CREB-AP1 Protein Complexes Regulate Transcription of the Collagen XXIV Gene (Col24a1) in Osteoblasts

Matsuo, Noritaka; Tanaka, Shizuko; Gordon, Marion K.; Koch, Manuel; Yoshioka, Hidekatsu; Ramirez, Francesco

doi:10.1074/jbc.m509923200

Cited by 41 publications

(29 citation statements)

References 49 publications

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“…In addition, allicin treatment ameliorated the repression of PI3K/AKT and CREB/ERK signaling by hydrogen peroxide, and might also be associated with the anti-oxidative stress effect of allicin. Previously, PI3K and CREB have been implicated in chondrocyte-like cell proliferation and differentiation (Carpio et al, 2001;Matsuo et al, 2006). In the present study, allicin treatment of C28/I2 cells increased PI3K activity, and the phosphorylation of AKT, CREB, and ERK.…”

Section: Discussionsupporting

confidence: 53%

Hypoxia-induced apoptosis and mitochondrial dysfunction in chondrocytes arising from CREB phosphorylation reduction

et al. 2016

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ABSTRACT. Chondrocytes, which are embedded within the growthplate or the intervertebral disc, are sensitive to environmental stresses, such as inflammation and hypoxia. However, little is known about the molecular signaling pathways underlying hypoxia-induced mitochondrial dysfunction and apoptosis in chondrocytes. We first examined the apoptosis, caspase-3 activity, and apoptosis-associated markers in human chondrocyte cell line C28/I2 under normoxia or hypoxia. We then investigated mitochondrial dysfunction and the activation of cyclic adenosine monophosphate response elementbinding protein (CREB) signaling in the same human chondrocyte cell line. Our results indicated that hypoxia induced apoptosis and reduced CREB phosphorylation in chondrocytes. Upregulated mitochondrial superoxide and reactive oxygen species levels, and reduced mitochondrial membrane potential and complex IV activity were observed in hypoxia-treated C28/I2 cells. In conclusion, the present study confirmed reduced CREB phosphorylation, apoptosis induction, and mitochondrial dysfunction in the hypoxia-treated chondrocyte cells. This implies the key role played by CREB signaling in hypoxiainduced mitochondrial dysfunction and apoptosis in chondrocytes.

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Section: Discussionsupporting

confidence: 53%

Hypoxia-induced apoptosis and mitochondrial dysfunction in chondrocytes arising from CREB phosphorylation reduction

et al. 2016

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“…In addition, the allicin treatment also ameliorated the repressed PI3K/AKT and CREB/ERK signaling by H 2 O 2 that may also be associated with the anti-OS effect of allicin. Previously, PI3K and CREB were demonstrated to be involved in osteoblast-like cell proliferation and differentiation (42,43). In the present study, allicin treatment on MC3T3-E1 cells led to increased PI3K activity, phosphorylation of AKT, CREB and ERK.…”

Section: A B C Dsupporting

confidence: 47%

Allicin inhibits oxidative stress-induced mitochondrial dysfunction and apoptosis by promoting PI3K/AKT and CREB/ERK signaling in osteoblast cells

Ding

Zhao

Jiang

2016

Experimental and Therapeutic Medicine

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Abstract.Osteoporosis is a disease of the skeleton that is characterized by the loss of bone mass and degeneration of bone microstructure, resulting in an increased risk of fracture. Oxidative stress, which is known to promote oxidative damage to mitochondrial function and also cell apoptosis, has been recently indicated to be implicated in osteoporosis. However, there are few agents that counteract oxidative stress in osteoporosis. In the present study, the protective effects of allicin against the oxidative stress-induced mitochondrial dysfunction and apoptosis were investigated in murine osteoblast-like MC3T3-E1 cells. The results demonstrated that allicin counteracted the reduction of cell viability and induction of apoptosis caused by hydrogen peroxide (H 2 O 2 ) exposure. The inhibition of apoptosis by allicin was confirmed by the inhibition of H 2 O 2 -induced cytochrome c release and caspase-3 activation. Moreover, the inhibition of apoptosis by allicin was identified to be associated with the counteraction of H 2 O 2 -induced mitochondrial dysfunction. In addition, allicin was demonstrated to be able to significantly ameliorate the repressed phosphoinositide 3-kinase (PI3K)/AKT and cyclic adenosine monophosphate response element-binding protein (CREB)/extracellular-signal-regulated kinase (ERK) signaling pathways by H 2 O 2 , which may also be associated with the anti-oxidative stress effects of allicin. In conclusion, allicin protects osteoblasts from H 2 O 2 -induced oxidative stress and apoptosis in MC3T3-E1 cells by improving mitochondrial function and the activation of PI3K/AKT and CREB/ERK signaling. The present study implies a promising role of allicin in oxidative stress-associated osteoporosis.

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“…These binding motifs were also found to be active in many other ECM protein-coding genes, i.e. collagens such as Col11a2 (19) and Col24a1 (20), proteoglycan core proteins such as biglycan (21,22), decorin (23), glypican-3 (24) or murine glypican-4 (25). Binding sites for Sp1 and AP-1 are also involved in the transcriptional regulation of other enzymes participating in glycosaminoglycan biosynthesis, like UDP-glucose dehydrogenase (26,27).…”

Section: Discussionmentioning

confidence: 99%

Identification and Characterization of the Human Xylosyltransferase I Gene Promoter Region

Müller

Prante

Kleesiek

et al. 2009

Journal of Biological Chemistry

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Human xylosyltransferase I catalyzes the initial and rate-limiting step in the biosynthesis of glycosaminoglycans and proteoglycans. Furthermore, this enzyme has been shown to play a major role in the physiological development of bone and cartilage as well as in pathophysiological processes such as systemic sclerosis, dilated cardiomyopathy, or fibrosis. Here, we report for the first time the identification and characterization of the XYLT1 gene promoter region and important transcription factors involved in its regulation. Members of the activator protein 1 (AP-1) and specificity protein 1 (Sp1) family of transcription factors are necessary for the transcriptional regulation of the XYLT1 gene, which was proven by curcumin, tanshinone IIA, mithramycin A, and short interference RNA treatment. A stepwise 5 and 3 deletion of the predicted GCrich promoter region, which lacks a TATA and/or CAAT box, revealed that a 531-bp core promoter element is able to drive the transcription on a basal level. A binding site for transcription factors of the AP-1 family, which is essential for full promoter activity, was identified by site-directed mutagenesis located 730 bp 5 of the translation initiation site. The ability of this site to bind members of the AP-1 family was further verified by electrophoretic mobility shift assays. A promoter element containing this binding site was able to drive the transcription to about 79-fold above control in SW1353 chondrosarcoma cells. Our findings provide a first insight into the regulation of the XYLT1 gene and may contribute to understanding the processes taking place during extracellular matrix formation and remodeling in health and disease.

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CREB-AP1 Protein Complexes Regulate Transcription of the Collagen XXIV Gene (Col24a1) in Osteoblasts

Cited by 41 publications

References 49 publications

Hypoxia-induced apoptosis and mitochondrial dysfunction in chondrocytes arising from CREB phosphorylation reduction

Hypoxia-induced apoptosis and mitochondrial dysfunction in chondrocytes arising from CREB phosphorylation reduction

Allicin inhibits oxidative stress-induced mitochondrial dysfunction and apoptosis by promoting PI3K/AKT and CREB/ERK signaling in osteoblast cells

Identification and Characterization of the Human Xylosyltransferase I Gene Promoter Region

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