ArticleBiotechnology letters2023
CD44 mediates hyaluronan to promote the differentiation of human amniotic mesenchymal stem cells into chondrocytes.
Article in Biotechnology letters, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 15 citations in OpenAlex.
- Mucin-typebioRxiv : the preprint server for biology · 2025Article
- Integrated bioinformatics analysis identifies CHAD association with osteoporosis and in vitro chondrogenic effects of Wogonin.Scientific reports · 2025Article
- Review
- Mesenchymal Stem Cells from the Deciduous Tooth Pulp Lose their Ability to Suppress the Differentiation of Dendritic Cells during Long-Term Culturing.Bulletin of experimental biology and medicine · 2024Article
- The Hyaluronan/CD44 Axis: A Double-Edged Sword in Cancer.International journal of molecular sciences · 2023Review
- Extracellular matrix-induced signaling pathways in mesenchymal stem/stromal cells.Cell communication and signaling : CCS · 2023Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
objectivesCD44 is the major receptor for hyaluronan (HA), but its effect on HA-induced differentiation of human amnion mesenchymal stem cells into chondrocytes is unclear. This study aimed to investigate the effects and mechanisms of CD44 in HA-induced chondrogenesis.
methodsImmunocytochemistry and toluidine blue staining were used to assess the secretion of type II collagen and aggrecan, respectively. qRT-PCR and western blotting were performed to evaluate the expression of key genes and proteins.
resultsThe expression of aggrecan and type II collagen was downregulated after using the anti-CD44 antibody (A3D8). The transcriptional levels of chondrocytes‑associated genes SRY‑box transcription factor 9, aggrecan, and collagen type II alpha 1 chain were also decreased. Thus, CD44 may mediate HA-induced differentiation of hAMSCs into chondrocytes. Further investigation indicated that expression of phosphorylated (p)‑Erk1/2 and p‑Smad2 decreased following CD44 inhibition. The changes in the expression of p-Erk1/2 and p-Smad2 were consistent after using the ERK1/2 inhibitor (U0126) and agonist (EGF), respectively. After administering the p-Smad2 inhibitor, the expression levels of p-ERK1/2 and p-Smad2 appeared downregulated. The results showed crosstalk between Erk1/2 and Smad2. Moreover, inhibition of p-Erk1/2 and p-Smad2 significantly reduced the accumulation of aggrecan and type II collagen.
conclusionThese data indicate that CD44 mediates HA-induced differentiation of hAMSCs into chondrocytes by regulating Erk1/2 and Smad2 signaling.
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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 Socratic graph.