• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利：CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法，用中文像聊天一样搜索，搜遍4000万医学文献。AI智能推荐，让科研检索更轻松。

立即免费搜索

文件翻译

保留排版，准确专业，支持PDF/Word/PPT等文件格式，支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述，25分钟生成高质量综述，智能提取关键信息，辅助科研写作。

立即免费体验

氯化镉诱导大鼠前列腺前病变过程中溶血磷脂酸受体 1 的表达及其与细胞增殖、凋亡和血管生成的关系。

Expression of lysophosphatidic acid receptor 1 and relation with cell proliferation, apoptosis, and angiogenesis on preneoplastic changes induced by cadmium chloride in the rat ventral prostate.

机构信息

Histology Laboratory, Institute of Applied Molecular Medicine, Department of Basic Medical Sciences, School of Medicine, CEU-San Pablo University, Madrid, Spain.

出版信息

PLoS One. 2013;8(2):e57742. doi: 10.1371/journal.pone.0057742. Epub 2013 Feb 22.

DOI:10.1371/journal.pone.0057742
PMID:23451264
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3579784/
Abstract

BACKGROUND

Lysophosphatidic acid (LPA) is a phospholipid growth factor involved in cell proliferation, differentiation, migration, inflammation, angiogenesis, wound healing, cancer invasion, and survival. This study was directed to evaluate the immunoexpression of LPA-1, cell proliferation, apoptosis, and angiogenesis markers in preneoplastic lesions induced with cadmium chloride in rat prostate.

METHODS

The following parameters were calculated in ventral prostate of normal rats and rats that received Cd in drinking water during 24 months: percentages of cells immunoreactive to LPA-1 (LILPA1), PCNA (LIPCNA), MCM7 (LIMCM7), ubiquitin (LIUBI), apoptotic cells (LIAPO), and p53 (LIp53); volume fraction of Bcl-2 (VFBcl-2); and length of microvessels per unit of volume (LVMV/mm3). Data were analyzed using Student's t-test and Pearson correlation test.

RESULTS

The LILPA1 in dysplastic lesions and normal epithelium of Cd-treated rats was significantly higher than those in the control group. Markers of proliferation were significantly increased in dysplastic lesions, whereas some apoptotic markers were significantly decreased. No significant differences between groups were found in VFBcl-2. Dysplastic lesions showed a significant increase of LIp53. The length of microvessels per unit of volume was elevated in dysplastic acini. Statistically significant correlations were found only between LILPA1 and LIUBI.

CONCLUSIONS

Our results suggest that LPA-1 might be implicated in dysplastic lesions induced by cadmium chloride development. More studies are needed to confirm its potential contribution to the disease.

摘要

背景

溶血磷脂酸（LPA）是一种参与细胞增殖、分化、迁移、炎症、血管生成、伤口愈合、癌症侵袭和存活的磷脂生长因子。本研究旨在评估氯化镉诱导的大鼠前列腺癌前病变中 LPA-1、细胞增殖、细胞凋亡和血管生成标志物的免疫表达。

方法

计算正常大鼠和在饮用水中接受 Cd 处理 24 个月的大鼠前列腺腹侧的以下参数：对 LPA-1（LILPA1）、PCNA（LIPCNA）、MCM7（LIMCM7）、泛素（LIUBI）、凋亡细胞（LIAPO）和 p53（LIp53）有免疫反应的细胞百分比；Bcl-2 的体积分数（VFBcl-2）；和每单位体积的微血管长度（LVMV/mm3）。使用 Student's t 检验和 Pearson 相关检验分析数据。

结果

Cd 处理大鼠的发育不良病变和正常上皮中的 LILPA1 明显高于对照组。增殖标志物在发育不良病变中显著增加，而一些凋亡标志物则显著减少。VFBcl-2 各组间无显著差异。发育不良病变中 LIp53 明显增加。单位体积的微血管长度在发育不良的腺泡中升高。仅在 LILPA1 和 LIUBI 之间发现有统计学意义的相关性。

结论

我们的结果表明，LPA-1 可能参与了氯化镉诱导的发育不良病变的发生。需要进一步的研究来证实其对疾病的潜在贡献。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ab9/3579784/d00212f895e5/pone.0057742.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ab9/3579784/8c5f3278a835/pone.0057742.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ab9/3579784/effd72a5b9ef/pone.0057742.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ab9/3579784/de6025983fd7/pone.0057742.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ab9/3579784/c69eae10e10e/pone.0057742.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ab9/3579784/d00212f895e5/pone.0057742.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ab9/3579784/8c5f3278a835/pone.0057742.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ab9/3579784/effd72a5b9ef/pone.0057742.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ab9/3579784/de6025983fd7/pone.0057742.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ab9/3579784/c69eae10e10e/pone.0057742.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ab9/3579784/d00212f895e5/pone.0057742.g005.jpg

