CCAAT/Enhancer Binding Protein β Regulates Expression of Indian Hedgehog during Chondrocytes Differentiation

Ushijima, Takahiro; Okazaki, Ken; Tsushima, Hiroyuki; Ishihara, Kazuhíko; Doi, Toshio; Iwamoto, Yukihide

doi:10.1371/journal.pone.0104547

Cited by 10 publications

(9 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, Ihh gene deletion is currently not a therapeutic option as it is lethal in animals. RNA interference (RNAi) provides a means to knockdown Ihh without the severe side effects caused by chemical inhibitors [88]. In the future, it will be necessary to develop a safe and effective RNAi delivery system to target Ihh signaling for preventing and treating OA [89].…”

Section: Molecular Mechanisms Related To Oa Pathogenesismentioning

confidence: 99%

Osteoarthritis Pathogenesis: A Review of Molecular Mechanisms

et al. 2014

View full text Add to dashboard Cite

Osteoarthritis (OA), the most prevalent chronic joint disease, increases in prevalence with age, and affects majority of individuals over the age of 65 and is a leading musculoskeletal cause of impaired mobility in the elderly. Because the precise molecular mechanisms which are involved in the degradation of cartilage matrix and development of OA are poorly understood and there are currently no effective interventions to decelerate the progression of OA or retard the irreversible degradation of cartilage except for total joint replacement surgery. In this paper, the important molecular mechanisms related to OA pathogenesis will be summarized and new insights into potential molecular targets for the prevention and treatment of OA will be provided.

show abstract

Section: Molecular Mechanisms Related To Oa Pathogenesismentioning

confidence: 99%

Osteoarthritis Pathogenesis: A Review of Molecular Mechanisms

et al. 2014

View full text Add to dashboard Cite

show abstract

“…Cebpb -null mice are dwarf and show reduced expression of PHC/HC markers [161]. C/EBPβ was proposed to directly target the genes for the cyclin-dependent kinase inhibitor p57Kip2 and IHH, and to interact with RUNX2 to activate Ihh [161, 162]. C/EBPβ is also produced by ACCs, especially in osteoarthritic lesions, where it could have deleterious effects [161].…”

Section: Basic-domain Transcription Factorsmentioning

confidence: 99%

Transcriptional control of chondrocyte specification and differentiation

Liu

Samsa

Zhou

et al. 2017

Seminars in Cell & Developmental Biology

141

112

View full text Add to dashboard Cite

A milestone in the evolutionary emergence of vertebrates was the invention of cartilage, a tissue that has key roles in modeling, protecting and complementing the bony skeleton. Cartilage is elaborated and maintained by chondrocytes. These cells derive from multipotent skeletal progenitors and they perform highly specialized functions as they proceed through sequential lineage commitment and differentiation steps. They form cartilage primordia, the primary skeleton of the embryo. They then transform these primordia either into cartilage growth plates, temporary drivers of skeletal elongation and endochondral ossification, or into permanent tissues, namely articular cartilage. Chondrocyte fate decisions and differentiated activities are controlled by numerous extrinsic and intrinsic cues, and they are implemented at the gene expression level by transcription factors. The latter are the focus of this review. Meritorious efforts from many research groups have led over the last two decades to the identification of dozens of key chondrogenic transcription factors. These regulators belong to all types of transcription factor families. Some have master roles at one or several differentiation steps. They include SOX9 and RUNX2/3. Others decisively assist or antagonize the activities of these masters. They include TWIST1, SOX5/6, and MEF2C/D. Many more have tissue-patterning roles and regulate cell survival, proliferation and the pace of cell differentiation. They include, but are not limited to, homeodomain-containing proteins and growth factor signaling mediators. We here review current knowledge of all these factors, one superclass, class, and family at a time. We then compile all knowledge into transcriptional networks. We also identify remaining gaps in knowledge and directions for future research to fill these gaps and thereby provide novel insights into cartilage disease mechanisms and treatment options.

show abstract

“…4). Runx2 may interact with CCAAT/enhancer binding protein beta (C/EBPβ) at the putative C/EBPβ responsive element in the Ihh promoter and may thus cooperatively stimulate Ihh expression (Ushijima et al 2014). Embryos that are double heterozygous for Wnt9a and β-catenin have reduced Ihh expression; there is direct interaction between the β-catenin/lymphoid enhancer binding factor 1 (Lef1) complex and the Ihh promoter, suggesting that Ihh expression is regulated by the canonical Wnt signaling pathway (Spater et al 2006).…”

Section: Ihh Signalingmentioning

confidence: 99%

Developmental Regulation of the Growth Plate and Cranial Synchondrosis

Wei

Mishina

et al. 2016

J Dent Res

View full text Add to dashboard Cite

Long bones and the cranial base are both formed through endochondral ossification. Elongation of long bones is primarily through the growth plate, which is a cartilaginous structure at the end of long bones made up of chondrocytes. Growth plate chondrocytes are organized in columns along the longitudinal axis of bone growth. The cranial base is the growth center of the neurocranium. Synchondroses, consisting of mirror-image growth plates, are critical for cranial base elongation and development. Over the last decade, considerable progress has been made in determining the roles of the parathyroid hormone-related protein, Indian hedgehog, fibroblast growth factor, bone morphogenetic protein, and Wnt signaling pathways in various aspects of skeletal development. Furthermore, recent evidence indicates the important role of the primary cilia signaling pathway in bone elongation. Here, we review the development of the growth plate and cranial synchondrosis and the regulation by the above-mentioned signaling pathways, highlighting the similarities and differences between these 2 structures.

show abstract

CCAAT/Enhancer Binding Protein β Regulates Expression of Indian Hedgehog during Chondrocytes Differentiation

Cited by 10 publications

References 33 publications

Osteoarthritis Pathogenesis: A Review of Molecular Mechanisms

Osteoarthritis Pathogenesis: A Review of Molecular Mechanisms

Transcriptional control of chondrocyte specification and differentiation

Developmental Regulation of the Growth Plate and Cranial Synchondrosis

Contact Info

Product

Resources

About