Related Experiment Video
Updated: Dec 22, 2025

06:10
Real-Time Imaging of CCL5-Induced Migration of Periosteal Skeletal Stem Cells in Mice
Published on: September 16, 2020
2.5K
Inhibition of long non-coding RNA TSIX accelerates tibia fraction healing via binding and positively regulating the
1Department of Orthopedics Trauma, Trauma Center, Shanghai General Hospital of Nanjing Medical University, Shanghai, China. wangqiugen@yahoo.com.
Summary
Knocking down long chain non-coding RNA TSIX (lncRNA TSIX) promotes tibia fracture healing by inhibiting SOX6 expression. This suggests lncRNA TSIX/SOX6 may be a therapeutic target for fracture treatment.
Area of Science:
- Molecular Biology
- Genetics
- Orthopedics
Background:
- Fracture healing is a complex process influenced by gene expression.
- Long chain non-coding RNAs (lncRNAs) are increasingly recognized for their roles in biological processes.
- Tibial fractures (TF) require long-term treatment and have a slow recovery.
Purpose of the Study:
- To investigate the role of lncRNA TSIX in tibial fracture healing.
- To explore the molecular mechanism of lncRNA TSIX in fracture repair.
- To identify potential therapeutic targets for TF.
Main Methods:
- Tibial fracture models were established in male C57BL/6J mice.
- Osteoblast cell cultures were used as an in vitro model.
- Expression of lncRNA TSIX and osteogenesis-related genes (Col1a1, Col-II, Col-X) was analyzed.
- Proliferation and apoptosis were assessed.
- Hematoxylin-eosin (HE) staining was performed to evaluate fracture healing.
Main Results:
- lncRNA TSIX expression was upregulated in plasma of TF mice in a time-dependent manner.
- Overexpression of lncRNA TSIX inhibited osteoblast proliferation and promoted apoptosis.
- lncRNA TSIX positively regulated SOX6 expression, affecting osteogenesis-related genes.
- Knockdown of lncRNA TSIX improved fracture healing in vivo and in vitro.
Conclusions:
- lncRNA TSIX knockdown promotes tibia fracture healing by inhibiting SOX6 expression.
- The lncRNA TSIX/SOX6 axis is a potential therapeutic target for tibial fracture treatment.
Related Concept Videos
Inheritance of Chromatin Structures
7.2K
Epigenetics is the study of inherited changes in a cell's phenotype without changing the DNA sequences. It provides a form of memory for the differential gene expression pattern to maintain cell lineage, position-effect variegation, dosage compensation, and maintenance of chromatin structures such as telomeres and centromeres. For example, the structure and location of the centromere on chromosomes are epigenetically inherited. Its functionality is not dictated or ensured by the underlying...
7.2K
TGF - β Signaling Pathway
10.3K
The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
10.3K
X-Inactivation
41.2K
The human X chromosome contains over ten times the number of genes as in the Y chromosome. Since males have only one X chromosome, and females have two, one might expect females to produce twice as many of the proteins, with undesirable results.
41.2K
Experimental RNAi
7.2K
RNA interference (RNAi) is a cellular mechanism that inhibits gene expression by suppressing its transcription or activating the RNA degradation process. The mechanism was discovered by Andrew Fire and Craig Mello in 1998 in plants. Today, it is observed in almost all eukaryotes, including protozoa, flies, nematodes, insects, parasites, and mammals. This precise cellular mechanism of gene silencing has been developed into a technique that provides an efficient way to identify and determine the...
7.2K

