• 제목/요약/키워드: integrins

검색결과 55건 처리시간 0.025초

Transforming growth factor β1 enhances adhesion of endometrial cells to mesothelium by regulating integrin expression

  • Choi, Hee-Jung;Park, Mi-Ju;Kim, Bo-Sung;Choi, Hee-Jin;Joo, Bosun;Lee, Kyu Sup;Choi, Jung-Hye;Chung, Tae-Wook;Ha, Ki-Tae
    • BMB Reports
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    • 제50권8호
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    • pp.429-434
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    • 2017
  • Endometriosis is the abnormal growth of endometrial cells outside the uterus, causing pelvic pain and infertility. Furthermore, adhesion of endometrial tissue fragments to pelvic mesothelium is required for the initial step of endometriosis formation outside uterus. $TGF-{\beta}1$ and adhesion molecules importantly function for adhesion of endometrial tissue fragments to mesothelium outside uterus. However, the function of $TGF-{\beta}1$ on the regulation of adhesion molecule expression for adhesion of endometrial tissue fragments to mesothelium has not been fully elucidated. Interestingly, transforming growth factor ${\beta}1$ ($TGF-{\beta}1$) expression was higher in endometriotic epithelial cells than in normal endometrial cells. The adhesion efficiency of endometriotic epithelial cells to mesothelial cells was also higher than that of normal endometrial cells. Moreover, $TGF-{\beta}1$ directly induced the adhesion of endometrial cells to mesothelial cells through the regulation of integrin of ${\alpha}V$, ${\alpha}6$, ${\beta}1$, and ${\beta}4$ via the activation of the $TGF-{\beta}1/TGF-{\beta}RI/Smad2$ signaling pathway. Conversely, the adhesion of $TGF-{\beta}1-stimulated$ endometrial cells to mesothelial cells was clearly reduced following treatment with neutralizing antibodies against specific $TGF-{\beta}1-mediated$ integrins ${\alpha}V$, ${\beta}1$, and ${\beta}4$ on the endometrial cell membrane. Taken together, these results suggest that $TGF-{\beta}1$ may act to promote the initiation of endometriosis by enhancing integrin-mediated cell-cell adhesion.

다양한 세포외기질이 배양 골아세포의 이동에 미치는 영향 (The Effects of Various Extracellular Matrices on Motility of Cultured MC3T3-E1 Cell)

  • 박병윤;서상우;이원재;류창우;나동균;손현주;박종철
    • Archives of Plastic Surgery
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    • 제32권2호
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    • pp.143-148
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    • 2005
  • Chemotactic migration of bone forming cell, osteoblast, is an important event during bone formation, bone remodeling, and fracture healing. Migration of cells is mediated by adhesion receptors, such as integrins, that link the cell to extracellular matrix ligands, type I collagen, fibronectin, laminin and depend on interaction between integrin and extracellular ligand. Our study was designed to investigate the effect of extracellular matrix like fibronectin, laminin, type I collagen on migration of osteoblast. Migration distance and speed of MC3T3-E1 cell on extracellular matrix-coated glass were measured for 24 hours using 0.01% type I collagen, 0.01% fibronectin, 100 microliter/ml laminin. The migration distance and speed of MC3T3-E1 cell was compared using a video-microscopy system. To determine migration speed, cells were viewed with a 4 phase- contrast lens and video recorded. Images were captured using a color CCD camera and saved in 8-bit full-color mode. The migration distance on 0.01% type I collagen or 0.01% fibronectin was longer than that on $100{\mu}l/ml$ laminin-coated glass. The migration speed on fibronectin-coated glass was 68 micrometer/hour which was fastest. The migration speed on type I collagen-coated glass was similar with that on fibronectin-coated glass. The latter two migration speeds were faster than that on no-coated glass. On the other hand, the average migration speed on laminin-coated glass was 37micrometer/hour and not different from that of control group. In conclusion, the extracelluar matrix ligands such as type I collagen and fibronectin seem to play an important role in cell migration. The type I collagen or fibronectin coated scaffold is more effective for migration of osteoblast in tissue engineering process.

