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민현영 ․ 장원구 대구대학교 산업기술연구소 2018 産業技術硏究 Vol.29 No.2
Niacin (Vitamin B3) is a necessary nutrient for humans and animals. This study was conducted to examine the effect of niacin on osteoblast differentiation. Previous study shows that precursor of niacin suppress osteoclast formation. However, the mechanism of niacin in osteoblast differentiation is not well known. In this study we investigated the effect of niacin in osteoblasts. Niacin induced osteogenic differentiation marker genes including distal-less homeobox 5(Dlx5), runt-related transcription factor 2(Runx2), alkaline phosphatase(ALP), and osteocalcin(OC). These results suggest that niacin contributes to osteoblast differentiation by inducing the osteogenic genes.
p-Anisaldehyde가 조골세포 분화에 미치는 영향
김경민 ․ 이도원 ․ 김현준 ․ 김아랑 ․ 장원구 대구대학교 산업기술연구소 2018 産業技術硏究 Vol.29 No.2
p-Anisaldehyde is a natural fragrance extracted from Pimpinella anisum L., and used as a preservative. This study examined the effect of p-anisaldehyde on osteoblast differentiation. First, cytotoxicity tests were carried out after examining the concentrations that did not show toxicity to the cells. The expression of osteoblast differentiation marker gene was confirmed by RT-PCR and was not effective in the treatment with p-anisaldehyde alone. However, p-anisaldehyde decreased the expression levels of inhibitor of differentiation-1 (Id1), distalless related homeobox (Dlx5), and runt-related transcription factor 2 (Runx2), which are osteogenic differentiation marker genes, which are increased in osteogenic condition. alkaline phosphatase (ALP) activity was also confirmed by ALP staining that p-anisaldehyde reduced ALP activity. These results show that p-anisaldehyde is effective in reducing osteoblast differentiation.
Trimethylpyrazine이 조골세포 분화에 미치는 영향
손효은 ․ 장원구 대구대학교 산업기술연구소 2018 産業技術硏究 Vol.29 No.2
Trimethylpyrazine (TrMP) is known to be derived from cocoa and nuts. In present study, we examined the effects of TrMP on osteoblast differentiation. The mRNA expression of osteogenic genes in MC3T3-E1 cells were determined by RT-PCR. TrMP induced the expression of osteogenic genes such as, inhibitor of differentiation-1 (Id1), distalless related homeobox (Dlx5), runt related transcription factor 2(Runx2), alkaline phosphatase( ALP), osteocalcin (OC). Alizarin red s staining was performed to measure calcium deposition. TrMP increased calcium deposition in MC3T3-E1 cells. These results suggest that TrMP was induces osteoblast differentiation in MC3T3-E1.
( Won Gu Kim ),( Tae Yong Kim ),( Tae Hyuk Kim ),( Hye Won Jang ),( Young Suk Jo ),( Young Joo Park ),( Sun Wook Kim ),( Won Bae Kim ),( Min Ho Shong ),( Do Joon Park ),( Jae Hoon Chung ),( Young Kee 대한내과학회 2014 The Korean Journal of Internal Medicine Vol.29 No.3
Background/Aims: Follicular thyroid carcinoma (FTC) and Hurthle cell carcinoma(HCC) of the thyroid are relatively uncommon thyroid malignancies in iodine-sufficient areas. In this study we evaluated the clinical behavior, prognosticfactors and treatment outcomes of FTC and HCC in Korea. Methods: This multicenter study included 483 patients with FTC and 80 patientswith HCC who underwent an initial surgery between 1995 and 2006 in one of thefour tertiary referral hospitals in Korea. We evaluated clinicopathological factorsassociated with distant metastases and recurrence during a median of 6 years offollow-up. Results: HCC patients were significantly older (49 years vs. 43 years; p < 0.001) andhad more lymphovascular invasions (22% vs. 14%; p = 0.03) compared with FTCpatients. Distant metastases were confirmed in 40 patients (8%) in the FTC groupand in two patients (3%) in the HCC group (p = 0.07). Distant metastases weresignificantly associated with older age, widely invasive cancer and extrathyroidalinvasion. Only 14 patients (3%) had recurrent disease and there was no significantdifference between FTC and HCC groups (p = 0.38). Recurrence was associatedwith larger tumor size and cervical lymph node metastasis. Conclusions: HCC patients were older and had more lymphovascular invasionsthan FTC patients. However, FTC and HCC patients had similar initial clinicopathologicalfeatures. Older age, wide invasiveness and extrathyroidal invasionwere independent risk factors for predicting distant metastases in FTC and HCCpatients.