相似文献

1
Expression of lysophosphatidic acid receptor 1 and relation with cell proliferation, apoptosis, and angiogenesis on preneoplastic changes induced by cadmium chloride in the rat ventral prostate.氯化镉诱导大鼠前列腺前病变过程中溶血磷脂酸受体 1 的表达及其与细胞增殖、凋亡和血管生成的关系。
PLoS One. 2013;8(2):e57742. doi: 10.1371/journal.pone.0057742. Epub 2013 Feb 22.
2
Immunohistochemical study of cell proliferation, Bcl-2, p53, and caspase-3 expression on preneoplastic changes induced by cadmium and zinc chloride in the ventral rat prostate.镉和氯化锌诱导大鼠前列腺前体病变中细胞增殖、Bcl-2、p53和半胱天冬酶-3表达的免疫组织化学研究
J Histochem Cytochem. 2006 Sep;54(9):981-90. doi: 10.1369/jhc.5A6733.2006. Epub 2006 Apr 3.
3
Cadmium chloride-induced dysplastic changes in the ventral rat prostate: an immunohistochemical and quantitative study.氯化镉诱导的雄性大鼠前列腺腹叶发育异常改变：一项免疫组织化学及定量研究
Prostate. 2001 Jan 1;46(1):11-20. doi: 10.1002/1097-0045(200101)46:1<11::aid-pros1003>3.0.co;2-k.
4
Quantitative and immunohistochemical evaluation of PCNA, androgen receptors, apoptosis, and Glutathione-S-Transferase P1 on preneoplastic changes induced by cadmium and zinc chloride in the rat ventral prostate.镉和氯化锌诱导大鼠腹侧前列腺肿瘤前变化过程中PCNA、雄激素受体、细胞凋亡及谷胱甘肽-S-转移酶P1的定量与免疫组化评估
Prostate. 2005 Jun 1;63(4):347-57. doi: 10.1002/pros.20192.
5
Lysophosphatidic acid signaling promotes proliferation, differentiation, and cell survival in rat growth plate chondrocytes.溶血磷脂酸信号传导促进大鼠生长板软骨细胞的增殖、分化和细胞存活。
Biochim Biophys Acta. 2009 May;1793(5):836-46. doi: 10.1016/j.bbamcr.2009.01.020. Epub 2009 Feb 21.
6
Correlation of increased apoptosis and proliferation with development of prostatic intraepithelial neoplasia (PIN) in ventral prostate of the Noble rat.凋亡增加和增殖与诺布尔大鼠腹侧前列腺前列腺上皮内瘤变（PIN）发展的相关性。
Prostate. 2000 Jun 15;44(1):31-9. doi: 10.1002/1097-0045(20000615)44:1<31::aid-pros5>3.0.co;2-o.
7
Profile of cell proliferation and apoptosis activated by the intrinsic and extrinsic pathways in the prostate of aging rats.衰老大鼠前列腺中由内源性和外源性途径激活的细胞增殖和凋亡概况。
Prostate. 2017 Jun;77(9):937-948. doi: 10.1002/pros.23349.
8
The value of immunohistochemical research on PCNA, p53 and heat shock proteins in prostate cancer management: a review.PCNA、p53和热休克蛋白免疫组化研究在前列腺癌治疗中的价值：综述
Eur J Histochem. 2006 Jan-Mar;50(1):25-34.
9
Relation between Bcl-2, cell proliferation, and the androgen receptor status in prostate tissue and precursors of prostate cancer.前列腺组织及前列腺癌前体中Bcl-2、细胞增殖与雄激素受体状态之间的关系。
Prostate. 1998 Mar 1;34(4):251-8. doi: 10.1002/(sici)1097-0045(19980301)34:4<251::aid-pros2>3.0.co;2-k.
10
Modulation of neoangiogenesis in bronchial preneoplastic lesions.支气管肿瘤前病变中新生血管生成的调节
Oncol Rep. 1999 Jul-Aug;6(4):813-7. doi: 10.3892/or.6.4.813.

