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Effect of Conditioned Medium from IGF1-Induced Human Wharton's Jelly Mesenchymal Stem Cells (IGF1-hWJMSCs-CM) on Osteoarthritis.


ABSTRACT: Background:Osteoarthritis (OA) is a chronic disease that attacks joints and bones which can be caused by trauma or other joint diseases. Stem cell and Conditioned Medium (CM) of stem cells are developed for OA therapy, which is minimally invasive. It can decrease inflammation and be a replacement for knee surgery. This study aimed to utilize human Wharton's Jelly-Mesenchymal Stem Cells (hWJMSCs) as an alternative OA therapy. Methods:CM from hWJMSCs induced by IGF1 was collected. The OA cells model (IL1?-CHON002) culture was treated as follows: 1) with hWJMSCs-CM 15% (v/v); 2) with hWJMSCs-CM 30% (v/v); 3) with IGF1-hWJMSCs (IGF1-hWJMSCs-CM) 15% (v/v); 4) with IGF1-hWJMSCs-CM 30% (v/v). Parameters including inflammatory cytokines (IL10 and TNF?), extracellular matrix degradation (MMP3 expression), and chondrogenic marker (COL2 expression) were determined. Results:The most significant increase in COL2 chondrogenic markers was found in IL1?-CHON002 treatment using 15% CM of hWJMSCs induced with IGF1. CM of hWJMSCs can reduce inflammatory cytokines (TNF? and IL10) and matrix degradation mediator MMP3. Better result was gained from IGF1-induced hWJMSCs-CM. Conclusion:CM of IGF1-hWJMSCs reduce inflammation while repairing injured joint in the human chondrocyte OA model.

SUBMITTER: Kusuma HSW 

PROVIDER: S-EPMC7368112 | biostudies-literature | 2020 Jul-Sep

REPOSITORIES: biostudies-literature

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<h4>Background</h4>Osteoarthritis (OA) is a chronic disease that attacks joints and bones which can be caused by trauma or other joint diseases. Stem cell and Conditioned Medium (CM) of stem cells are developed for OA therapy, which is minimally invasive. It can decrease inflammation and be a replacement for knee surgery. This study aimed to utilize human Wharton's Jelly-Mesenchymal Stem Cells (hWJMSCs) as an alternative OA therapy.<h4>Methods</h4>CM from hWJMSCs induced by IGF1 was collected. T  ...[more]

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