• 제목/요약/키워드: transforming growth factor

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Update of genetic susceptibility in patients with Kawasaki disease

  • Yoon, Kyung Lim
    • Clinical and Experimental Pediatrics
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    • 제58권3호
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    • pp.84-88
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    • 2015
  • Kawasaki disease (KD) is an acute systemic vasculitis that predominantly affects children, and can result in coronary artery lesions (CAL). A patient with KD who is resistant to treatment with intravenous immunoglobulin (IVIG) has a higher risk of developing CAL. Incomplete KD has increased in prevalence in recent years, and is another risk factor for the development of CAL. Although the pathogenesis of KD remains unclear, there has been increasing evidence for the role of genetic susceptibility to the disease since it was discovered in 1967. We retrospectively reviewed previous genetic research for known susceptibility genes in the pathogenesis of KD, IVIG resistance, and the development of CAL. This review revealed numerous potential susceptibility genes including genetic polymorphisms of ITPKC, CASP3, the transforming growth factor-${\beta}$ signaling pathway, B lymphoid tyrosine kinase, FCGR2A, KCNN2, and other genes, an imbalance of Th17/Treg, and a range of suggested future treatment options. The results of genetic research may improve our understanding of the pathogenesis of KD, and aid in the discovery of new treatment modalities for high-risk patients with KD.

Topical delivery of smad3 antisense using cationic solid lipid nanoparticle(SLN): therapeutic potential use and prevention of keloids

  • Jin, Su-Eon;Park, Jeong-Sook;Kim, Chong-Kook
    • 대한약학회:학술대회논문집
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    • 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2-2
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    • pp.248.1-248.1
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    • 2003
  • Keloids are characterized by abnormal proliferation of fibroblasts and overproduction of collagen. Recently, it is reported that transforming growth factor beta (TGFb) and its signaling molecule, SMAD3 are related to the mitogenic effect of fibroblasts and a stimulatory factor for collagen synthesis. Cationic SLN was developed to improve the complex formation of DNA/SLN and enhance the uptake efficiency to cells. SLN was formulated by DC-Chol, DOPE, trimyristin as a solid core and other surfactant. The physical properties of the SLN and the ATS-SLN complex were characterized. (omitted)

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Putty형 탈회동종골을 이용한 골유도 재생술: 증례보고 (Guided Bone Regeneration Using a Putty-type Demineralized Bone Matrix: Case Report)

  • 장한성;김수관;문성용;오지수;박진주;정미애;양석진;정종원;김정선
    • Maxillofacial Plastic and Reconstructive Surgery
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    • 제33권5호
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    • pp.420-424
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    • 2011
  • Allomatrix (Wright Medical Tech, Inc., Arlington, Tenn, USA), is a newly designed, injectable putty with a reliable demineralized bone matrix (DBM), derived from human bone. The compound contains 86% DBM and other bone growth factors such as bone morphogenic protein (BMP)-2, BMP-4, insulin-like growth factor (IGF)-1, and transforming growth factor (TGF)-${\beta}1$. It has excellent osteoinduction abilities. In addition, DBM is known to have osteoconduction capacity as a scaffold due to its collagen matrix. This product contains a powder, which is a mix of DBM and surgical grade calcium sulfate as a carrier. A practitioner can blend the powder with calcium sulfate solution, making a putty-type material which has the advantages of ease of handling, better fixation, and no need for a membrane, because it can function as membrane itself. This study reports the clinical and radiographic results of various guided bone regeneration cases using Allomatrix, demonstrating its strong potential as a graft material.

Effects of the Peroxisome Proliferator Ciprofibrate and Prostaglandin $F_2\alpha$ Combination Treatment on Second Messengers in Cultured Rat Hepatocytes

  • Hong, Jin-Tae;Yun, Yeo-Pyo
    • Archives of Pharmacal Research
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    • 제21권2호
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    • pp.120-127
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    • 1998
  • Peroxisome proliferators induce hepatic peroxisome proliferation and hepatic tumors in rodents. These chemicals increase the expression of the peroxisomal $\beta$-oxidation pathway and the cytochrome P-450 4A family, which metabolizes lipids, including eicosanoids. Peroxisome proliferators transiently induce increased cell proliferation in vivo. However, peroxisome proliferators are weakly mitogenic and are not co-mitogenic with epidermal growth factor (EGF) in cultured hepatocytes. Earlier study found that the peroxisome proliferator ciprofibrate is cornitogenic with eicosanoids. In order to study possible mechanisms of the comitogenicity of peroxisome proliferator ciprofibrate and eicosanoids' we hypothesized that the co-mitogenicity may result from synergistic or additive increases of second messengers in mitogenic signal pathways. We therefore examined the effect of the peroxisome proliferator ciprofibrate, prostaglandin $F_2_{\alpha}$($PGF_2{\alpha}$) and the combination of ciprofibrate and $PGF_2{\alpha}$ with or without growth factors on the protein kinase C (PKC) activity, and inositol-1, 4, 5-triphosphate ($IP_{3-}$) and intracellular calcium ($[Ca^{2+}]_i$) concentrations in cultured rat hepatocytes. The combination of ciprofibrate and $PGF_2{\alpha}$ significantly increased particulate PKC activity. The combination of ciprofibrate and $PGF_2{\alpha}$ also significantly increased EGF, transforming growth factor-$\alpha$ ($TGF_2{\alpha}$) and hepatic growth factor (HGF)-induced particulate PKC activity. The combination of ciprofibrate and $PGF_2_\alpha$greatly increased $[Ca^{2+}]_i$. However, the increases of PKC activity and $[Ca^{2+}]_i$ by ciprofibrate and $PGF_2{\alpha}$ alone were much smaller. Neither ciprofibrate or $PGF_2{\alpha}$ alone nor the combination of ciprofibrate and $PGF_2{\alpha}$ significantly increased the formation of $IP_3$. The combination of ciprofibrate and $PGF_2{\alpha}$, however, blocked the inhibitory effect of $TGF-{\beta}$ on particulate PKC activity and formation of $IP_3$ induced by EGF. These results show that co-mitogenicity of the peroxisome proliferator ciprofibrate and eicosanoids may result from the increase in particulate PKC activity and intracellular calcium concentration but not from the formation of $IP_3$.