引用本文的文献

1
G Protein-Coupled Receptors at the Crossroad between Physiologic and Pathologic Angiogenesis: Old Paradigms and Emerging Concepts.G 蛋白偶联受体在生理和病理性血管生成中的十字路口：旧范式与新兴概念。
Int J Mol Sci. 2017 Dec 14;18(12):2713. doi: 10.3390/ijms18122713.
2
Modeling cadmium-induced endothelial toxicity using human pluripotent stem cell-derived endothelial cells.利用人多能干细胞衍生的内皮细胞建立镉诱导的内皮细胞毒性模型。
Sci Rep. 2017 Nov 1;7(1):14811. doi: 10.1038/s41598-017-13694-5.
3
Epigenetic modifications due to heavy metals exposure in children living in polluted areas.

本文引用的文献

1
Lysophosphatidic acid enhances vascular endothelial growth factor-C expression in human prostate cancer PC-3 cells.溶血磷脂酸增强人前列腺癌细胞 PC-3 中血管内皮生长因子-C 的表达。
PLoS One. 2012;7(7):e41096. doi: 10.1371/journal.pone.0041096. Epub 2012 Jul 20.
2
Effects of TRPM8 on the proliferation and angiogenesis of prostate cancer PC-3 cells in vivo.瞬时受体电位阳离子通道亚家族M成员8（TRPM8）对体内前列腺癌PC-3细胞增殖和血管生成的影响。
Oncol Lett. 2011 Nov;2(6):1213-1217. doi: 10.3892/ol.2011.410. Epub 2011 Sep 2.
3
Transcriptional Regulation of the p53 Tumor Suppressor Gene in S-Phase of the Cell-Cycle and the Cellular Response to DNA Damage.
受污染地区儿童因重金属暴露导致的表观遗传修饰。
Curr Genomics. 2014 Dec;15(6):464-8. doi: 10.2174/138920291506150106153336.
4
A review of molecular events of cadmium-induced carcinogenesis.镉诱导致癌的分子事件综述。
J Environ Pathol Toxicol Oncol. 2014;33(3):183-94. doi: 10.1615/jenvironpatholtoxicoloncol.2014011075.
细胞周期S期p53肿瘤抑制基因的转录调控及细胞对DNA损伤的反应
Biochem Res Int. 2012;2012:808934. doi: 10.1155/2012/808934. Epub 2012 Jul 11.
4
Cadmium induces p53-dependent apoptosis in human prostate epithelial cells.镉诱导人前列腺上皮细胞中 p53 依赖性细胞凋亡。
PLoS One. 2012;7(3):e33647. doi: 10.1371/journal.pone.0033647. Epub 2012 Mar 20.
5
Ki-67 and minichromosome maintenance-7 (MCM7) expression in canine pituitary corticotroph adenomas.Ki-67 和 minichromosome maintenance-7（MCM7）在犬垂体促肾上腺皮质细胞瘤中的表达。
Domest Anim Endocrinol. 2011 Nov;41(4):207-13. doi: 10.1016/j.domaniend.2011.07.002. Epub 2011 Aug 23.
6
Diagnostic and prognostic signatures from the small non-coding RNA transcriptome in prostate cancer.前列腺癌中小非编码 RNA 转录组的诊断和预后特征。
Oncogene. 2012 Feb 23;31(8):978-91. doi: 10.1038/onc.2011.304. Epub 2011 Jul 18.
7
Non-Edg family LPA receptors: the cutting edge of LPA research.非 Edg 家族 LPA 受体：LPA 研究的前沿。
J Biochem. 2011 Sep;150(3):223-32. doi: 10.1093/jb/mvr087. Epub 2011 Jul 11.
8
Oncogenic activity of MCM7 transforming cluster.MCM7转化簇的致癌活性。
World J Clin Oncol. 2011 Feb 10;2(2):120-4. doi: 10.5306/wjco.v2.i2.120.
9
LPA5 is abundantly expressed by human mast cells and important for lysophosphatidic acid induced MIP-1β release.LPA5 在人肥大细胞中大量表达，对于溶血磷脂酸诱导的 MIP-1β 释放很重要。
PLoS One. 2011 Mar 28;6(3):e18192. doi: 10.1371/journal.pone.0018192.
10
Minichromosome maintenance protein 7 as a potential prognostic factor for progression-free survival in high-grade serous carcinomas of the ovary.微染色体维持蛋白 7 作为卵巢高级别浆液性癌无进展生存期的潜在预后因素。
Mod Pathol. 2011 Feb;24(2):277-87. doi: 10.1038/modpathol.2010.202. Epub 2010 Nov 12.