논문 상세보기

CCR5 deficiency in aged mice causes a decrease in bone mass KCI 등재후보

  • 언어KOR
  • URLhttps://db.koreascholar.com/Article/Detail/386096
구독 기관 인증 시 무료 이용이 가능합니다. 4,000원
대한구강생물학회 (The Korean Academy of Oral Biology)
초록

The CC chemokine receptor 5 (CCR5) is a G protein-coupled receptor that regulates chemotaxis and effector functions of immune cells. It also serves as the major co-receptor for the entry of human immunodeficiency virus (HIV). Recently, CCR5 inhibitors have been developed and used for the treatment or prevention of HIV infections. Additionally, it has been identified that CCR5 controls bone homeostasis by regulating osteoclastogenesis and the communication between osteoblasts and osteoclasts. However, the effects of CCR5 inhibition on bone tissue in elderly patients are unknown. This study aimed to examine the bone phenotype of aged CCR5 knockout (KO) mice. Femoral and tibial bones were isolated from 12-month and 18-month old wild-type (WT) and CCR5 KO mice, and microcomputed tomography and histology analyses were performed. Twelve-month-old CCR5 KO mice exhibited a decreased trabecular bone mass and cortical bone thickness in both femoral and tibial bones compared with agematched WT mice. Eighteen-month-old mice also showed a decreased trabecular bone mass in femurs compared with control WT mice, but not in tibial bones. Unlike in 12-month-old mice, the cortical margin of femurs and tibias in 18-month-old mice were rough, likely because they were aggravated by the deficiency of CCR5. Overall, our data suggest that the deficiency of CCR5 with aging can cause severe bone loss. When CCR5 inhibitors or CCR5 inactivating technologies are used in elderly patients, a preventive strategy for bone loss should be considered.

목차
Introduction
Materials and Methods
    1. 실험 동물
    2. 마이크로전산화단층촬영(microCT)
    3. 골지표 분석 및 3차원 이미지 재구성
    4. 조직학적 관찰
    5. 통계 분석
Results
    1. 12개월령 CCR5 결핍 마우스에서 대퇴골 및 경골의 변화
    2. 18개월령 CCR5 결핍 마우스에서 대퇴골 및 경골의 변화
Discussion
References
저자
  • Eun-Ji Oh(Department of Pharmacology and Dental Therapeutics, School of Dentistry, Chonnam National University)
  • Yaran Zang(Department of Pharmacology and Dental Therapeutics, School of Dentistry, Chonnam National University/Hard-tissue Biointerface Research Center, School of Dentistry, Chonnam National University)
  • Jung-Woo Kim(Department of Pharmacology and Dental Therapeutics, School of Dentistry, Chonnam National University/Hard-tissue Biointerface Research Center, School of Dentistry, Chonnam National University)
  • Mi Nam Lee(Department of Pharmacology and Dental Therapeutics, School of Dentistry, Chonnam National University/Hard-tissue Biointerface Research Center, School of Dentistry, Chonnam National University)
  • Ju Han Song(Department of Pharmacology and Dental Therapeutics, School of Dentistry, Chonnam National University/Hard-tissue Biointerface Research Center, School of Dentistry, Chonnam National University)
  • Sin-Hye Oh(Department of Pharmacology and Dental Therapeutics, School of Dentistry, Chonnam National University)
  • Seung Hee Kwon(Department of Pharmacology and Dental Therapeutics, School of Dentistry, Chonnam National University/Hard-tissue Biointerface Research Center, School of Dentistry, Chonnam National University)
  • Jin-Woo Yang(Department of Pharmacology and Dental Therapeutics, School of Dentistry, Chonnam National University/Hard-tissue Biointerface Research Center, School of Dentistry, Chonnam National University)
  • Jeong-Tae Koh(Department of Pharmacology and Dental Therapeutics, School of Dentistry, Chonnam National University/Hard-tissue Biointerface Research Center, School of Dentistry, Chonnam National University) Correspondence to