Jang, Won-Gu,Jeong, Byung-Chul,Kim, Eun-Jung,Choi, Hyuck,Oh, Sin-Hye,Kim, Don-Kyu,Koo, Seung-Hoi,Choi, Hueng-Sik,Koh, Jeong-Tae American Society for Biochemistry and Molecular Bi 2015 The Journal of biological chemistry Vol.290 No.21
<P>Endoplasmic reticulum (ER) stress transducers, such as old astrocyte specifically induced substance (OASIS) and activating transcription factor 6 (ATF6), which are induced by bone morphogenetic protein 2 (BMP2), regulate bone formation and osteoblast differentiation. Here, we examined the role of cAMP response element-binding protein H(CREBH), a member of the same family of ER membrane-bound basic leucine zipper (bZIP) transcription factors as OASIS and ATF6, in osteoblast differentiation and bone formation. Proinflammatory cytokine TNF alpha increased CREBH expression by up-regulating the nuclear factor-kappa B (NF-kappa B) signaling pathway in osteoblasts, increased the level of N-terminal fragment of CREBH in the nucleus, and inhibited BMP2 induction of osteoblast specific gene expression. Overexpression of CREBH suppressed BMP2-induced up-regulation of the osteogenic markers runt-related transcription factor 2 (Runx2), alkaline phosphatase (ALP), and osteocalcin (OC) in MC3T3-E1 cells and primary osteoblasts, as well as BMP2-induced ALP activity and OC protein production. In contrast, knockdown of CREBH attenuated the inhibitory effect of TNF alpha on BMP2-induced osteoblast differentiation. Mechanistic studies revealed that CREBH increased the expression of Smad ubiquitination regulatory factor 1 (Smurf1), leading to ubiquitin-dependent degradation of Smad1, whereas knock-down of CREBH inhibited TNF alpha-mediated degradation of Smad1 by Smurf1. Consistent with these in vitro findings, administration of Ad-CREBH inhibited BMP2-induced ectopic and orthotopic bone formation in vivo. Taken together, these results suggest that CREBH is a novel negative regulator of osteoblast differentiation and bone formation.</P>
Kisspeptin-10 induces osteogenic differentiation through GPR54-mediated BMP2 expression and activity
Won-Gu Jang 한국수정란이식학회 2016 한국수정란이식학회 학술대회 Vol.2016 No.10
Kisspeptin-10 (KP-10) has been reported to act as a tumor metastasis suppressor via its receptor, G protein-coupled receptor 54 (GRP54). The KP-10/GPR54/BMPs signaling pathway plays an important role in embryonic kidney development. However, its function in osteoblast differentiation is unknown. The aim of this study was to confirm the molecular mechanism for the action of KP-10 on osteoblast differentiation. Expression of the Bone morphogenetic protein-2 (BMP2) and osteogenic genes were determined by RT-PCR and real-time PCR analysis in C3H10T1/2 cells. Transient transfection assays were performed to confirm the effects of KP-10 on BMP2-Luc activity. BMP2 and phospho-Smad1/5/9 protein levels were determined by Western blot analysis. Alkaline phosphatase (ALP) staining experiment was performed to evaluate ALP activity. To further confirm the effect of KP-10-induced GPR54, we used GPR54 Knock out (KO) C3H10T1/2 cells. KP-10 significantly increased osteogenic gene such as Runx2, ALP and Dlx5 in C3H10T1/2 cells. The ALP staining levels were also increased by KP-10. Interestingly, BMP2 mRNA, protein expression and promoter activity were also increased by KP-10. However, KP-10-induced BMP2 expressions were not increased in GPR54 KO cells. These results suggest that KP-10 increases BMP2 expression through GPR54. Next, Western blot analysis shown Smad1/5/9 phosphorylation were enhanced in a time-dependent manner by KP-10 treatment. It is well known that BMP2 increased phosphorylation of Smad1/5/9 via BMP2 receptor. In addition, KP-10 increased NFATc4 mRNA levels and NFATc4 overexpression enhance BMP2 mRNA levels. To confirm the KP-10-induced BMP2 action, we used KP-10-treated medium in wild type cells and GPR54 KO cells. The osteogenic genes were not elevated by KP-10-treated medium (GPR54 KO cells) whereas increased expression levels by KP-10 medium (wild type cells). These data indicate that KP-10 induced osteoblast differentiation through NFATc4-mediated BMP2 signaling.
BMP2 Protein Regulates Osteocalcin Expression via Runx2-mediated<i>Atf6</i>Gene Transcription
Jang, Won-Gu,Kim, Eun-Jung,Kim, Don-Kyu,Ryoo, Hyun-Mo,Lee, Keun-Bae,Kim, Sun-Hun,Choi, Hueng-Sik,Koh, Jeong-Tae American Society for Biochemistry and Molecular Bi 2012 The Journal of biological chemistry Vol.287 No.2
( Won Gu Jang ),( Eun Jung Kim ),( Jeong Tae Koh ) 생화학분자생물학회(구 한국생화학분자생물학회) 2011 BMB Reports Vol.44 No.11
Tunicamycin, an endoplasmic reticulum (ER) stress inducer, specifically inhibits N-glycosylation. The cyclic AMP (cAMP) response element-binding protein H (CREBH) was previously shown to be regulated by UPR-dependent proteolytic cleavage in the liver. On the other hand, the role of CREBH in other tissues is unknown. In the present study, tunicamycin increased the level of CREBH activation (cleavage) as well as mRNA expression in osteoblast cells. Adenoviral (Ad) overexpression of CREBH suppressed BMP2-induced expression of alkaline phosphatase (ALP) and osteocalcin (OC). Interestingly, the BMP2-induced OASIS (structurally similar to CREBH, a positive regulator of osteoblast differentiation) expression was also inhibited by CREBH overexpression. In addition, inhibition of CREBH expression using siRNA reversed the tunicamycin-suppressed ALP and OC expression. These results suggest that CREBH inhibited osteoblast differentiation via suppressing BMP2-induced ALP, OC and OASIS expression in mouse calvarial derived osteoblasts. [BMB reports 2011; 44(11): 735-740]