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630 nm-OLED Accelerates Wound Healing in Mice Via Regulation of Cytokine Release and Genes Expression of Growth Factors

  • Mo, SangJoon;Chung, Phil-Sang;Ahn, Jin Chul
    • Current Optics and Photonics
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    • 제3권6호
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    • pp.485-495
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    • 2019
  • Photobiomodulation (PBM) using organic light emitting diodes (OLEDs) surface light sources have recently been claimed to be the next generation of PBM light sources. However, the differences between light emitting diodes (LEDs) and OLED mechanisms in vitro and in vivo have not been well studied. In vivo mouse models were used to investigate the effects of OLED irradiation on cellular function and cutaneous wound healing compared to LED irradiation. Mice in the LED- and OLED-irradiated groups were subjected to irradiation with 6 J/㎠ LED and OLED (630 nm), respectively, for 14 days after wounding, and some mice were sacrificed for the experiments on days 3, 7, 10, and 14. To evaluate wound healing, we performed hematoxylin-eosin and Masson's trichrome staining and quantified collagen density by computerized image analysis. The results showed that the size of the wound, collagen density, neo-epidermis thickness, number of new blood vessels, and number of fibroblasts and neutrophils was significantly influenced by LED and OLED irradiation. The tissue levels of interleukin (IL)-β, IL-6 and tumor necrosis factor (TNF)-α were investigated by immunohistochemical staining. LED and OLED irradiation resulted in a significant increase in the tissue IL-β and IL-6 levels at the early stage of wound healing (P < 0.01), and a decrease in the tissue TNF-α level at all stages of wound healing (P < 0.05), compared to the no-treatment group. The expression levels of the genes encoding vascular endothelial growth factor and transforming growth factor-beta 1 were significantly increased in LED and OLED-irradiated wound tissue at the early stage of wound healing (P < 0.01) compared to the no-treatment group. Thus, OLED as well as LED irradiation accelerated wound healing by modulating the synthesis of anti-inflammatory cytokines and the expression levels of genes encoding growth factors, promoting collagen regeneration and reducing scarring. In conclusion, this suggests the possibility of OLED as a new light source to overcome the limitations of existing PBMs.

High Glucose Induces Connective Tissue Growth Factor Expression and Extracellular Matrix Accumulation in Rat Aorta Vascular Smooth Muscle Cells Via Extracellular Signal-Regulated Kinase 1/2

  • Ha, Yu Mi;Lee, Dong Hyup;Kim, Mina;Kang, Young Jin
    • The Korean Journal of Physiology and Pharmacology
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    • 제17권4호
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    • pp.307-314
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    • 2013
  • Connective tissue growth factor (CTGF) is a potent pro-fibrotic factor, which is implicated in fibrosis through extracellular matrix (ECM) induction in diabetic cardiovascular complications. It is an important downstream mediator in the fibrotic action of transforming growth factor ${\beta}$ ($TGF{\beta}$) and is potentially induced by hyperglycemia in human vascular smooth muscle cells (VSMCs). Therefore, the goal of this study is to identify the signaling pathways of CTGF effects on ECM accumulation and cell proliferation in VSMCs under hyperglycemia. We found that high glucose stimulated the levels of CTGF mRNA and protein and followed by VSMC proliferation and ECM components accumulation such as collagen type 1, collagen type 3 and fibronectin. By depleting endogenous CTGF we showed that CTGF is indispensable for the cell proliferation and ECM components accumulation in high glucose-stimulated VSMCs. In addition, pretreatment with the MEK1/2 specific inhibitors, PD98059 or U0126 potently inhibited the CTGF production and ECM components accumulation in high glucose-stimulated VSMCs. Furthermore, knockdown with ERK1/2 MAPK siRNA resulted in significantly down regulated of CTGF production, ECM components accumulation and cell proliferation in high glucose-stimulated VSMCs. Finally, ERK1/2 signaling regulated Egr-1 protein expression and treatment with recombinant CTGF reversed the Egr-1 expression in high glucose-induced VSMCs. It is conceivable that ERK1/2 MAPK signaling pathway plays an important role in regulating CTGF expression and suggests that blockade of CTGF through ERK1/2 MAPK signaling may be beneficial for therapeutic target of diabetic cardiovascular complication such as atherosclerosis.

