Role of notch-1 intracellular domain in activation of rheumatoid synoviocytes

Nakazawa, Minako; Ishii, Hidetoki; Aono, Hiroyuki; Takai, Miwa; Honda, Tomohiro; Aratani, Satoko; Fukamizu, Akiyoshi; Nakamura, Hiroshi; Yoshino, Shinichi; Kobata, Tetsuji; Nishioka, Kusuki; Nakajima, Takeshi

doi:10.1002/1529-0131(200107)44:7<1545::aid-art278>3.0.co;2-q

Cited by 62 publications

(48 citation statements)

References 36 publications

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“…AOS is an autosomal dominant disorder caused by mutations in RBPJ and/or NOTCH1 genes resulting in Notch LOF, although no additional molecular mechanisms underlying this disease are known (Hassed et al, 2012;Stittrich et al, 2014). Notch signaling defects, either GOF or LOF, have also been implicated in osteoarthritis (Mahjoub et al, 2012;Hosaka et al, 2013;Mirando et al, 2013;Sassi et al, 2014;Liu et al, 2015), rheumatoid arthritis (Nakazawa et al, 2001;Park et al, 2015) and osteoporosis (Engin et al, 2008;Hilton et al, 2008;Majewski et al, 2011;Simpson et al, 2011), and have been associated with a predisposition to pathologic fractures (Kung et al, 2010). Studies like the one presented here further our understanding of the molecular players and events that Notch signaling might control during normal skeletal development, as well as our understanding of how they contribute to the pathology of certain skeletal diseases and injury processes.…”

Section: Discussionsupporting

confidence: 90%

HES factors regulate specific aspects of chondrogenesis and chondrocyte hypertrophy during cartilage development

Rutkowski

Kohn

Sharma

et al. 2016

Journal of Cell Science

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RBPjκ-dependent Notch signaling regulates multiple processes during cartilage development, including chondrogenesis, chondrocyte hypertrophy and cartilage matrix catabolism. Select members of the HES-and HEY-families of transcription factors are recognized Notch signaling targets that mediate specific aspects of Notch function during development. However, whether particular HES and HEY factors play any role(s) in the processes during cartilage development is unknown. Here, for the first time, we have developed unique in vivo genetic models and in vitro approaches demonstrating that the RBPjκ-dependent Notch targets HES1 and HES5 suppress chondrogenesis and promote the onset of chondrocyte hypertrophy. HES1 and HES5 might have some overlapping function in these processes, although only HES5 directly regulates Sox9 transcription to coordinate cartilage development. HEY1 and HEYL play no discernable role in regulating chondrogenesis or chondrocyte hypertrophy, whereas none of the HES or HEY factors appear to mediate Notch regulation of cartilage matrix catabolism. This work identifies important candidates that might function as downstream mediators of Notch signaling both during normal skeletal development and in Notch-related skeletal disorders.

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Section: Discussionsupporting

confidence: 90%

HES factors regulate specific aspects of chondrogenesis and chondrocyte hypertrophy during cartilage development

Rutkowski

Kohn

Sharma

et al. 2016

Journal of Cell Science

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“…In addition, it was recently reported that RSF expressed high levels of both Wnt and Frizzled, a receptor-ligand pair implicated in both limb bud and bone marrow stem cell development (Sen et al, 2002). In supporting our observations, Nakazawa et al (2001) reported that Notch-1 was overexpressed in rheumatoid synoviocytes and TNF induced nuclear translation of NICD in RSF.…”

Section: Discussionmentioning

confidence: 87%

Induction of Notch signaling by tumor necrosis factor in rheumatoid synovial fibroblasts

et al. 2003

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“…The antibodies used in this study were raised against the intracellular domain of each Notch homologue, and some signals were detected in the nuclei as well as the cytoplasmic domain in the RA and OA synovium. We previously reported that Notch-1 expression was characteristically detected in the nuclei of RA synoviocytes [20]. Although additional experiments should be done, the present study revealed that not only Notch-1 but also other Notch homologues might also be translocated into the nuclei.…”

Section: Discussionmentioning

confidence: 99%

“…Nuclear staining of Notch-1 was characteristically elevated in RA compared with that of OA (Fig. 1), which is consistent with our previous results [20].…”

Section: Expression Of Notch-1 -2 -3 and -4 In The Synovium From Rmentioning

confidence: 99%

Expression of Notch homologues in the synovium of rheumatoid arthritis and osteoarthritis patients

Ishii

Nakazawa

Yoshino

et al. 2001

Rheumatology International

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Notch is known as a receptor that controls differentiation or proliferation in various cells and is associated with several diseases. The objective of the present study was to clarify whether human Notch homologues Notch-1, -2, -3, and -4 are expressed in synovium and synoviocytes from rheumatoid arthritis (RA) and osteoarthritis (OA) patients. Immunohistochemical staining showed that Notch-1, -2, and -3 were clearly expressed in the synovium from both RA and OA, whereas Notch-4 was only slightly detected. We further performed Western blotting with the same antibodies used in immunohistochemical staining. Notch-1 and -2 were strongly detected in both RA and OA, and the expression of Notch-3 was slightly detected, while there was no Notch-4 expression in both RA and OA synoviocytes. In contrast, all Notch homologues were strongly expressed in the synovium at the developmental stage obtained from the infant. These results indicate that the expression pattern of Notch among synovium from OA and RA patients differed from that of normal subjects.

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Role of notch-1 intracellular domain in activation of rheumatoid synoviocytes

Cited by 62 publications

References 36 publications

HES factors regulate specific aspects of chondrogenesis and chondrocyte hypertrophy during cartilage development

HES factors regulate specific aspects of chondrogenesis and chondrocyte hypertrophy during cartilage development

Induction of Notch signaling by tumor necrosis factor in rheumatoid synovial fibroblasts

Expression of Notch homologues in the synovium of rheumatoid arthritis and osteoarthritis patients

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