A study on role of triiodothyronine (T3) hormone on the improvement of articular cartilage surface architecture

Jia, Peng; Zhang, Xinglin; Zuo, Hai-ning; Lü, Xing; Gai, Pengzhou

doi:10.1016/j.etp.2017.05.010

Cited by 5 publications

(4 citation statements)

References 22 publications

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“…As mentioned previously, such a strong response in aggrecan and runx2 by HT-2 in comparison to the T 3 effect was surprising, since T 3 is known to induce hypertrophic differentiation. In tissue engineering applications, T 3 has been shown to increase the expression and synthesis of type II collagen [24], and improve articular cartilage surface architecture [25]. As the metabolite of T-2 toxin, it would be reasonable to assume that the HT-2 toxin will share similarity with the T-2 toxin, which leads to cartilage destruction by the degradation of the extracellular matrix [26,27].…”

Section: Discussionmentioning

confidence: 99%

Cytotoxic Properties of HT-2 Toxin in Human Chondrocytes: Could T3 Inhibit Toxicity of HT-2?

Zhang

Shao

Zhang

et al. 2019

Toxins

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Thyroid hormone triiodothyronine (T3) plays an important role in coordinated endochondral ossification and hypertrophic differentiation of the growth plate, while aberrant thyroid hormone function appears to be related to skeletal malformations, osteoarthritis, and Kashin-Beck disease. The T-2 toxin, present extensively in cereal grains, and one of its main metabolites, HT-2 toxin, are hypothesized to be potential factors associated with hypertrophic chondrocyte-related osteochondropathy, known as the Kashin-Beck disease. In this study, we investigated the effects of T3 and HT-2 toxin on human chondrocytes. The immortalized human chondrocyte cell line, C-28/I2, was cultured in four different groups: controls, and cultures with T3, T3 plus HT-2 and HT-2 alone. Cytotoxicity was assessed using an MTT assay after 24-h-exposure. Quantitative RT-PCR was used to detect gene expression levels of collagen types II and X, aggrecan and runx2, and the differences in runx2 were confirmed with immunoblot analysis. T3 was only slightly cytotoxic, in contrast to the significant, dose-dependent cytotoxicity of HT-2 alone at concentrations ≥ 50 nM. T3, together with HT-2, significantly rescued the cytotoxic effect of HT-2. HT-2 induced significant increases in aggrecan and runx2 gene expression, while the hypertrophic differentiation marker, type X collagen, remained unchanged. Thus, T3 protected against HT-2 induced cytotoxicity, and HT-2 was an inducer of the pre-hypertrophic state of the chondrocytes.

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Section: Discussionmentioning

confidence: 99%

Cytotoxic Properties of HT-2 Toxin in Human Chondrocytes: Could T3 Inhibit Toxicity of HT-2?

Zhang

Shao

Zhang

et al. 2019

Toxins

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“… 143 Thyroxine, triiodothyronine, and IL-1β have also been employed to promote hypertrophic markers' expression or improve cartilage remodeling. 42 , 144 , 145 Of note, previously to the hypertrophic stimulus, it is required that MSCs differentiate into chondrocytes to create the cartilaginous template. For that, MSCs are required to be in a 3D environment, which can be achieved by creating cell aggregates or seeding MSCs in 3D bioengineered matrices.…”

Section: Design Principles For Endochondral Tissue Engineeringmentioning

confidence: 99%

Close-to-native bone repair via tissue-engineered endochondral ossification approaches

Nadine¹,

Fernandes²,

Correia³

et al. 2022

iScience

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“…Thyroid hormone and T 3 have been shown to induce morphological and hypertrophic marker expression without inducing proliferation. 167 Furthermore, inflammatory cytokines, such as interleukin-1β, have been used to induce inflammation to improve hypertrophic cartilaginous construct remodeling into bone tissue without hampering mineralization. 29,168 Endochondral priming duration.…”

Section: Optimal Endochondral Priming Medium and Durationmentioning

confidence: 99%

Bone defect reconstruction via endochondral ossification: A developmental engineering strategy

Liu

Yan

et al. 2021

J Tissue Eng

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Traditional bone tissue engineering (BTE) strategies induce direct bone-like matrix formation by mimicking the embryological process of intramembranous ossification. However, the clinical translation of these clinical strategies for bone repair is hampered by limited vascularization and poor bone regeneration after implantation in vivo. An alternative strategy for overcoming these drawbacks is engineering cartilaginous constructs by recapitulating the embryonic processes of endochondral ossification (ECO); these constructs have shown a unique ability to survive under hypoxic conditions as well as induce neovascularization and ossification. Such developmentally engineered constructs can act as transient biomimetic templates to facilitate bone regeneration in critical-sized defects. This review introduces the concept and mechanism of developmental BTE, explores the routes of endochondral bone graft engineering, highlights the current state of the art in large bone defect reconstruction via ECO-based strategies, and offers perspectives on the challenges and future directions of translating current knowledge from the bench to the bedside.

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A study on role of triiodothyronine (T3) hormone on the improvement of articular cartilage surface architecture

Cited by 5 publications

References 22 publications

Cytotoxic Properties of HT-2 Toxin in Human Chondrocytes: Could T3 Inhibit Toxicity of HT-2?

Cytotoxic Properties of HT-2 Toxin in Human Chondrocytes: Could T3 Inhibit Toxicity of HT-2?

Close-to-native bone repair via tissue-engineered endochondral ossification approaches

Bone defect reconstruction via endochondral ossification: A developmental engineering strategy

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