We previously demonstrated that atherogenic Ldlr−/−Apobec1−/− (LDb) double knockout mice lacking both low-density lipoprotein receptor (LDLR) and apolipoprotein B mRNA-editing catalytic polypeptide-1 (Apobec1) had increased serum IL-17 levels,...
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https://www.riss.kr/link?id=A106501822
김영욱 (The University of Texas Health Science Center at Houston) ; Patrick Kee (The University of Texas Health Science Center at Houston) ; Delia Danila (The University of Texas Health Science Center at Houston) ; Ba-Bie Teng (The University of Texas Health Science Center at Houston)
2019
English
PCSK9 ; IL-17 ; Atherosclerosis ; T-cells
KCI우수등재,SCOPUS,SCIE
학술저널
1-16(16쪽)
0
0
상세조회0
다운로드다국어 초록 (Multilingual Abstract)
We previously demonstrated that atherogenic Ldlr−/−Apobec1−/− (LDb) double knockout mice lacking both low-density lipoprotein receptor (LDLR) and apolipoprotein B mRNA-editing catalytic polypeptide-1 (Apobec1) had increased serum IL-17 levels,...
We previously demonstrated that atherogenic Ldlr−/−Apobec1−/− (LDb) double knockout mice lacking both low-density lipoprotein receptor (LDLR) and apolipoprotein B mRNA-editing catalytic polypeptide-1 (Apobec1) had increased serum IL-17 levels, with T cell programming shifted towards Th17 cells. In this study, we assessed the role of proprotein convertase subtilisin/kexin type 9 (PCSK9) in T cell programming and atherogenesis. We deleted the Pcsk9 gene from LDb mice to generate Ldlr−/−Apobec1−/−Pcsk9−/− (LTp) triple knockout mice. Atherosclerosis in the aortic sinus and aorta were quantitated. Lymphoid cells were analyzed by flow cytometry, ELISA and real-time PCR. Despite of dyslipidemia, LTp mice developed barely detectable atherosclerotic lesions. The IL-17, was very low in plasma and barely detectable in the aortic sinus in the LTp mice. In the spleen, the number of CD4+CD8− cells and splenocytes were much lower in the LDb mice than LTp mice, whereas, the IL-17-producing cells of γδTCR+ T cells and effector memory CD4+ T cells (CD44hiCD4+) in the spleen were significantly higher in the LDb mice than in the LTp mice. The Rorc mRNA expression levels were elevated in LDb mice compared to LTp mice. When re-stimulated with an anti-CD3 Ab, CD44hiCD4+ T cells from LDb mice secreted more IL-17 than those from LTp mice. T cells from LDb mice (with PCSK9) produce more IL-17 at basal and stimulated conditions when compared with LTp mice (without PCSK9). Despite the dyslipidemic profile and the lack of LDLR, atherogenesis is markedly reduced in LTp mice. These results suggest that PCSK9 is associated with changes in T cell programming that contributes to the development of atherosclerosis.
참고문헌 (Reference)
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학술지 이력
연월일 | 이력구분 | 이력상세 | 등재구분 |
---|---|---|---|
2025 | 평가예정 | 해외DB학술지평가 신청대상 (해외등재 학술지 평가) | |
2022-01-01 | 평가 | 등재학술지 유지 (해외등재 학술지 평가) | |
2021-12-01 | 평가 | 등재로 하락 (재인증) | |
2016-02-22 | 학회명변경 | 영문명 : Korean Association Of Immunbiologists -> The Korean Association of Immunologists | |
2016-01-01 | 평가 | 우수등재학술지 선정 (계속평가) | |
2012-01-01 | 평가 | 등재 1차 FAIL (등재유지) | |
2009-01-01 | 평가 | 등재학술지 선정 (등재후보2차) | |
2008-01-01 | 평가 | 등재후보 1차 PASS (등재후보1차) | |
2007-01-01 | 평가 | 등재후보학술지 유지 (등재후보2차) | |
2006-01-01 | 평가 | 등재후보 1차 PASS (등재후보1차) | |
2004-07-01 | 평가 | 등재후보학술지 선정 (신규평가) |
학술지 인용정보
기준연도 | WOS-KCI 통합IF(2년) | KCIF(2년) | KCIF(3년) |
---|---|---|---|
2016 | 0.36 | 0.36 | 0.29 |
KCIF(4년) | KCIF(5년) | 중심성지수(3년) | 즉시성지수 |
0.24 | 0.2 | 0.636 | 0 |