发信人: pcd (在郁金香的国度), 信区: S_LifeScience
标 题: 张峻峰老师课题组又一篇Gut文章上线!
发信站: 南京大学小百合站 (Fri Sep 6 11:55:02 2013)
本实验室的研究成果继2010年之后又一次被Gut收录，其最新影响因子10.732，特此报喜！
Huang Z, Shi T, Zhou Q, Shi S, Zhao R, Shi H, Dong L, Zhang C, Zeng K, Chen J,
Zhang J. miR-141 Regulates colonic leukocytic trafficking by targeting CXCL12
beta during murine colitis and human Crohn's disease. Gut. 2013.
链接：
http://www.ncbi.nlm.nih.gov/pubmed/24000293
Abstract
OBJECTIVE: Emerging evidence suggests that microRNA (miRNA)-mediated gene
regulation influences a variety of autoimmune disease processes, including
Crohn's disease (CD), but the biological function of miRNAs in CD remains
unclear. We examine miRNA level in colon tissues and study the potential
functions of miRNAs that regulate pathological genes during the inflammation
process. DESIGN: miRNA levels were assayed in the inflamed colon of 2,4,6-
trinitrobenzene sulfonic acid (TNBS)-induced and IL-10 knockout (KO) chronic
colitis mice and CD patients by microarray or qRT-PCR. The influence of
differently expressed miR-141 on its putative target genes, CXCL12beta, and
leukocyte migration was investigated in colonic epithelia cells, colitis
models and CD patients. The role of miR-141 was further studied in the
experimental colitis mice by intracolonic administration of miR-141 precursors
or inhibitors. RESULTS: An inverse correlation between miR-141 and CXCL12beta
/total-CXCL12 was observed predominantly in the epithelial cells of the
inflamed colons from colitic mice and CD patients. Further study demonstrated
that miR-141 directly regulated CXCL12beta expression and CXCL12beta-mediated
leukocyte migration. Upregulation or downregulation of miR-141 in the TNBS-
induced or IL-10 KO colitic colon regulated leukocyte infiltration and
alleviated or aggravated experimental colitis, respectively. Additionally,
colonic overexpression of CXCL12beta abolished the therapeutic effect of miR-1
41 in TNBS-induced colitis. CONCLUSIONS: This study showed that the pathway of
miR-141 targeting CXCL12beta is a possible mechanism underlying inflammatory
cell trafficking during colonic inflammation process. Inhibiting colonic CXCL1
2beta expression and blocking colonic immune cell recruitment by using miRNA
precursors represents a promising approach that may be valuable for CD
treatment.
--
※ 来源:．南京大学小百合站 http://bbs.nju.edu.cn [FROM: 114.212.207.179]
标 题: 张峻峰老师课题组又一篇Gut文章上线!
发信站: 南京大学小百合站 (Fri Sep 6 11:55:02 2013)
本实验室的研究成果继2010年之后又一次被Gut收录，其最新影响因子10.732，特此报喜！
Huang Z, Shi T, Zhou Q, Shi S, Zhao R, Shi H, Dong L, Zhang C, Zeng K, Chen J,
Zhang J. miR-141 Regulates colonic leukocytic trafficking by targeting CXCL12
beta during murine colitis and human Crohn's disease. Gut. 2013.
链接：
http://www.ncbi.nlm.nih.gov/pubmed/24000293
Abstract
OBJECTIVE: Emerging evidence suggests that microRNA (miRNA)-mediated gene
regulation influences a variety of autoimmune disease processes, including
Crohn's disease (CD), but the biological function of miRNAs in CD remains
unclear. We examine miRNA level in colon tissues and study the potential
functions of miRNAs that regulate pathological genes during the inflammation
process. DESIGN: miRNA levels were assayed in the inflamed colon of 2,4,6-
trinitrobenzene sulfonic acid (TNBS)-induced and IL-10 knockout (KO) chronic
colitis mice and CD patients by microarray or qRT-PCR. The influence of
differently expressed miR-141 on its putative target genes, CXCL12beta, and
leukocyte migration was investigated in colonic epithelia cells, colitis
models and CD patients. The role of miR-141 was further studied in the
experimental colitis mice by intracolonic administration of miR-141 precursors
or inhibitors. RESULTS: An inverse correlation between miR-141 and CXCL12beta
/total-CXCL12 was observed predominantly in the epithelial cells of the
inflamed colons from colitic mice and CD patients. Further study demonstrated
that miR-141 directly regulated CXCL12beta expression and CXCL12beta-mediated
leukocyte migration. Upregulation or downregulation of miR-141 in the TNBS-
induced or IL-10 KO colitic colon regulated leukocyte infiltration and
alleviated or aggravated experimental colitis, respectively. Additionally,
colonic overexpression of CXCL12beta abolished the therapeutic effect of miR-1
41 in TNBS-induced colitis. CONCLUSIONS: This study showed that the pathway of
miR-141 targeting CXCL12beta is a possible mechanism underlying inflammatory
cell trafficking during colonic inflammation process. Inhibiting colonic CXCL1
2beta expression and blocking colonic immune cell recruitment by using miRNA
precursors represents a promising approach that may be valuable for CD
treatment.
--
※ 来源:．南京大学小百合站 http://bbs.nju.edu.cn [FROM: 114.212.207.179]
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