Carboxy-terminal telopeptide levels of type I collagen hydrogels modulated the encapsulated cell fate for regenerative medicine.
Niu C., Xiong Y., Yang L., Xiao X., Yang S., Huang Z.
Laboratory Study, published in Int J Biol Macromol (2022) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Laboratory Study
- Journal
- Int J Biol Macromol (2022)
- Country
- Netherlands
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 36566813
- DOI
- 10.1016/j.ijbiomac.2022.12.186
- Citations
- 5
Abstract (original English)
The cellular microenvironment has a profound impact on cell proliferation, interaction, and differentiation. In cell encapsulation for disease therapy, type I collagen is an important biomaterial due to its ability to mimic the extracellular matrix. Telopeptides (carboxy-terminal, CTX, and amino-terminal, NTX) protruding from the triple helix structure of type I collagen are cross-link sites, but also mediate the signal transmission in tissue homeostasis. It is worth investigating the features of the hydrogel microenvironment shaped by the tissue-derived type I collagen with various telopeptide levels, which is paramount for encapsulated cell development. Here, we found the fate of encapsulated human adipose-derived stem cells (hADSCs) and human umbilical vein endothelial cells (HUVECs) behaved differently towards decreasing CTX levels in the collagen hydrogels. Even among collagen hydrogels with a small magnitude of CTX variation, similar stiffness and microstructure, the apparent CTX modulation on the proliferation, cell-interaction, and genes expression of encapsulated hADSCs, as well as morphology and tubule structure formation of endothelial cells were observed, suggesting the biological roles of CTX and its modulation on microenvironment for cell development.
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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