• Title/Summary/Keyword: 아교질 mRNA 발현

Search Result 5, Processing Time 0.025 seconds

Low-Intensity Pulsed Ultrasound Promotes Healing with Increases Collagen Deposition and Collagen mRNA Expression in Skin Wound of Rat (저강도 맥동초음파에의한 피부 상처 치유 촉진과 아교질 축적 및 아교질 mRNA 발현 증가)

  • Lee, Jae-Hyoung;Jeka, Seung-Joo;Kwon, Pil-Seung
    • Journal of the Korean Society of Physical Medicine
    • /
    • v.8 no.3
    • /
    • pp.449-456
    • /
    • 2013
  • 목적: 본 연구는 저강도 맥동 초음파적용이 흰쥐의 전층 상처 치유와 아교질 축적 및 아교질 mRNA발현에 미치는 영향을 규명할 목적으로 시행하였다. 방법: 12마리의 Sprague-Dawley계 흰쥐를 저강도 맥동 초음파군(n=6)과 대조군(n=6)에 무작위 배정하고 등에 $19.63mm^2$ 크기의 전층 적출 상처를 만든 다음 저강도 맥동 초음파군은 3 MHz, 순환주기 20%, SATA 강도 $0.4W/cm^2$로 1일 1회, 1회 5분씩 초음파를 적용하고, 대조군은 가짜 초음파를 적용하였다. 7일간 처치 후 초음파군과 대조군의 아교질 축적, 아교질 mRNA 발현, 상처치유율, 절반치유시간을 비교하였다. 결과: 초음파군의 아교질 축적(p<05)과 아교질 mRNA 발현(p<.01)이 대조군보다 유의하게 증가하였고, 상처치유율(p<.05)과 절반치유시간(p<.0)도 초음파군의 대조군보다 유의하게 빨랐다. 결론: 본 연구에서 전층 상처에 저강도 맥동 초음파를 적용한 결과 상처 치유가 촉진되었고 육아조직에 아교질 축적이 증가하였다. 이러한 결과는 맥동 초음파의 기계적 자극이 제 1형 아교질 mRNA 전사활동을 촉진시키는 것으로 사료된다.

The Effect of Over-expression and Inactivation of Nuclear Factor I-C on the Dentin Matrix Gene Expression of MDPC-23 Odontoblasts (Nuclear Factor I-C 과발현과 발현억제가 MDPC-23 상아모세포주의 상아질 기질유전자 발현에 미치는 영향)

  • Bae, Hyun-Sook;Cho, Young-Sik
    • Journal of dental hygiene science
    • /
    • v.9 no.4
    • /
    • pp.427-433
    • /
    • 2009
  • Nuclear factor I-C (NFI-C) null mice demonstrated aberrant odontoblast differentiation and abnormal dentin formation. In order to elucidate the mechanisms responsible for these changes, we evaluated the expression of dentin matrix gene after over-expression and inactivation of NFI-C in MDPC-23 cells by reverse transcription-polymerase chain reaction (RT-PCR) analysis. Collagen type I (Col I), osteocalcin (OC), and dentin sialophosphoprotein (DSPP) expression was decreased after inactivation of NFI-C. However, bone sialoprotein (BSP) expression was dramatically increased after inactivation of NFI-C. ALP and DMP4 expression was not changed after inactivation of NFI-C. The expression of alkaline phoshatase (ALP) and dentin matrix protein 4 (DMP4) was increased after over-expression of NFI-C, while Col I, OC, DSPP, and BSP expression was decreased. These findings suggest that odontoblasts after loss of NFI-C lost the phenotype of odontoblasts and acquired those of osteoblasts.

  • PDF

THE ADHESION OF ODONTOBLAST TO TYPE I COLLAGEN (상아모세포의 I 형 아교질에 대한 부착)

  • Ahn, Myung-Ki;Jeong, Tae-Sung;Kim, Shin
    • Journal of the korean academy of Pediatric Dentistry
    • /
    • v.37 no.3
    • /
    • pp.308-316
    • /
    • 2010
  • Odontoblasts are anchorage dependent cells adhering to a substrate via cell adhesive molecules. Receptor ligands such as integrins bind to these proteins and are known to function as signal transduction molecules in a series of critical recognition events of cell-substratum. The aim of this study is to examine the interaction of odontoblast (MDPC-23 cell) with type I Col and the effect of TGF-${\beta}1$ and TNF-$\alpha$ on the expression of cell adhesion molecules. In this study, MDPC-23 cells adhered to type I Col dose-dependently. Immunofluorescence data demonstrated that integrin ${\alpha}1$, ${\alpha}2$ and CD44 were expressed on cell surface, and FAK and paxillin were localized in focal adhesion plaques in MDPC-23 cells adhesion to Col. Cytokine TGF-${\beta}1$ increased the adhesion of MDPC-23 cells to Col and the expression level of integrin ${\alpha}1$, 4{\alpha}2$ and chondroitin sulfate on MDPC-23 cells. RT-PCR data demonstrated that cytokine TGF-${\beta}1$ increased the amount of integrin ${\alpha}1$ mRNA in MDPC-23 cells. Therefore, MDPC-23 cells adhere to collagen type I Col and expressed a complex pattern of integrins and proteoglycans, including ${\alpha}1$, ${\alpha}2$, chondroitin sulfate and CD44 detected by immunoblotting and immunofluorescence assay. TGF-${\beta}1$ treatment enhanced the expression of adhesion molecules such as integrin ${\alpha}1$, ${\alpha}2$ and chondroitin sulfate.

