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.

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.
复制标题

DOI:
10.1371/journal.pone.0057742
复制
发表时间:
2013
期刊:
影响因子:
3.7
通讯作者:
Santamaria L
Santamaria L
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Arriazu R;Durán E;Pozuelo JM;Santamaria L

文献摘要

参考文献

被引文献

相似文献

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的免疫表达、细胞增殖、凋亡和血管生成标志物。计算正常大鼠和染镉大鼠腹侧前列腺中LPA-1(LILPA 1)、PCNA(LIPCNA)、MCM 7(LIMCM 7)、泛素(LIUBI)、凋亡细胞(LIAPO)和p53(LIp 53)免疫反应阳性细胞的百分比,Bcl-2(VFBcl-2)的体积分数;和每单位体积的微血管长度(LVMV/mm 3)。使用Student t检验和Pearson相关性检验分析数据。LILPA 1在镉处理组大鼠的不典型增生病变和正常上皮中的表达明显高于对照组。增生标志物显着增加,而一些凋亡标志物显着减少。VFBcl-2在组间无显著差异。异型增生病变显示LIp 53的显著增加。每单位体积的微血管长度在发育不良的腺泡中升高。仅LILPA 1和LIUBI之间存在统计学显著相关性。我们的研究结果表明,LPA-1可能牵连在镉的发展引起的发育异常病变。需要更多的研究来证实它对疾病的潜在贡献。
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. 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. 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. 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.
DOI: 10.1002/pros.20192
发表时间: 2005-06-01
期刊: PROSTATE
影响因子: 2.8
作者:
Arriazu, R;Pozuelo, JM;Santamaría, L
通讯作者: Santamaría, L
DOI: 10.1055/s-2006-958465
发表时间: 2007-02-01
影响因子: 5.7
作者:
Delves, George H.;Stewart, Alistair B.;Lwaleed, Bashir A.
通讯作者: Lwaleed, Bashir A.
DOI: 10.1210/en.2005-1635
发表时间: 2006-10-01
期刊: ENDOCRINOLOGY
影响因子: 4.8
作者:
Guo, Rishu;Kasbohm, Elizabeth A.;Daaka, Yehia
通讯作者: Daaka, Yehia
DOI: 10.1371/journal.pone.0018192
发表时间: 2011-03-28
期刊: PloS one
影响因子: 3.7
作者:
Lundequist A;Boyce JA
通讯作者: Boyce JA
DOI: 10.1083/jcb.119.3.493
发表时间: 1992-11
期刊: The Journal of cell biology
影响因子: --
作者:
Gavrieli Y;Sherman Y;Ben-Sasson SA
通讯作者: Ben-Sasson SA