دورية أكاديمية

O-Phenanthroline as modulator of the hypoxic and catabolic response in cartilage tissue-engineering models.

التفاصيل البيبلوغرافية
العنوان: O-Phenanthroline as modulator of the hypoxic and catabolic response in cartilage tissue-engineering models.
المؤلفون: Georgi N; Department of Developmental BioEngineering, MIRA Institute for Biomedical Technology and Technical Medicine, University of Twente, Enschede, The Netherlands., Landman EB; Department of Developmental BioEngineering, MIRA Institute for Biomedical Technology and Technical Medicine, University of Twente, Enschede, The Netherlands., Klein TJ; Cartilage Regeneration Laboratory, Institute of Health and Biomedical Innovation, Queensland University of Technology, Kelvin Grove, Australia., van Blitterswijk CA; Department of Tissue Regeneration, MIRA Institute for Biomedical Technology and Technical Medicine, University of Twente, Enschede, The Netherlands., Karperien M; Department of Developmental BioEngineering, MIRA Institute for Biomedical Technology and Technical Medicine, University of Twente, Enschede, The Netherlands.
المصدر: Journal of tissue engineering and regenerative medicine [J Tissue Eng Regen Med] 2017 Mar; Vol. 11 (3), pp. 724-732. Date of Electronic Publication: 2014 Nov 21.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: John Wiley & Sons Country of Publication: England NLM ID: 101308490 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1932-7005 (Electronic) Linking ISSN: 19326254 NLM ISO Abbreviation: J Tissue Eng Regen Med Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Chichester, West Sussex, UK : John Wiley & Sons
مواضيع طبية MeSH: Models, Biological*, Cartilage, Articular/*pathology , Phenanthrolines/*pharmacology , Tissue Engineering/*methods, Animals ; Cell Count ; Cell Hypoxia/drug effects ; Chondrogenesis/drug effects ; Chondrogenesis/genetics ; Cobalt/pharmacology ; Extracellular Matrix/drug effects ; Extracellular Matrix/metabolism ; Extremities/embryology ; Gene Expression Regulation/drug effects ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Interleukin-1beta/pharmacology ; Male ; Mice ; Middle Aged ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; SOX9 Transcription Factor/genetics ; SOX9 Transcription Factor/metabolism ; Tumor Necrosis Factor-alpha/pharmacology
مستخلص: Hypoxia has been shown to be important for maintaining cartilage homeostasis as well as for inducing chondrogenic differentiation. Ensuring low oxygen levels during in vitro culture is difficult, therefore we assessed the chondro-inductive capabilities of the hypoxia-mimicking agent O-phenanthroline, which is also known as a non-specific matrix metalloproteinase (MMP) inhibitor. We found that O-phenanthroline reduced the expression of MMP3 and MMP13 mRNA levels during chondrogenic differentiation of human chondrocytes (hChs), as well as after TNFα/IL-1β exposure in an explant model. Interestingly, O-phenanthroline significantly inhibited matrix degradation in a TNFα/IL-1β-dependent model of cartilage degeneration when compared to control and natural hypoxia (2.5% O 2 ). O-Phenanthroline had limited ability to improve the chondrogenic differentiation or matrix deposition in the chondrogenic pellet model. Additionally, O-phenanthroline alleviated MMP-induced cartilage degradation without affecting chondrogenesis in the explant culture. The data presented in this study indicate that the inhibitory effect of O-phenanthroline on MMP expression is dominant over the hypoxia-mimicking effect. Copyright © 2014 John Wiley & Sons, Ltd.
(Copyright © 2014 John Wiley & Sons, Ltd.)
فهرسة مساهمة: Keywords: cartilage; chondrogenesis; degradation; differentiation; phenanthroline
المشرفين على المادة: 0 (HIF1A protein, human)
0 (Hypoxia-Inducible Factor 1, alpha Subunit)
0 (Interleukin-1beta)
0 (Phenanthrolines)
0 (RNA, Messenger)
0 (SOX9 Transcription Factor)
0 (Tumor Necrosis Factor-alpha)
3G0H8C9362 (Cobalt)
EVS87XF13W (cobaltous chloride)
W4X6ZO7939 (1,10-phenanthroline)
تواريخ الأحداث: Date Created: 20141122 Date Completed: 20171120 Latest Revision: 20180129
رمز التحديث: 20231215
DOI: 10.1002/term.1969
PMID: 25414128
قاعدة البيانات: MEDLINE
الوصف
تدمد:1932-7005
DOI:10.1002/term.1969