1,4-Butanediol diglycidyl ether-cross-linked hyaluronan inhibits fibrosis in rat primary tenocytes by down-regulating autophagy modulation.

Abstract

Epidural fibrosis, an inevitable part of the postoperative healing process, is one of the important causes of failed back surgery syndrome after spinal surgery. The aim of this study was to examine the inhibitory effect of a novel material 1,4-butanediol diglycidyl ether-cross-linked hyaluronan (cHA) on fibrosis in primary tenocytes. cHA inhibited migration, cell proliferation, and suppressed the expression of fibronectin, but not transforming growth factor-β, in primary tenocytes. cHA significantly increased matrix metalloproteinase-3 but decreased collagen-1 and microtubule-associated protein light chain 3-II expression in a dose-dependent manner compared with control groups. We therefore concluded that suppressing autophagy activity may be involved in the anti-fibrotic effect of cHA in primary tenocytes. Further, cHA may have the potential for preventing epidural fibrosis and subsequent failed back syndrome in patients with laminectomy in the future.

• Authors: Dur-Zong Hsu, I-Ming Jou
• Journal: Journal of materials science. Materials in medicine (J Mater Sci Mater Med) Vol. 27 Issue 5 Pg. 84 (May 2016) ISSN: 1573-4838 [Electronic] United States
• PMID: 26968759 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Butylene Glycols
• Collagen Type I
• Hyaluronic Acid
• 1,4-bis(2,3-epoxypropoxy)butane
• Matrix Metalloproteinase 3

Topics

• Animals
• Autophagy (drug effects)
• Butylene Glycols (chemistry, pharmacology)
• Cell Movement
• Collagen Type I (genetics, metabolism)
• Dose-Response Relationship, Drug
• Down-Regulation
• Fibrosis
• Gene Expression Regulation (drug effects)
• Hyaluronic Acid (chemistry, pharmacology)
• Materials Testing
• Matrix Metalloproteinase 3 (genetics, metabolism)
• Rats
• Tenocytes (drug effects)