A Novel Role for Adipose Ephrin-B1 in Inflammatory Response

Mori, Takuya; Maeda, Norikazu; Inoue, Kana; Sekimoto, Ryohei; Tsushima, Yu; Matsuda, Koichiro; Yamaoka, Mitsuaki; Suganami, Takayoshi; Nishizawa, Hitoshi; Ogawa, Yoshihiro; Funahashi, Tohru; Shimomura, Iichiro

doi:10.1371/journal.pone.0076199

Cited by 19 publications

(16 citation statements)

References 37 publications

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“…Isolation of total RNA and synthesis of cDNA were performed as described elsewhere (28). Real‐time quantitative PCR was performedwith the ViiATM7 real‐time PCR system (Thermo Fisher Scientific) using Power SYBR green PCR master mix (Thermo Fisher Scientific), according to the manufacturer's instruction.…”

Section: Methodsmentioning

confidence: 99%

Adiponectin association with T‐cadherin protects against neointima proliferation and atherosclerosis

et al. 2017

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Adiponectin, an adipocyte-derived protein abundant in the circulation, is thought to be protective against atherosclerosis. However, it is not fully understood how the association of adiponectin with vascular cells and its antiatherogenic effect are connected. In this study, T-cadherin was essential for accumulation of adiponectin in the neointima and atherosclerotic plaque lesions, and the adiponectin-T-cadherin association protected against vascular injury. In the apolipoprotein E-knockout (ApoE-KO) mice, adiponectin and T-cadherin colocalized on endothelial cells and synthetic smooth muscle cells in the aortic intima. Notably, aortic adiponectin protein disappeared in T-cadherin/ApoE double-knockout (Tcad/ApoE-DKO) mice with significant elevation of blood adiponectin concentration. Furthermore, in Tcad/ApoE-DKO mice, carotid artery ligation resulted in a significant increase of neointimal thickness compared with ApoE-KO mice. Finally, on a high-cholesterol diet, Tcad/ApoE-DKO mice increased atherosclerotic plaque formation, despite a 5-fold increase in plasma adiponectin level compared with that in ApoE-KO mice. , knockdown of T-cadherin from human aortic smooth muscle cells (HASMCs) with synthetic phenotype significantly reduced adiponectin accumulation on HASMCs and negated the inhibitory effect of adiponectin on proinflammatory change. Collective evidence showed that adiponectin accumulates in the vasculature T-cadherin, and the adiponectin-T-cadherin association plays a protective role against neointimal and atherosclerotic plaque formations.-Fujishima, Y., Maeda, N., Matsuda, K., Masuda, S., Mori, T., Fukuda, S., Sekimoto, R., Yamaoka, M., Obata, Y., Kita, S., Nishizawa, H., Funahashi, T., Ranscht, B., Shimomura, I. Adiponectin association with T-cadherin protects against neointima proliferation and atherosclerosis.

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Section: Methodsmentioning

confidence: 99%

Adiponectin association with T‐cadherin protects against neointima proliferation and atherosclerosis

et al. 2017

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“…EFNB1 has several basic functions in cell adhesion, migration, and patterning 15 – 18 to regulate many developmental roles, including bone formation, 19 , 20 skeletogenesis, 21 neuronal wiring, 22 , 23 angiogenesis, 24 and retinocollicular mapping, 25 in addition to disease monitoring such as inflammation 26 and blood pressure monitoring. 27 Previous characterization of the EFNB1 protein structure 28 enabled the location of the highly conserved arginine to be determined within the essential receptor-binding domain in the extracellular region.…”

Section: Discussionmentioning

confidence: 99%

Isolated Sagittal Synostosis in a Boy with Craniofrontonasal Dysplasia and a Novel EFNB1 Mutation

Chauhan¹,

Hoover

Scanga

et al. 2015

Plastic and Reconstructive Surgery - Global Open

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Summary:Craniofrontonasal syndrome (CFNS) is a rare X-linked disorder that shows greater severity in females and is largely attributed to mutations in EFNB1. A 7-year-old boy presented with hypertelorism, broad nasal root, midfacial hypoplasia, mandibular prognathia, ptosis, and scaphocephaly was clinically diagnosed with CFNS. Three-dimensional computed tomographic scans confirmed the isolated sagittal synostosis. His mother also showed clinical features of CFNS, but less severe. Genetic tests uncovered a novel C to T mutation at nucleotide 466 (c.466C>T) in exon 1 of EFNB1 for both. To the best of our knowledge, this is the only reported incident of CFNS in a male child exhibiting isolated sagittal synostosis.

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“…Moreover, Eph-ephrin communication has been reported in white adipose tissue, where ephrin-A4 and ephrin-A5 were found to be a downstream signaling pathway to aldehyde dehydrogenase, which stimulates the development and innervation of white adipose tissue (Shen et al, 2018 ). Also, ephrin-B1 was identified to be down-regulated in mature adipocytes of obese mice and shown to suppress the adipose inflammatory response (Mori et al, 2013 ).…”

Section: The Role Of Eph-ephrin Signaling Within the Mesenchymal Linementioning

confidence: 99%

Eph-Ephrin Signaling Mediates Cross-Talk Within the Bone Microenvironment

Arthur

Gronthos

2021

Front. Cell Dev. Biol.

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Skeletal integrity is maintained through the tightly regulated bone remodeling process that occurs continuously throughout postnatal life to replace old bone and to repair skeletal damage. This is maintained primarily through complex interactions between bone resorbing osteoclasts and bone forming osteoblasts. Other elements within the bone microenvironment, including stromal, osteogenic, hematopoietic, endothelial and neural cells, also contribute to maintaining skeletal integrity. Disruption of the dynamic interactions between these diverse cellular systems can lead to poor bone health and an increased susceptibility to skeletal diseases including osteopenia, osteoporosis, osteoarthritis, osteomalacia, and major fractures. Recent reports have implicated a direct role for the Eph tyrosine kinase receptors and their ephrin ligands during bone development, homeostasis and skeletal repair. These membrane-bound molecules mediate contact-dependent signaling through both the Eph receptors, termed forward signaling, and through the ephrin ligands, referred to as reverse signaling. This review will focus on Eph/ ephrin cross-talk as mediators of hematopoietic and stromal cell communication, and how these interactions contribute to blood/ bone marrow function and skeletal integrity during normal steady state or pathological conditions.

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A Novel Role for Adipose Ephrin-B1 in Inflammatory Response

Cited by 19 publications

References 37 publications

Adiponectin association with T‐cadherin protects against neointima proliferation and atherosclerosis

Adiponectin association with T‐cadherin protects against neointima proliferation and atherosclerosis

Isolated Sagittal Synostosis in a Boy with Craniofrontonasal Dysplasia and a Novel EFNB1 Mutation

Eph-Ephrin Signaling Mediates Cross-Talk Within the Bone Microenvironment

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