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[ subject:"Biomedical engineering." ]
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Co-delivering Lysophosphatidic Acid ...
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Wilkinson, Miles Walter.
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Co-delivering Lysophosphatidic Acid With Adipose-derived Stromal Cells to Improve Survival and Contributions to Bone Regeneration.
紀錄類型:
書目-電子資源 : Monograph/item
正題名/作者:
Co-delivering Lysophosphatidic Acid With Adipose-derived Stromal Cells to Improve Survival and Contributions to Bone Regeneration./
作者:
Wilkinson, Miles Walter.
面頁冊數:
107 p.
附註:
Source: Masters Abstracts International, Volume: 53-03.
Contained By:
Masters Abstracts International53-03(E).
標題:
Biomedical engineering. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=1560236
ISBN:
9781321024418
Co-delivering Lysophosphatidic Acid With Adipose-derived Stromal Cells to Improve Survival and Contributions to Bone Regeneration.
Wilkinson, Miles Walter.
Co-delivering Lysophosphatidic Acid With Adipose-derived Stromal Cells to Improve Survival and Contributions to Bone Regeneration.
- 107 p.
Source: Masters Abstracts International, Volume: 53-03.
Thesis (M.S.)--University of California, Davis, 2014.
This item is not available from ProQuest Dissertations & Theses.
Skeletal grafts containing osteogenically pre-differentiated adipose derived stromal cells are an attractive means of regenerating critical size defects. Yet, a defect's ischemic milieu often leads to a loss of implant efficacy marked by diminished cell function and apoptosis. We hypothesized that the adjuvant delivery of lysophosphatidic acid (LPA) would protect adipose derived stromal cells (ASC) from serum deprivation/hypoxia (SD/H) induced apoptosis, thereby enhancing their contributions to bone repair. Human ASC were osteogenically induced for 7 days and their resistance to apoptosis, pro-angiogenic, and osteogenic potential was examined in the presence of LPA in SD/H conditions in vitro. LPA receptor expression was upregulated in SD/H. The presentation of 25 microM LPA reduced vulnerability of ASC to apoptosis while retaining vascular endothelial growth factor (VEGF) secretion. SD/H-induced reduction in the osteogenic differentiation marker alkaline phosphatase was not abrogated by the addition of LPA. Syngeneic ASC were subsequently delivered into a rat calvarial defect in LPA-loaded fibrin gels to assess its capacity to potentiate bone healing. Bone formation quantified at 4 and 12 weeks using microcomputed tomography indicated no early differences in bone volume or density. Laser Doppler perfusion imaging did not reveal any perfusion differences. Cytochemical staining analysis and fluorescent microscopy revealed no differences in cell persistence between groups but did show that cell proximity coincide with the deposition of collagen. These results indicate that LPA elicits SD/H-induced apoptosis protection and signals VEGF secretion in vitro, but these benefits did not translate toward the survival of ASC and contributions to bone formation.
ISBN: 9781321024418Subjects--Topical Terms:
535387
Biomedical engineering.
Co-delivering Lysophosphatidic Acid With Adipose-derived Stromal Cells to Improve Survival and Contributions to Bone Regeneration.
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Skeletal grafts containing osteogenically pre-differentiated adipose derived stromal cells are an attractive means of regenerating critical size defects. Yet, a defect's ischemic milieu often leads to a loss of implant efficacy marked by diminished cell function and apoptosis. We hypothesized that the adjuvant delivery of lysophosphatidic acid (LPA) would protect adipose derived stromal cells (ASC) from serum deprivation/hypoxia (SD/H) induced apoptosis, thereby enhancing their contributions to bone repair. Human ASC were osteogenically induced for 7 days and their resistance to apoptosis, pro-angiogenic, and osteogenic potential was examined in the presence of LPA in SD/H conditions in vitro. LPA receptor expression was upregulated in SD/H. The presentation of 25 microM LPA reduced vulnerability of ASC to apoptosis while retaining vascular endothelial growth factor (VEGF) secretion. SD/H-induced reduction in the osteogenic differentiation marker alkaline phosphatase was not abrogated by the addition of LPA. Syngeneic ASC were subsequently delivered into a rat calvarial defect in LPA-loaded fibrin gels to assess its capacity to potentiate bone healing. Bone formation quantified at 4 and 12 weeks using microcomputed tomography indicated no early differences in bone volume or density. Laser Doppler perfusion imaging did not reveal any perfusion differences. Cytochemical staining analysis and fluorescent microscopy revealed no differences in cell persistence between groups but did show that cell proximity coincide with the deposition of collagen. These results indicate that LPA elicits SD/H-induced apoptosis protection and signals VEGF secretion in vitro, but these benefits did not translate toward the survival of ASC and contributions to bone formation.
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