혈소판 풍부혈장의 임상적 응용 (USE OF PLATELET-RICH PLASMA)

  • 하정완;김수관;조세인;이철우;정태영;김수흥;김영균
    • Maxillofacial Plastic and Reconstructive Surgery
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    • 제23권5호
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    • pp.452-457
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    • 2001
  • Platelet-rich plasma is an autologous source of platelet-derived growth factor and transforming growth factor beta that is obtained by sequestering and concentrating platelets by gradient density centrifugation. We have used platelet-rich plasma for bone graft, especially allobone graft, at implant surgery, sinus lift procedure, and cyst enucleation. This article is retrospective study from October 1999 to November 2000. All cases were good healing and clinical success.

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Chemical Synthesis and Determination of Biological Activity of the Epidermal Growth Factor-Like Domain of Mouse Betacellulin

  • Shin, Song-Yub;Kang, Shin-Won;Ha, Jong-Myung
    • BMB Reports
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    • 제28권2호
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    • pp.87-93
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    • 1995
  • To investigate the biological functions of the EGF-like domain of mouse betacellulin (BTC), mouse BTC(33-80), a 48-residue peptide corresponding to the EGF-like domain, was synthesized by stepwise solidphase methods using a 9-fluorenylmethoxycarbonyl (Fmoc) strategy. The homogeneity of synthetic mouse BTC(33-80) was confirmed by analytical reversed phase (RP)-HPLC, amimo acid analysis, and fast atom bombardment mass spectrometer (FAB-MS). Three disulfide bond pairings of synthetic mouse BTC(33-80) were established by amino acid analysis of cysteine-containing fragments derived from thermolytic digestion. These were consistent with the pairings of EGF and transforming growth factor ($TGF-{\alpha}$). The EGF-Iike domain of mouse BTC showed equipotent activity in both EGF-receptor binding on A-431 epidermoid carcinoma cells, and mitogenesis on NIH-3T3 fibroblast cells, as compared with authentic h-EGF. Results suggest that the EGF-Iike domain of BTC plays a significant role in mitogenic activity with an EGF-receptor mediated system.

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Clinical application of serum anti-Müllerian hormone in women

  • Oh, So Ra;Choe, Sun Yi;Cho, Yeon Jean
    • Clinical and Experimental Reproductive Medicine
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    • 제46권2호
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    • pp.50-59
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    • 2019
  • Anti-$M{\ddot{u}}llerian$ hormone (AMH), a peptide growth factor of the transforming growth $factor-{\beta}$ family, is a reliable marker of ovarian reserve. Regarding assisted reproductive technology, AMH has been efficiently used as a marker to predict ovarian response to stimulation. The clinical use of AMH has recently been extended and emphasized. The uses of AMH as a predictive marker of menopause onset, diagnostic tool for polycystic ovary syndrome, and assessment of ovarian function before and after gynecologic surgeries or gonadotoxic agents such as chemotherapy have been investigated. Serum AMH levels can also be affected by environmental and genetic factors; thus, the effects of factors that may alter AMH test results should be considered. This review summarizes the findings of recent studies focusing on the clinical application of AMH and factors that influence the AMH level and opinions on the use of the AMH level to assess the probability of conception before reproductive life planning as a "fertility test."

4-Hexylresorcinol induced angiogenesis potential in human endothelial cells

  • Kim, Min-Keun;Kim, Seong-Gon;Lee, Suk Keun
    • Maxillofacial Plastic and Reconstructive Surgery
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    • 제42권
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    • pp.23.1-23.11
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    • 2020
  • Background: 4-Hexylresorcinol (4HR) is able to increase angiogenesis. However, its molecular mechanism in the human endothelial cells has not been clarified. Methods: As endothelial cells are important in angiogenesis, we treated the human umbilical vein endothelial cells (HUVECs) with 4HR and investigated protein expressional changes by immunoprecipitation high-performance liquid chromatography (IP-HPLC) using 96 antisera. Results: Here, we found that 4HR upregulated transforming growth factor-β (TGF-β)/SMAD/vascular endothelial growth factor (VEGF) signaling, RAF-B/ERK and p38 signaling, and M2 macrophage polarization pathways. 4HR also increased expression of caspases and subsequent cellular apoptosis. Mechanistically, 4HR increased TGF-β1 production and subsequent activation of SMADs/VEGFs, RAF-B/ERK and p38 signaling, and M2 macrophage polarization. Conclusion: Collectively, 4HR activates TGF-β/SMAD/VEGF signaling in endothelial cells and induced vascular regeneration and remodeling for wound healing.