Expression of Growth Factors and Secretory Leukocyte Protease Inhibitor (SLPI) in RAW264.7 Cells after Lipopolysaccharide (LPS) Stimulation (대식세포주 (RAW264.7)에서 박테리아성 지질다당류 (LPS) 자극에 의한 분비백혈구단백분해효소억제제 (SLPI)와 성장인자들의 발현)

  • Son, Wook-Hee;Choi, Baik-Dong;Jeong, Soon-Jeong;Wang, Guan-Lin;Hwang, Ho-Keel;Jeong, Moon-Jin
    • Applied Microscopy
    • /
    • v.37 no.2
    • /
    • pp.93-102
    • /
    • 2007
  • Secretory leukocyte protease inhibitor (SLPI) was known as one of bacterial lipopolysaccharide (LPS)-induced products of macrophage. Macrophages play an important role in the development of inflammatory responses by secreting an array of cytokines and chemokines in a tissue microenvironment. To identify the function and relationship between potent growth factors and SLPI after LPS stimulation, we conducted reverse transcriptase polymerase chain reaction (RT-PCR) and Western blots for the detection of mRNA and protein expression of SLPI and growth factors such as VEGF, PDGF, bFGF after 100 ng LPS stimulation on the RAW264.7 cells. The result of RT-PCR was showed SLPI mRNA expression was increased from 60 min to 48h in RAW 264.7 cells after incubation with LPS. VEGF and PDGF mRNA was expressed highly at initial stage by LPS stimulation. The mRNA of bFGF and type I collagen was very weakly expressed after LPS stimulation. SLPI protein level was increased likely the mRNA levels in RAW 267.7 cells. Additionally, phase contrast and scanning electron microscopic observation demonstrated that the LPS induce the change of morphology of the RAW264.7 cells. From these results, it suggest that expression of SLPI by LPS treatment may associate with VEGF and PDGF expression in RAW264.7 cells.

Establishment of a Radiation-Induced Fibrosis Model in BALB/c Mice (BALB/c 마우스를 이용한 방사선섬유증 모델 확립)

  • Ryu, Seung-Hee;Lee, Sang-Wook;Moon, Soo-Young;Oh, Jeong-Yoon;Yang, Youn-Joo;Park, Jin-Hong
    • Radiation Oncology Journal
    • /
    • v.28 no.1
    • /
    • pp.32-38
    • /
    • 2010
  • Purpose: Although radiation-induced fibrosis is one of the common sequelae occurring after irradiation of skin and soft tissues, the treatment methods are not well standardized. This study aimed to establish the skin fibrosis mouse model by fractionated radiation for the further mechanism studies or testing the efficacy of therapeutic candidates. Materials and Methods: The right hind limbs of BALB/c mice received two fractions of 20 Gy using a therapeutic linear accelerator. Early skin damages were scored and tissue fibrosis was assessed by the measurement of a leg extension. Morphological changes were assessed by H&E staining and by Masson's Trichrome staining. TGF-${\beta}1$ expression from soft tissues was also detected by immunohistochemistry and PCR. Results: Two fractions of 20 Gy irradiation were demonstrated as being enough to induce early skin damage effects such as erythema, mild skin dryness, dry and wet desquamation within several weeks of radiation. After 13 weeks of irradiation, the average radiation-induced leg contraction was $11.1{\pm}6.2mm$. Morphologic changes in irradiated skin biopsies exhibited disorganized collagen and extracellular matrix fibers, as well as the accumulation of myofibroblasts compared to the non-irradiated skin. Moreover, TGF-${\beta}1$ expression in tissue was increased by radiation. Conclusion: These results show that two fractions of 20 Gy irradiation can induce skin fibrosis in BALB/c mice accompanied by other common characteristics of skin damages. This animal model can be a useful tool for studying skin fibrosis induced by radiation.