Corin is a key regulator of endochondral ossification and bone development via modulation of vascular endothelial growth factor A expression.
Nordberg RC., Wang H., Wu Q., Loboa EG.
Animal Study on Cartilage Damage, published in J Tissue Eng Regen Med (2018) — 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
- Animal Study
- Journal
- J Tissue Eng Regen Med (2018)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 30352487
- DOI
- 10.1002/term.2760
- Citations
- 8
Abstract (original English)
Corin has been studied extensively within the vascular system and is known to regulate blood pressure. We have shown that corin is one of the most highly upregulated genes during osteogenic differentiation of human adipose-derived stem cells (hASCs). This study tested the hypothesis that, through modulation of angiogenic signalling pathways, corin is a critical regulator of osteogenic differentiation and endochondral ossification. In vitro, corin expression in hASC was suppressed via siRNA knockdown and vascular endothelial growth factor A (VEGF-A) expression was quantified via reverse transcription polymerase chain reaction. In vivo, a murine corin knockout model (female, 10 weeks) was used to determine the effect of corin deficiency on long bone development. Wild-type and corin knockout long bones were compared via haematoxylin and eosin staining to assess tissue characteristics and cellular organization, three-point bending to assess mechanical characteristics, and immunohistochemistry to visualize VEGF-A expression patterns. Corin knockdown significantly (p < 0.05) increased VEGF-A mRNA expression during osteogenic differentiation. In vivo, corin knockout reduced tibial growth plate thickness (p < 0.01) and severely diminished the hypertrophic region. Corin knockout femurs had significantly increased stiffness (p < 0.01) and maximum loads (p < 0.01) but reduced postyield de
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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