Argonaute2 regulation for K+ channel-mediated human adipose tissue-derived stromal cells self-renewal and survival in nucleus.
Kim BS., Im YB., Jung SJ., Park CH., Kang SK.
Laboratory Study, published in Stem Cells Dev (2012) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Laboratory Study
- Journal
- Stem Cells Dev (2012)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 22014067
- DOI
- 10.1089/scd.2011.0388
Abstract (original English)
Argonaute2 (Ago2) is a well-known factor that has intrinsic endonuclease activity and is a part of the fundamental gene regulatory machinery. Recently, we showed that nuclear Ago2 regulates voltage-gated potassium (Kv) channels and that Ago2/Kv1.3 has crucial functions in the self-renewal and cell de-aging processes in adipose tissue-derived stromal cells (ATSCs). In the nucleus, Ago2 bound to the promoter regions of calcium-activated potassium channel 3, potassium channel subfamily K member 1 (KCNK1), and voltage-gated potassium channel 2, and the expression of these genes was significantly upregulated at the level of transcription. We detected an active K+ channel that plays a critical role in Ago2-mediated ATSC self-renewal through the control of membrane potential during cell self-renewal and differentiation. Among the several regulatory subunits of voltage-dependent K+ (Kv) channels, Kv1.3 and Kv1.5 have been shown to impact tissue differentiation and cell growth in cultured ATSCs following their direct binding to the regulatory region of the Kv channel gene. In ATSCs, interference with Ago2 or K+ channel gene expression or treatment with tetraethylammonium significantly downregulated stemness gene expression, induced cell cycle arrest, and inhibited the ability of cells to transdifferentiate into neurons or β-cells via Oct4 knockdown. Blockage of the K+ channel significan
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
How we grade evidenceBrowse all related research
Filter the research library by this study's title keywords, author, or publication year.