Insulin-like growth factor-1 boosts the developing process of condylar hyperplasia by stimulating chondrocytes proliferation

Chen, Y.; Jin, Ke; Long, Xing; Meng, Qinggong; Deng, Mohong; Fang, Wei; Li, J.; Cai, Hengxing; Chen, S.

doi:10.1016/j.joca.2011.12.013

Cited by 36 publications

(25 citation statements)

References 37 publications

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“…The presence of IGF-1 was found mainly in the proliferative and hypertrophic chondrocyte layer, vice versa only a few in the calcified chondrocyte layer. There was the correlation of IGF-1 gene with age and cartilaginous thickness [4,11,18]. The study of SNPs can help to discover the multifactorial etiologies which interaction among of genetic factors with hormonal, neurological, biochemical, and biomechanical [1,8,10].…”

Section: Discussionmentioning

confidence: 99%

“…IGF-1 gene expression depends on to the etiology of mandibular growth in Class III malocclusion [9,10]. IGF-1 promotes human TMJ cartilage overgrowth in the developing process of condylar hyperplasia by enhancing chondrocytes proliferation through MAPK (Mitogen-activated protein kinase)-eERK pathway [11]. Distribution of IGF-1 in condylar hyperplasia patients has been a complicated expression of facial asymmetry in postnatal growth abnormality of the mandibular condyle [4].…”

Section: Introductionmentioning

confidence: 99%

“…There were 13 tagging SNPs of IGF-1 in that showed a minor allele frequency ≥5% in the association of high myopia of Chinese population and reported that potential SNPs of IGF-1 gene were worthy to be studied related to any phenotype [12,13]. In dentistry, IGF-1 gene expression affects cell growth regulation and proliferation of the affected organs in skeletal maturity, especially in mandibular condylar cartilage which is related to stimulation of proliferation and promoting myoblastic differentiation or osteoblastic tissues [4,11]. TThe similarity of period in mandibular growth and increasing of spinal curve degree in growing subjects as multidisiplinary approched nowadays in treatment of growing subjects.…”

Section: Introductionmentioning

confidence: 99%

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IDENTIFICATION OF SNPs IGF-1 GENE IN VERTICAL MANDIBULAR ASYMMETRY PATIENTS WITH IDIOPATHIC SCOLIOSIS SYMPTOM

Sofyanti

Siregar

Siregar³

et al. 2018

Asian J Pharm Clin Res

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

IDENTIFICATION OF SNPs IGF-1 GENE IN VERTICAL MANDIBULAR ASYMMETRY PATIENTS WITH IDIOPATHIC SCOLIOSIS SYMPTOM

Sofyanti

Siregar

Siregar³

et al. 2018

Asian J Pharm Clin Res

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“…IGF-1 plays an important role in cell proliferation; it is mainly expressed in the liver although also in brain, heart, lung, bone, placenta, and testes and also produced by chondrocytes [72] thus having an autocrine and/or paracrine regulation [73].…”

Section: Insulin-like Growth Factormentioning

confidence: 99%

Current Applications of Mesenchymal Stem Cells for Cartilage Tissue Engineering

Fuentes-Mera¹,

Camacho²,

Moncada‐Saucedo³

et al. 2017

Mesenchymal Stem Cells - Isolation, Characterization and Applications

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Articular cartilage injuries caused by traumatic/mechanical progressive degeneration result in joint pain, swelling, the consequent loss of joint function, and eventually osteoarthritis. Articular tissue possesses a poor ability to regenerate that further complicates the therapeutic approaches. Mesenchymal stem cells (MSCs) have emerged as a promising alternative treatment. Recently, it has been reported that a wide variety of strategies ranging from merely using cells in the injured area to employ biofunctional substitutes in which cells are harmonizing with scafolding and growth factors to create an engineered cartilage tissue.This chapter reviews the state-of the-art in cartilage tissue engineering focused on tissue engineering approaches designed to recapitulate the native development of cartilage and its tridimensional structure as an osteochondral unit. Since the production of hypertrophied tissue is one of the most critical challenges to overcome in chondral tissue regeneration, here we show new strategies to minimize hypertrophy in cartilage. Finally, the eicacy and safety of diferent treatments of cartilage in current clinical trials will be discussed.While the framework provides new features and beneits concerning the strategies for articular tissue regeneration, this chapter presents a set of tools to improve approaches to orthopedic regenerative medicine based on the use of MSCs.Keywords: MSCs, MSCs-subpopulations, cartilage regeneration, cartilage tissue engineering, hypertrophy © 2017 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. IntroductionThe chondrocytes are the only cells found in cartilage. The chondrocytes demonstrate distinctive properties such as being metabolically active in order to maintain the renewal of the extracellular matrix (ECM) by synthesizing collagens, proteoglycans, hyaluronic acid, and glycoproteins. Restoration of the cartilage damage is still challenging for orthopedic medicine due to its poor ability to regenerate [1].Mesenchymal stem cells (MSCs) have potential applications in tissue engineering, and regenerative medicine represents an atractive option for repairing lesions in cartilage. Stem cellbased therapies that harmonize with tissue-engineering technologies, and biomaterials are vital for the continuous advance of cartilage regenerative medicine [2,3].Once the relationship between structure function in normal and damaged tissues is understood and the development of biological substitutes for the repair or regeneration can be reached. To develop a biological substitute, tissue engineering uses scafolds, cells, and growth factors. Each of these elements alone is able to promote tissue regeneration, but composites fabricated in combination would be more efective [4,5].The objective of the present chapter is, therefore, t...