인체 특발성 폐섬유증에서 Intercellular Adhesion Molecule-1의 발현에 관한 연구 (Expression of Intercellular Adhesion Molecule-1 in Human Idiopathic Pulmonary Fibrosis)

  • 박성수;신동호;김태화;이동후;이정희;이중달
    • Tuberculosis and Respiratory Diseases
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    • 제40권2호
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    • pp.185-191
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    • 1993
  • 연구배경 : ICAM-1은 90 kD의 당단백으로서 ${\beta}_2$ integrin과 관계를 가지며, 특발성 폐섬유증의 병인론에 있어서 ICAM-1의 발현과 밀접한 관계가 있다고 보고되고 있다. 특발성 폐섬유종에 있어서 ICAM-1의 발현 정도는 상향조절된다. 특발성 폐섬유증에 있어서 ICAM-1의 발현 양상에 대한 보고는 드물다. 방법 : 본 연구는 특발성 폐섬유증에 있어서 ICAM-1의 발현 양상을 연구하고자 개흉폐생검으로 채취된 특발성 간질성 폐섬유증 3예의 6절편과 폐절제시 채취한 3예의 정상조직을 연구재료로 하여 ICAM-1의 단세포군항체를 이용하여 연역조직화학적 검색을 실시하였다. 결과 : ICAM-1은 3예의 정상조직의 기관지 상피세포나 폐포 세포에서는 발현되지 않았다. 3예의 특발성 폐섬유증 6절편 중 5절편에서 폐포벽의 간질성 섬유아 세포들에서 발현되었고, 1절편에서는 증식된 폐포내 폐포세포에서 발현되었다. 그 정도는 비균질적인 양상을 보였다. 3예의 6절편 중 5절편에서 강한 발현을 1절편에서는 약한 발현정도를 나타냈다. 결론 : 위의 연구 결과를 종합하여 보면, ICAM-1의 발현 증가는 특발성 폐섬유증의 병인과 상당한 관련이 있음을 암시해 주는 것으로 추정된다.

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고콜레스테롤혈증을 유발한 토끼의 대동맥 판막에서 ${\beta}_3$ Integrin 발현의 변화 (Altered Expression of ${\beta}_3$ Integrin on Sclerotic Aortic Valves in a Hypercholesterolemic Rabbit Model)

  • 박찬범;김영두;최미선;진웅;문석환;김용한;김치경;조건현;권종범
    • Journal of Chest Surgery
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    • 제41권6호
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    • pp.687-694
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    • 2008
  • 배경: 대동맥 판막 경화증은 고령에서 흔히 나타나며, 대동맥 판막 협착증처럼 좌심실 유출로를 폐쇄하지는 않으나 심혈관질환으로의 사망 위험성이 50%나 증가되며, 심근경색증의 위험성이 높다. 그러나, 대동맥 판막경화증에서 ${\beta}_3$ integrin의 관련성은 잘 알려져 있지 않다. 대상 및 방법: 20마리의 뉴질랜드산 토끼들을 2군으로 나눈 후, 1군(10마리)에서는 정상식이를 시행하였고, 2군(10마리)에서는 1% 콜레스테롤식이를 시행하였다. 12주간 식이후 실험동물을 희생시켜 대동맥 판막 및 상행대동맥을 채취하였다. 각군의 토끼들의 혈장에서 총 콜레스테롤, 중성지방, 저밀도(LDL)-콜레스테롤, 고밀도(HDL)-콜레스테롤 수치를 측정하였으며, 대동맥 판막과 대동맥에서 HE 염색을 시행하였고, 대동맥 판막에서 근육섬유모세포, 대식세포에 대한 면역조직화학염색을 시행하였으며, ${\beta}_3$, integrin에 대한 정량적검사를 위하여 Real-time polymerase chain reaction (RT-PCR)을 시행하였다. 결과: 총 콜레스테롤($2148.3{\pm}1012.5\;mg/dL$ versus $53.7{\pm}31.8\;mg/dL$, p<0.05), 중성지방($240.4{\pm}218.3\;mg/dL$ versus $31.6{\pm}6.4\;mg/dL$, p<0.05), 저밀도-콜레스테롤 수치($2,065.3{\pm}960.9\;mg/dL$ versus $29.1{\pm}30.9\;mg/dL$, p<0.05)는 정상식이군과 비교해서 콜레스테롤 식이군에서 의미 있게 증가하였다. 대동맥판막의 면역 조직화학염색에서 근육섬유모세포와 대식세포는 콜레스테롤식이군에서 발현이 증가되었다. RT-PCR을 이용한 정량적 검사에서 ${\beta}_3$ integrin mRNA의 발현은 대동맥판막과 대동맥 모두 콜레스테롤 식이군에서 의미 있게 감소되어 있었다(p<0.05). 결론 : 콜레스테롤식이에 의한 고콜레스테롤혈증은 토끼의 대동맥 판막에서 대동맥 판막경화증을 유발하였다. 석회화 대동맥 판막의 초기 상태인대동맥 판막 경화증은 초기죽상경화병변과 유사한 과정을 보이며, 이는 ${\beta}_3$, integrin의 감소가 중요한 역할을 한다고 생각된다.

