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肥胖症小鼠模型模拟出生创伤后单核细胞趋化蛋白 3 的表达。

Expression of monocyte chemotactic protein 3 following simulated birth trauma in a murine model of obesity.

机构信息

Department of Urology, University Hospitals Case Medical Center, Case Western Reserve University, Cleveland, OH 44113, USA.

出版信息

Urology. 2010 Dec;76(6):1517.e12-7. doi: 10.1016/j.urology.2010.07.466. Epub 2010 Oct 23.

DOI:10.1016/j.urology.2010.07.466
PMID:20970834
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4169711/
Abstract

OBJECTIVE

To determine the effect of obesity on simulated birth trauma in leptin-deficient obese mice as measured by relative monocyte chemotactic protein 3 (MCP-3) expression.

MATERIALS AND METHODS

A total of 25 wild-type and 25 obese C57BL/6 virgin female mice underwent 1 hour of vaginal distension (VD), sham VD, or anesthesia without VD. Pelvic organ tissues were then harvested either immediately or 24-hours post VD and subsequent real-time polymerase chain reaction analysis was performed.

RESULTS

Urethral MCP-3 levels in wild-type mice were elevated from baseline at 0 hours with a return to baseline at 24 hours in both VD and sham VD groups. In obese mice, there was a 6-fold elevation in MCP-3 levels at 0 hours after sham VD vs control (P <.05), which then returned to baseline levels at 24 hours. After undergoing VD, MCP-3 levels increased to 6-fold baseline values (P = .002) at 0 hours, with continued elevation in MCP-3 levels to 15 times control levels (P = .0003) at 24 hours.

CONCLUSIONS

MCP-3 is significantly over-expressed in the urethral tissues of both wild-type and obese mice immediately after any urethral manipulation. At 24 hours, the MCP-3 expression patterns become divergent between VD and sham VD in obese mice. With a greater degree of trauma, MCP-3 continued to rise at 24 hours, suggesting that the underlying obesity resulted in alterations in response to tissue injury, paralleling the degree of injury. Such associations warrant further investigation into the role of MCP-3 as a chemokine for stem cell migration, with implications for subsequent tissue repair mechanisms after birth trauma.

摘要

目的

通过相对单核细胞趋化蛋白 3(MCP-3)表达来确定肥胖对瘦素缺乏肥胖小鼠模拟分娩损伤的影响。

材料与方法

共 25 只野生型和 25 只肥胖 C57BL/6 处女雌性小鼠接受 1 小时阴道扩张(VD)、假 VD 或无 VD 麻醉。然后立即或 VD 后 24 小时采集盆腔器官组织,并进行实时聚合酶链反应分析。

结果

野生型小鼠的尿道 MCP-3 水平在 0 小时时从基线升高,在 VD 和假 VD 组中均在 24 小时时恢复到基线。在肥胖小鼠中,假 VD 后 0 小时 MCP-3 水平升高 6 倍,与对照组相比(P <.05),然后在 24 小时时恢复到基线水平。接受 VD 后,MCP-3 水平在 0 小时时升高至 6 倍基线值(P =.002),24 小时时 MCP-3 水平继续升高至 15 倍对照组水平(P =.0003)。

结论

在任何尿道操作后,野生型和肥胖小鼠的尿道组织中 MCP-3 均显著过表达。24 小时时,肥胖小鼠的 VD 和假 VD 之间的 MCP-3 表达模式变得不同。随着创伤程度的增加,MCP-3 在 24 小时时继续升高,这表明肥胖导致对组织损伤的反应发生改变,与损伤程度平行。这些关联需要进一步研究 MCP-3 作为趋化因子对干细胞迁移的作用,这对分娩损伤后组织修复机制有影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9890/4169711/59ca88d3d096/nihms584499f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9890/4169711/49e74ac296ea/nihms584499f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9890/4169711/3add6352eec7/nihms584499f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9890/4169711/59ca88d3d096/nihms584499f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9890/4169711/49e74ac296ea/nihms584499f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9890/4169711/3add6352eec7/nihms584499f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9890/4169711/59ca88d3d096/nihms584499f3.jpg

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本文引用的文献

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Cytokine expression after vaginal distention of different durations in virgin Sprague-Dawley rats.处女Sprague-Dawley大鼠不同时长阴道扩张后的细胞因子表达
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A mouse model of simulated birth trauma induced stress urinary incontinence.一种模拟分娩创伤诱导压力性尿失禁的小鼠模型。
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