Autor: |
Wei-Chi Hsieh, Kuan-Hsing Chen, Yi-Wen Chuang, C.H. Lin, Heng-Jung Hsu |
Rok vydání: |
2018 |
Předmět: |
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Zdroj: |
Annals of Physical and Rehabilitation Medicine. 61:e416 |
ISSN: |
1877-0657 |
DOI: |
10.1016/j.rehab.2018.05.969 |
Popis: |
Introduction/Background Lysophosphatidic acid (LPA) is a natural form of phospholipids contained in platelet-rich plasma (PRP), which is often used in treating osteoarthritis. Abnormal synovial fluid production is related to osteoarthritis, which may due to dysregulated vascular permeability mediated by synoviocytes related angiogenesis factors expression. In this study, we investigated the effect of LPA on the angiogenic factors expression in synoviocytes from normal and osteoarthritis tissue. Material and method Primary culture of human fibroblast-like synoviocytes (HFLS) from normal (N) and osteoarthritis (OA) tissue and human umbilical vein endothelial cells (HUVEC) were used in this study. The expression patterns of LPA receptors on HFLS-N and HFLS-OA were determined by qRT-PCR. The effect of LPA on the angiogenetic capability was evaluated by determining the effect of conditioned medium from LPA treated HFLS-N and HFLS-OA on HUVEC endothelial cell permeability and tube formation assays. Specific LPA modulated angiogenetic factors were screened by angiogenesis protein array and confirmed by ELISA. The role of specific angiogenesis protein was confirmed by recombinant protein. Results The expression levels of LPA specific receptors between HFLS-N and HFLS-OA are different. LPA may enhance the angiogenesis effect of HFLS-N but not in HFLS-OA on endothelial cell permeability and tube formation on the matrix gel. Meanwhile, the LPA activated angiogenesis related factors MMP-9, IGFBP-1 and Prolactin are at least partly involved in promoting the angiogenetic capability of HFLS-N. Conclusion HFLS-OA may lose the ability to express MMP-9, IGFBP-1 and Prolactin. The clinical significances of MMP-9, IGFBP-1 and Prolactin need further investigations. |
Databáze: |
OpenAIRE |
Externí odkaz: |
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