Abstract

Background:The delay in wound healing, decrease in the long bones resilience to fracture, and delay in fracture healing are among common complications DM patients, and they still remain as challenging issues to be solved. The mechanism has not been fully understood yet, but high sugar and/or insulin deficiency or unresponsiveness to insulin in blood are potential causes to blame. Extracellular matrix degradation/remodeling is one of the important mechanisms whereby cell differentiation, bone remodeling and wound repair can be regulated. ADAMTS proteins play important roles in cartilage/bone metabolism. This study aimed to determine whether ADAMTS/TIMP proteins were affected by insulin application in OUMS-27 cells.Material and methods:OUMS-27 cells were induced by 10μg/mL insulin for 1,3,7,and 11days. Cells were harvested, mRNA and protein extractions were performed. Total mRNA and cDNA levels were measured by qRT-PCR and protein levels were detected by WB.Results:ADAMTS1,5, and 7 levels were significantly decreased, while TIMP-3 levels were detected increased (mRNA/protein concentrations).Conclusions:Pathologies and disturbances of cartilage/bone metabolism, delayed fracture healing in particular, in patients with DM may result from insulin deficiency. ADAMTS genes that play a role in healing process are increased during insulin deficiency, which consequently interrupts healing process by causing cartilage ECM degradation.

Highlights

  • Glucose is an essential nutrient for metabolism and structural needs for the growth centers of the hyaline cartilage and the bone growth center

  • In order to assess the effects of insulin on ADAMTS gene expression in cultured OUMS-27 cells, Quantitative real-time (qRT)-PCR was performed on mRNA eluted from cell lysate

  • We investigated the effects of insulin in chondrosarcoma cells in vitro

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Summary

Introduction

Glucose is an essential nutrient for metabolism and structural needs for the growth centers of the hyaline cartilage and the bone growth center. It is found that DM decreases the bone formation, results in osteopenia and delayed fracture healing [8]. A disintegrin and metalloproteinase with a thrombospondin type 1 motif (ADAMTS) proteins play important roles in cartilage/bone metabolism. This study aimed to determine whether ADAMTS/Tissue inhibitors of metalloproteinases (TIMP) proteins were affected by insulin application in OUMS-27 (chondrosarcoma) cells. Results: ADAMTS1,5, and 7 levels were significantly decreased, while TIMP-3 levels were detected increased (mRNA/protein concentrations). Conclusion: Pathologies and disturbances of cartilage/bone metabolism, delayed fracture healing in particular, in patients with DM may result from insulin deficiency. ADAMTS genes that play a role in healing process are increased during insulin deficiency, which interrupts healing process by causing cartilage extracellular matrix (ECM) degradation

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