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Adipose-derived stromal vascular fraction prevent bone bridge formation on growth plate injury in rat (in vivo studies) an experimental research.

ABSTRACT: The growth plate is cartilage tissue found at the end of long bones in children, responsible for longitudinal bone growth. Injuries to the growth plate cartilage often lead to unwanted bony repair, resulting in growth disturbances such as limb length discrepancy and angulation deformity in children. There is currently no clinical treatment that can fully repair an injured growth plate. Tissue engineering is promising for regeneration of growth plate. Adipose-derived stromal vascular fraction highlight the promising potential as tissue engineering therapy for inducing regeneration of injured growth plate and able to reduce the formation of bony repair that can lead to deformity and limb length discrepancy. Using an animal model of growth plate injury, bone bridge formation is evaluated after 28 days using Enzyme-linked Immunoassay, radiology, histopathology and Immunofloresence examination. Radiological analyses performed by evaluation of grey value using ImageJ software and diameter bone bridge measured from the end to end distance between uninjured growth plate evaluated by histopatology examination. Enzyme-linked Immunoassay and immunofloresence are used to evaluate chondrocyte and chondrogenic marker within the defect. The result shows in group with Adipose-derived stromal vascular fraction have a significant lower bone bridge formation compare to positive control group. This current study represents the first work that has utilized this animal model to investigate whether Adipose-derived stromal vascular fraction can be used to initiate regeneration at the injured growth plate.

SUBMITTER: Sananta P

PROVIDER: S-EPMC7645312 | biostudies-literature | 2020 Dec

REPOSITORIES: biostudies-literature

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Adipose-derived stromal vascular fraction prevent bone bridge formation on growth plate injury in rat (in vivo studies) an experimental research.

Sananta Panji P I Gede Made Oka Rahaditya R Suryanto Dradjat Prof Respati PR Suroto Heri H Mustamsir Edi E Kalsum Umi U Andarini Sri S

Annals of medicine and surgery (2012) 20200928

The growth plate is cartilage tissue found at the end of long bones in children, responsible for longitudinal bone growth. Injuries to the growth plate cartilage often lead to unwanted bony repair, resulting in growth disturbances such as limb length discrepancy and angulation deformity in children. There is currently no clinical treatment that can fully repair an injured growth plate. Tissue engineering is promising for regeneration of growth plate. Adipose-derived stromal vascular fraction hig ...[more]

PMID: 33194176

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Project description:Human adipose-derived stromal vascular fraction (hSVF) cells are an easily accessible, heterogeneous cell system that can spontaneously self-assemble into functional microvasculatures in vivo. However, the mechanisms underlying vascular self-assembly and maturation are poorly understood, therefore we utilized an in vitro model to identify potential in vivo regulatory mechanisms. We utilized passage one (P1) hSVF because of the rapid UEA1+ endothelium (EC) loss at even P2 culture. We exposed hSVF cells to a battery of angiogenesis inhibitors and found that the pan-Wnt inhibitor IWP2 produced the most significant hSVF-EC networking decrease (~25%). To determine which Wnt isoform(s) and receptor(s) may be involved, hSVF was screened by PCR for isoforms associated with angiogenesis, with only WNT5A and its receptor, FZD4, being expressed for all time points observed. Immunocytochemistry confirmed Wnt5a protein expression by hSVF. To see if Wnt5a alone could restore IWP2-induced EC network inhibition, recombinant human Wnt5a (0-150 ng/ml) was added to IWP2-treated cultures. The addition of rhWnt5a significantly increased EC network area and significantly decreased the ratio of total EC network length to EC network area compared to untreated controls. To determine if Wnt5a mediates in vivo microvascular self-assembly, 3D hSVF constructs containing an IgG isotype control, anti-Wnt5a neutralizing antibody or rhWnt5a were implanted subcutaneously for 2w in immune compromised mice. Compared to IgG controls, anti-Wnt5a treatment significantly reduced vessel length density by ~41%, while rhWnt5a significantly increased vessel length density by ~62%. However, anti-Wnt5a or rhWnt5a did not significantly affect the density of segments and nodes, both of which measure vascular complexity. Taken together, this data demonstrates that endogenous Wnt5a produced by hSVF plays a regulatory role in microvascular self-assembly in vivo. These findings also suggest that manipulating Wnt signaling could enhance control of hSVF vascularization in tissue engineering applications.

Dataset Information

Adipose-derived stromal vascular fraction prevent bone bridge formation on growth plate injury in rat (in vivo studies) an experimental research.

Publications

Adipose-derived stromal vascular fraction prevent bone bridge formation on growth plate injury in rat (in vivo studies) an experimental research.

Similar Datasets

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