TY - JOUR
T1 - Nicotine alters MicroRNA expression and hinders human adult stem cell regenerative potential
AU - Ng, Tsz Kin
AU - Carballosa, Carlos M.
AU - Pelaez, Daniel
AU - Wong, Hoi Kin
AU - Choy, Kwong Wai
AU - Pang, Chi Pui
AU - Cheung, Herman S.
PY - 2013/3/1
Y1 - 2013/3/1
N2 - Adult stem cells are critical for the healing process in regenerative medicine. However, cigarette smoking inhibits stem cell recruitment to tissues and delays the wound-healing process. This study investigated the effect of nicotine, a major constituent in the cigarette smoke, on the regenerative potentials of human mesenchymal stem cells (MSC) and periodontal ligament-derived stem cells (PDLSC). The cell proliferation of 1.0 μM nicotine-treated MSC and PDLSC was significantly reduced when compared to the untreated control. Moreover, nicotine also retarded the locomotion of these adult stem cells. Furthermore, their osteogenic differentiation capabilities were reduced in the presence of nicotine as evidenced by gene expression (RUNX2, ALPL, BGLAP, COL1A1, and COL1A2), calcium deposition, and alkaline phosphatase activity analyses. In addition, the microRNA (miRNA) profile of nicotine-treated PDLSC was altered; suggesting miRNAs might play an important role in the nicotine effects on stem cells. This study provided the possible mechanistic explanations on stem cell-associated healing delay in cigarette smoking.
AB - Adult stem cells are critical for the healing process in regenerative medicine. However, cigarette smoking inhibits stem cell recruitment to tissues and delays the wound-healing process. This study investigated the effect of nicotine, a major constituent in the cigarette smoke, on the regenerative potentials of human mesenchymal stem cells (MSC) and periodontal ligament-derived stem cells (PDLSC). The cell proliferation of 1.0 μM nicotine-treated MSC and PDLSC was significantly reduced when compared to the untreated control. Moreover, nicotine also retarded the locomotion of these adult stem cells. Furthermore, their osteogenic differentiation capabilities were reduced in the presence of nicotine as evidenced by gene expression (RUNX2, ALPL, BGLAP, COL1A1, and COL1A2), calcium deposition, and alkaline phosphatase activity analyses. In addition, the microRNA (miRNA) profile of nicotine-treated PDLSC was altered; suggesting miRNAs might play an important role in the nicotine effects on stem cells. This study provided the possible mechanistic explanations on stem cell-associated healing delay in cigarette smoking.
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UR - http://www.scopus.com/inward/citedby.url?scp=84874078543&partnerID=8YFLogxK
U2 - 10.1089/scd.2012.0434
DO - 10.1089/scd.2012.0434
M3 - Article
C2 - 23030247
AN - SCOPUS:84874078543
VL - 22
SP - 781
EP - 790
JO - Stem Cells and Development
JF - Stem Cells and Development
SN - 1547-3287
IS - 5
ER -