ArticleExperimental and therapeutic medicine2021
Bcl-xL mutant promotes cartilage differentiation of BMSCs by upregulating TGF-β/BMP expression levels.
Article in Experimental and therapeutic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Current status, trend and progress of stem cells in tracheal tissue engineering research: an overview and perspectives.Stem cell research & therapy · 2025Review
- Effects of calcium-sensitive receptors on chondrogenic differentiation of rat bone marrow mesenchymal stem cells.Cell and tissue banking · 2025Article
- Review
- Upregulated miR-9-5p inhibits osteogenic differentiation of bone marrow mesenchymal stem cells under high glucose treatment.Journal of bone and mineral metabolism · 2022Article
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 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bcl-xL is a transmembrane molecule in the mitochondria, with apoptosis-related and pro-metabolic functions, that also plays a role in chondrogenesis and differentiation. A Bcl-xL mutant, in which the GRI sequence is replaced by ELN, has no anti-apoptotic effect, while other biological functions of this mutant remain unchanged. The present study investigated the impact of this Bcl-xL mutant on cartilage differentiation and the expression levels of TGF-β and bone morphogenetic protein (BMP). Human bone marrow mesenchymal stem cells (BMSCs) were transfected with Bcl-xL and Bcl-xL mutant (∆Bcl-xL) overexpression vectors. The cells were divided into four groups: Control (not subjected to any transfection), EV (empty pcDNA3.1-Bcl-xL vector), OV (Bcl-xL overexpression) and ∆OV (∆Bcl-xL overexpression). Saffron and toluidine blue staining was performed to observe cartilage tissue formation. Flow cytometry was conducted to measure BMSC apoptosis. The expression levels of TGF-β and BMP were evaluated using reverse transcription-quantitative PCR (RT-qPCR) and western blotting. Compared with that in the control group, the expression levels of Bcl-xL in the OV group increased significantly (P<0.05). Western blotting and RT-qPCR results revealed that OV and ∆OV treatment increased the expression levels of TGF-β and BMP in transfected cells, compared to their expression in the control and EV groups (P<0.05). Saffron and toluidine blue staining results showed that cartilage formation was increased in the ∆OV and ∆OV + Bax-/Bak-groups to similar degrees. Cell apoptosis in the ∆OV group did not change compared with that in the control group. The Bcl-xL mutant promoted cartilage differentiation of BMSCs and upregulated TGF-β/BMP expression. This enhancement of chondrogenic differentiation was not related to the expression of Bax and Bak. Taken together, these findings provided for improved application of bone tissue engineering technology in the treatment of articular cartilage defects.
Indexed as
Identifiers
What 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.