Journal
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
Volume 305, Issue 4, Pages C377-C391Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpcell.00404.2012
Keywords
human adipose tissue-derived mesenchymal stem cells; TGF-beta(1); ion channel; vascular smooth muscle
Categories
Funding
- National Research Foundation of Korea (NRF)
- Ministry of Education, Science and Technology [2011-0019422, 2010-0021126, 2010-0020224, 2012R1A2A1A03007595]
- National Research Foundation of Korea [2010-0021126] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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Human adipose tissue-derived mesenchymal stem cells (hASCs) have the power to differentiate into various cell types including chondrocytes, osteocytes, adipocytes, neurons, cardiomyocytes, and smooth muscle cells. We characterized the functional expression of ion channels after transforming growth factor-beta(1) (TGF-beta(1))-induced differentiation of hASCs, providing insights into the differentiation of vascular smooth muscle cells. The treatment of hASCs with TGF-beta(1) dramatically increased the contraction of a collagen-gel lattice and the expression levels of specific genes for smooth muscle including alpha-smooth muscle actin, calponin, smooth mucle-myosin heavy chain, smoothelin-B, myocardin, and h-caldesmon. We observed Ca2+, big-conductance Ca2+-activated K+ (BKCa), and voltage-dependent K+ (K-v) currents in TGF-beta(1)-induced, differentiated hASCs and not in undifferentiated hASCs. The currents share the characteristics of vascular smooth muscle cells (SMCs). RT-PCR and Western blotting revealed that the L-type (Ca(v)1.2) and T-type (Ca(v)3.1, 3.2, and 3.3), known to be expressed in vascular SMCs, dramatically increased along with the Ca-v beta(1) and Ca-v beta(3) subtypes in TGF-beta(1)-induced, differentiated hASCs. Although the expression-level changes of the alpha-subtype BKCa channels varied, the major alpha-subtype BKCa channel (K(Ca)1.1) clearly increased in the TGF-beta(1)-induced, differentiated hASCs. Most of the K-v subtypes, also known to be expressed in vascular SMCs, dramatically increased in the TGF-beta(1)-induced, differentiated hASCs. Our results suggest that TGF-beta(1) induces the increased expression of vascular SMC-like ion channels and the differentiation of hASCs into contractile vascular SMCs.
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