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Nicotine alters MicroRNA expression and hinders human adult stem cell regenerative potential
Tsz Kin Ng1, Carlos M Carballosa, Daniel Pelaez
1Geriatric Research, Education and Clinical Center, Miami Veterans Affairs Medical Center, Miami, Florida 33125, USA.
Abstract:
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.
Insights
Nicotine, found in cigarette smoke, impairs adult stem cell functions like proliferation and healing. This research explains how nicotine hinders stem cell potential, impacting regenerative medicine and wound healing.
Area of Science:
- Regenerative Medicine
- Stem Cell Biology
- Toxicology
Background:
- Adult stem cells are crucial for tissue repair and regenerative medicine.
- Cigarette smoking is known to impede wound healing and stem cell function.
- Nicotine is a primary toxicant in cigarette smoke.
Purpose of the Study:
- To investigate the impact of nicotine on the regenerative capabilities of human mesenchymal stem cells (MSC) and periodontal ligament-derived stem cells (PDLSC).
- To elucidate the mechanisms by which nicotine affects stem cell proliferation, migration, and differentiation.
Main Methods:
- Treatment of MSC and PDLSC with 1.0 μM nicotine.
- Assessment of cell proliferation and locomotion.
- Analysis of osteogenic differentiation via gene expression (RUNX2, ALPL, BGLAP, COL1A1, COL1A2), calcium deposition, and alkaline phosphatase activity.
- MicroRNA (miRNA) profiling of nicotine-treated PDLSC.
Main Results:
- Nicotine significantly reduced the proliferation and locomotion of both MSC and PDLSC.
- Osteogenic differentiation potential was diminished by nicotine exposure.
- Alterations in the miRNA profile of nicotine-treated PDLSC were observed, suggesting a role for miRNAs in nicotine's effects.
Conclusions:
- Nicotine negatively affects critical stem cell functions, including proliferation, migration, and osteogenic differentiation.
- The findings provide mechanistic insights into why cigarette smoking delays wound healing and hinders regenerative medicine.
- MicroRNAs may mediate some of the detrimental effects of nicotine on stem cells.
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