Evidence that CXCL16 is a potent mediator of angiogenesis and is involved in endothelial progenitor cell chemotaxis : studies in mice with K/BxN serum-induced arthritis.
Evidence that CXCL16 is a potent mediator of angiogenesis and is involved in endothelial progenitor cell chemotaxis : studies in mice with K/BxN serum-induced arthritis.
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DOI：
10.1002/art.37981
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发表时间：
2013-07
影响因子：
--
通讯作者：
Ruth, Jeffrey H.
中科院分区：
文献类型：
--
作者：
Isozaki, Takeo;Arbab, Ali S.;Haas, Christian S.;Amin, M. Asif;Arendt, Monica D.;Koch, Alisa E.;Ruth, Jeffrey H.
我们检测了CXCL16在类风湿性关节炎(RA)滑膜中招募内皮细胞(ECs)形成新生血管的可能性。我们利用RA滑膜组织(ST)严重联合免疫缺陷(SCID)小鼠嵌合系统检测了人真皮微血管内皮细胞(HMVEC)和人内皮祖细胞(EPC)在移植的人滑膜中的募集情况。以CXCR6基因缺陷(CXCR6−/−)和野生型(Wt)C57BL/6小鼠为模型，制备K/BxN血清诱导的关节炎模型，并观察其血管生成情况。用免疫荧光和CXCL16信号活性检测人脐血HMVECs和EPC中CXCR6的表达。我们发现CXCR6在人内皮祖细胞和人脐静脉内皮细胞上有显著表达，并可被白介素1β(IL-1β)上调。SCID小鼠移植体内注射RA SF，CXCL16免疫耗竭后，EPC募集显著减少。使用K/BxN血清诱导的炎性关节炎模型，与野生型(Wt)小鼠相比，CXCR6−/−小鼠的血红蛋白(Hb)水平显著降低，这与CXCR6−/−小鼠的单核细胞减少和T细胞向关节炎关节组织的募集有关。我们还发现，HMVEC和EPC对CXCL16刺激有反应，但具有独特的信号转导途径和归巢特性。这些结果表明，CXCL16及其受体CXCR6可能是一对与RA关节内EPC募集和血管形成高度相关的中枢配体-受体对。
We examined the possibility that CXCL16 recruits endothelial cells (ECs) to developing neovasculature in rheumatoid arthritis (RA) synovium. We utilized the RA synovial tissue (ST) severe combined immunodeficient (SCID) mouse chimera system to examine human dermal microvascular endothelial cell (HMVEC) and human endothelial progenitor cell (EPC) recruitment into engrafted human synovium injected intragraft with RA synovial fluid (SF) immunodepleted of CXCL16. CXCR6 deficient (CXCR6−/−) and wild-type (Wt) C57BL/6 mice were primed to develop K/BxN serum induced arthritis and evaluated for angiogenesis. HMVECs and EPCs from human cord blood were also examined for CXCR6 expression by immunofluorescence and signaling activity for CXCL16. We found that CXCR6 is prominently expressed on human EPCs and HMVECs and can be upregulated by interleukin-1β (IL-1β). SCID mice injected intragraft with RA SF immunodepleted of CXCL16 showed a significant reduction in EPC recruitment. Using the K/BxN serum induced inflammatory arthritis model, CXCR6−/− mice showed profound reductions in hemoglobin (Hb) levels that correlated with reductions in monocyte and T-cell recruitment to arthritic joint tissue in CXCR6−/− compared to wildtype (Wt) mice. We also found that HMVECs and EPCs respond to CXCL16 stimulation but have unique signal transduction pathways and homing properties. These results indicate that CXCL16 and its receptor CXCR6 may be a central ligand-receptor pair that can be highly correlated with EPC recruitment and blood vessel formation in the RA joint.
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影响因子：
4.4
作者：
Woods, JM;Katschke, KJ;Kock, AE
通讯作者：
Kock, AE
缺乏内皮选择素的小鼠中关节炎的加速发育。
影响因子：
4.9
作者：
Ruth JH;Amin MA;Woods JM;He X;Samuel S;Yi N;Haas CS;Koch AE;Bullard DC
通讯作者：
Bullard DC
DOI：
10.1084/jem.175.4.1135
发表时间：
1992-04-01
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Peacock DJ;Banquerigo ML;Brahn E
通讯作者：
Brahn E
影响因子：
--
作者：
Nanki, T;Shimaoka, T;Miyasaka, N
通讯作者：
Miyasaka, N
影响因子：
--
作者：
Haas, Christian S.;Amin, M. Asif;Koch, Alisa E.
通讯作者：
Koch, Alisa E.