Localization of chondromodulin-I at the feto-maternal interface and its inhibitory actions on trophoblast invasion in vitro

Miura, Shigenori; Shukunami, Chisa; Mitsui, Kaori; Kondo, Jun; Hiraki, Yuji

doi:10.1186/1471-2121-12-34

Cited by 7 publications

(3 citation statements)

References 37 publications

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“…Further, hypoxia-associated reduced expression of Chm-1 might also be a factor for mid-to-late valve disease progression [58]. During implantation, Chm-1 was shown to have an inhibitory effect on trophoblast migration and invasion, which implies that Chm-1 may affect the regulation of tissue differentiation and angiogenesis during embryonic development [59]. Further studies are required to advance our understanding of the role of Chm-1 in the development of infective endocarditis, and embryogenesis.…”

Section: The Role Of Chm-1 In Cancer and Heart Diseasementioning

confidence: 99%

Chondromodulin-1 in health, osteoarthritis, cancer, and heart disease

Zhu

Qiu

Bennett

et al. 2019

Cell. Mol. Life Sci.

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The human chondromodulin-1 (Chm-1, Chm-I, CNMD, or Lect1) gene encodes a 334 amino acid type II transmembrane glycoprotein protein with characteristics of a furin cleavage site and a putative glycosylation site. Chm-1 is expressed most predominantly in healthy and developing avascular cartilage, and healthy cardiac valves. Chm-1 plays a vital role during endochondral ossification by the regulation of angiogenesis. The anti-angiogenic and chondrogenic properties of Chm-1 are attributed to its role in tissue development, homeostasis, repair and regeneration, and disease prevention. Chm-1 promotes chondrocyte differentiation, and is regulated by versatile transcription factors, such as Sox9, Sp3, YY1, p300, Pax1, and Nkx3.2. Decreased expression of Chm-1 is implicated in the onset and progression of osteoarthritis and infective endocarditis. Chm-1 appears to attenuate osteoarthritis progression by inhibiting catabolic activity, and to mediate anti-inflammatory effects. In this review, we present the molecular structure and expression profiling of Chm-1. In addition, we bring a summary to the potential role of Chm-1 in cartilage development and homeostasis, osteoarthritis onset and progression, and to the pathogenic role of Chm-1 in infective endocarditis and cancers. To date, knowledge of the Chm-1 receptor, cellular signalling, and the molecular mechanisms of Chm-1 is rudimentary. Advancing our understanding the role of Chm-1 and its mechanisms of action will pave the way for the development of Chm-1 as a therapeutic target for the treatment of diseases, such as osteoarthritis, infective endocarditis, and cancer, and for potential tissue regenerative bioengineering applications.

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Section: The Role Of Chm-1 In Cancer and Heart Diseasementioning

confidence: 99%

Chondromodulin-1 in health, osteoarthritis, cancer, and heart disease

Zhu

Qiu

Bennett

et al. 2019

Cell. Mol. Life Sci.

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“…Cnmd is a protein primarily expressed in healthy adult cartilage and is notably present in the avascular cartilage during endochondral bone formation [ 6 , 10 , 11 ]. While its predominant expression is observed in cartilage, Cnmd has also been found in various other tissues, such as cardiac valves [ 68 ], intervertebral discs [ 6 , 69 ], thymus [ 70 ], retina [ 71 , 72 ], and in the decidua during the early implantation period in mice [ 73 ] ( Figure 6 ).…”

Section: Cnmd: Gene and Proteinmentioning

confidence: 99%

A Narrative Review of the Roles of Chondromodulin-I (Cnmd) in Adult Cartilage Tissue

Reyes Alcaraz,

Pattappa,

Miura

et al. 2024

IJMS

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Articular cartilage is crucial for joint function but its avascularity limits intrinsic repair, leading to conditions like osteoarthritis (OA). Chondromodulin-I (Cnmd) has emerged as a key molecule in cartilage biology, with potential implications for OA therapy. Cnmd is primarily expressed in cartilage and plays an important role in chondrocyte proliferation, cartilage homeostasis, and the blocking of angiogenesis. In vivo and in vitro studies on Cnmd, also suggest an involvement in bone repair and in delaying OA progression. Its downregulation correlates with OA severity, indicating its potential as a therapeutic target. Further research is needed to fully understand the mode of action of Cnmd and its beneficial implications for managing OA. This comprehensive review aims to elucidate the molecular characteristics of Cnmd, from its expression pattern, role in cartilage maintenance, callus formation during bone repair and association with OA.

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“…ChM‐I inhibits the chemotactic migration of endothelial cells by destabilizing the actin cytoskeleton and lamellipodial extension 18. Thus, ChM‐I is considered to be responsible for the avascular nature of cartilage, cardiac valves, decidua, and the eye 13, 19, 20. However, the role, function, and distribution of ChM‐I is unclear in the meniscus.…”

mentioning

confidence: 99%

Chondromodulin‐I derived from the inner meniscus prevents endothelial cell proliferation

Fujii

Furumatsu

Yokoyama

et al. 2012

Journal Orthopaedic Research

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The meniscus is a fibrocartilaginous tissue that plays an important role in controlling complex biomechanics of the knee. A perimeniscal capillary plexus supplies the outer meniscus, whereas the inner meniscus is composed of avascular tissue. Anti-angiogenic molecules, such as chondromodulin-I (ChM-I) and endostatin, have pivotal roles in preserving the avascularity of cartilage. However, the anti-angiogenic role of ChM-I is unclear in the meniscus. We hypothesized that the inner meniscus might maintain its avascular feature by expressing ChM-I. Immunohistochemical analyses revealed that ChM-I was mainly detected in the inner and superficial zones of the meniscus. On the other hand, endostatin distribution was similar between the inner and outer meniscus. In Western blot, ChM-I was detected only in the inner meniscus, whereas endostatin was equally observed in both inner and outer menisci. In addition, ChM-I concentration of the inner meniscus-derived conditioned medium was higher than that of the outer meniscusderived medium. ChM-I removal from the inner meniscus-derived medium and functional blocking of ChM-I significantly increased endothelial cell proliferation. In this study, we demonstrated that the inner meniscus contained larger amounts of ChM-I, and that the inner meniscus-derived ChM-I inhibited endothelial cell proliferation. Our results suggest that ChM-I may be a key anti-angiogenic factor for maintaining the avascularity of the inner meniscus. ß

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Localization of chondromodulin-I at the feto-maternal interface and its inhibitory actions on trophoblast invasion in vitro

Cited by 7 publications

References 37 publications

Chondromodulin-1 in health, osteoarthritis, cancer, and heart disease

Chondromodulin-1 in health, osteoarthritis, cancer, and heart disease

A Narrative Review of the Roles of Chondromodulin-I (Cnmd) in Adult Cartilage Tissue

Chondromodulin‐I derived from the inner meniscus prevents endothelial cell proliferation

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