자궁내막증 환자의 자궁내막내 성호르몬 수용체, Integrins, Cyclooxygenase의 발현과 변이 양상 (Expression Pattern of Progesterone Receptor, Integrin, Cyclooxygenase (COX) in Human Endometrium of Patients with Endometriosis)

  • 김미란;박동욱;권혁찬;황경주;주희재;조동제;김세광;오기석
    • Clinical and Experimental Reproductive Medicine
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    • 제27권2호
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    • pp.117-131
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    • 2000
  • Objectives: To develop a new immunohistochemical marker system for supplementation of the Noyes histological classification of the endometrium in women of child bearing age with regular menstrual cycles, and to employ this system to evaluate pathologic factors involved in endometriosis, and thus to ascertain if it is useful in diagnosis. Materials and Methods: Endometrial biopsies were sampled from the posterior fundus of 41 (24 proliferative phases, 17 secretory phases) women with regular menstrual cycles (28-32 days), and each sample was immunohistochemically stained according to Noyes et al (1975) for determination of expression for estrogen receptor (ER), progesterone receptor (PR), integrin ${\alpha}_1$, ${\alpha}_4$, ${\beta}_3$, COX-1 and COX-2. Then, the PR, integrin ${\beta}_3$ and COX-2 which were clearly expressed in the luteal phase was with endometrial samples were obtained from 20 cases of normal patients (group 1) and 25 cases with endometriosis (group 2) after confirming the day of ovulation by sex steroid level measurements 7-8 days after ovulation Results: In the regular menstruation group the expression of ER showed a tendency to be increased in the proliferative phase and decreased in the secretory phase, and was the highest in the proliferative phase. However, PR in the stromal cells showed no change in the entire menstrual cycle while in the epithelial cells, PR reached a peak in the late proliferative phase and was almost absent in the secretory phase. Integrin (${\alpha}_1$, ${\alpha}_4$, and ${\beta}_3$ expression in the epithelial cells was absent in the proliferative phase but ${\alpha}_1$ was strongly expressed starting from the early secretory phase into the entire secretory phase. ${\alpha}_4$ was expressed strongly in the early and mid secretory phases and disappeared in the late proliferative phase, while ${\beta}_3$ appeared after the mid secretory phase and continued to be expressed until the late secretory phase. Expression in the stromal cells was weak overall and did not show any cyclic pattern. COX-1 expression was shown as a cyclic pattern in the stromal and epithelial cells and was particularly strongly expressed in the mid secretory phase of epithelial cells, and in the mid secretory and menstruation phase of stromal cells. In the endometrial epithelial cells there was strong expression during the entire cycle with stronger expression in the secretory phase compared to the prolferative phase. COX-2 was clearly expressed in the late proliferative, early and mid secretory phases in the stromal cells. No expression was observed in the proliferative phase of the epithelial cells, but which began to appear in the early secretory phase reaching a significant pattern from the mid secretory phase onwards. There was almost no expression in the stromal cells. In the cases with endometriosis showing normal endometrial maturation according to the Noyes classification, PR expression was increased while Integrin-${\beta}_3$의 expression was significantly decreased compared to the normal group. Also, COX-2 expression was slightly decreased in the stromal cells of patients with endometriosis while it was significantly increased in the stromal cells. Conclusion: Immunohistochemical markers can supplement the original Noyes classification of histological endometrial dating and therefore ascertain existing pathologic conditions. Particularly for patients with endometriosis with normally mature endometrial cells, changes in COX-2 and integrin expression patterns may assist in elucidating pathophysiologic mechanisms and therefore aid in the diagnosis of abnormal implantation conditions, and consequently determine a treatment modality.

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