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“…A study by Fu confirmed that cyclic mechanical stretch-enhanced myoblast proliferation was dependent on activated IGF-1R [7]. IGF-1R has been shown to play a vital role in the modulation of chondrocyte activity and functions following chemical stimuli [8]. However, it is presently obscure whether IGF-1R is involved in modulating mechanical stress-initiated mitogenic effects in chondrocytes.…”

Section: Introductionmentioning

confidence: 98%

Periodic Mechanical Stress Stimulates Cav-1-Dependent IGF-1R Mitogenic Signals in Rat Chondrocytes Through ERK1/2

Tang

Jiang

Sun

et al. 2018

Cell Physiol Biochem

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Background/Aims: The biological effects of periodic mechanical stress on the mitogenesis of chondrocytes have been studied extensively over the past few years. However, the mechanisms underlying the ability of chondrocytes to sense and respond to mechanical stimuli remain to be determined. In the current study, we analyzed the mechanisms by which periodic mechanical stress is translated into biochemical signals and verified the key role of non-integrin mechanosensors including Caveolin-1 (Cav-1), and insulin-like growth factor-1 receptor (IGF-1R) in chondrocyte proliferation. Methods: Two steps were undertaken in the experiment. In the first step, the cells were maintained under static conditions or periodic mechanical stress for 0 h and 1 h prior to Western blot analysis. In the second step, the cells were pretreated with short hairpin RNA (shRNA) targeted to Cav-1 or IGF-1R or control scrambled shRNA. Moreover, they were pretreated with their selective inhibitors methyl β-cyclodextrin (MCD) or Linsitinib (OSI-906). They were maintained under static conditions or periodic mechanical stress for 1 h prior to Western blot analysis, and for 3 days, 8 h per day, prior to direct cell counting and CCK-8 assay, respectively. Results: Periodic mechanical stress significantly induced sustained phosphorylation of Cav-1 at Tyr 14 and IGF-1R at Tyr 1135/1136 . Proliferation was inhibited by pretreatment with Cav-1 inhibitor MCD and by shRNA targeted to Cav-1 in chondrocytes in response to periodic mechanical stress. Meantime, MCD and shRNA targeted to Cav-1 also attenuated IGF-1R, and extracellular signal-regulated kinase (ERK)1/2 activation. In addition, inhibiting IGF-1R activity by Linsitinib and shRNA targeted to

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Insulin-like growth factor-1 boosts the developing process of condylar hyperplasia by stimulating chondrocytes proliferation

Abstract: IGF-1 promotes human TMJ cartilage overgrowth in the developing process of CH by enhancing chondrocytes proliferation via MAPK-ERK pathway.

Cited by 36 publications

References 37 publications

IDENTIFICATION OF SNPs IGF-1 GENE IN VERTICAL MANDIBULAR ASYMMETRY PATIENTS WITH IDIOPATHIC SCOLIOSIS SYMPTOM

IDENTIFICATION OF SNPs IGF-1 GENE IN VERTICAL MANDIBULAR ASYMMETRY PATIENTS WITH IDIOPATHIC SCOLIOSIS SYMPTOM

Current Applications of Mesenchymal Stem Cells for Cartilage Tissue Engineering

Periodic Mechanical Stress Stimulates Cav-1-Dependent IGF-1R Mitogenic Signals in Rat Chondrocytes Through ERK1/2

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