ArticleAmerican journal of translational research2018
Low-dose nicotine reduces the homing ability of murine BMSCs during fracture healing.
Article in American journal of translational research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 18 citations in OpenAlex.
- LINC00662 regulates osteogenic differentiation of BMSCs and inhibits fracture healing via miR-330-3p/PTEN axis.BMC musculoskeletal disorders · 2025Article
- Smoking and osteoimmunology: Understanding the interplay between bone metabolism and immune homeostasis.Journal of orthopaedic translation · 2024Review
- Isomangiferin promotes the migration and osteogenic differentiation of rat bone marrow mesenchymal stem cells.Open life sciences · 2024Article
- LIPUS as a potential strategy for periodontitis treatment: A review of the mechanisms.Frontiers in bioengineering and biotechnology · 2023Review
- Smoking Alters Inflammation and Skeletal Stem and Progenitor Cell Activity During Fracture Healing in Different Murine Strains.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2021Article
- The Life of a Fracture: Biologic Progression, Healing Gone Awry, and Evaluation of Union.JBJS reviews · 2020Review
- Nicotine Suppresses the Invasiveness of Human Trophoblasts by Downregulation of CXCL12 Expression through the Alpha-7 Subunit of the Nicotinic Acetylcholine Receptor.Reproductive sciences (Thousand Oaks, Calif.) · 2020Article
- Downregulation of microRNA-16-5p accelerates fracture healing by promoting proliferation and inhibiting apoptosis of osteoblasts in patients with traumatic brain injury.American journal of translational research · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Wound and fracture healing are affected by exposure to nicotine and other compounds in cigarettes. This study examined the effects of exposure to low-dose nicotine at sub-toxic concentrations on the proliferation, differentiation and migration of bone marrow stem cells (BMSCs) in vitro and their homing to fracture site in C57BL/6 mice. BMSCs were investigated in cells treated with or without nicotine (1 μM to 1 mM). Different concentrations of nicotine exhibited varied effects on BMSCs growth regulation and bone differentiation. CCK8 test significantly increased at a high nicotine concentration of 1 mM while calcium nodule staining with Alizarin red decreased at the same concentration. In vitro scratch test, Transwell tests and in vivo BMSCs homing tests showed negative effects on BMSCs migration at 10 μM to 1 mM nicotine test. Real-time PCR analysis revealed the down-regulation of SDF-1, CXCR4 and CXCR7, which were members of the potent chemotactic signaling system. Western blot analysis indicated the down-regulated expression levels of periostin expressed by nicotine-treated osteoblasts (1 μM to 100 μM). Micro CT results showed that nicotine delayed the fracture healing in mice. Our data suggest that exposure to low-dose nicotine concentrations may affect bone formation by inhibiting the migration and homing of BMSCs, which may be an important risk factor for bone healing delay in smoking patients.
Indexed as
Identifiers
30323867PMC6176232W2985851467What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.