current (Ito), a delayed rectifier K+ current (IKDR), and an inward-rectifier K+ current (Kir) were heterogeneously present in these cells, and a TTX-sensitive Na+ current (INa,TTX) was also recorded. In the RT-PCR analysis, Kv1.1, heag1, Kv4.2, Kir2.1, MaxiK, and hNE-Na were detected. In particular, INa,TTX showed a significant passage-dependent increase. This is the first report showing that functional ion channel profiling depend on the cellular passage of hBM-MSCs
Asunto(s)

Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Células Madre / Médula Ósea / Células Madre Mesenquimatosas / Esclerosis Amiotrófica Lateral / Canales Iónicos Límite: Humanos Idioma: Inglés Revista: The Korean Journal of Physiology and Pharmacology Año: 2008 Tipo del documento: Artículo

Similares

MEDLINE

...
LILACS

LIS

Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Células Madre / Médula Ósea / Células Madre Mesenquimatosas / Esclerosis Amiotrófica Lateral / Canales Iónicos Límite: Humanos Idioma: Inglés Revista: The Korean Journal of Physiology and Pharmacology Año: 2008 Tipo del documento: Artículo