Tardy Felicia Magee, Benghuzzi Hamed, Tucci Michelle
Clinical Health Sciences Graduate Program, School of Health Related Professions, Departments of Pathology and Orthopedic Surgery, University of Mississippi Medical Center, Jackson, Mississippi, USA.
Biomed Sci Instrum. 2002;38:191-6.
Increasing evidence reveals that low-density lipoproteins (LDL) and gender are significant risk factors in the development of cardiovascular disease (CVD). The long-term objective of this investigation is to determine the possible relationship between sex hormones, LDL, and the development of CVD. The specific aims of this investigation include: (1) to evaluate the effect of estrogen (E) and testosterone (T) on the proliferation of MRC-5 cells, (2) to investigate the role of E and T on the viability of MRC-5 cells exposed to physiological and supraphysiological levels of LDL, and (3) to evaluate the morphological changes associated with E, T, and LDL, alone or in combination, on MRC-5 cells. Proliferation rates, biochemical marker analysis, and morphological evaluations were performed following standard laboratory procedures. The results of the investigation revealed that physiological and supraphysiological levels of LDL, alone, or in combination with E and T, induced significant changes in the functional and structural capacities of MRC-5 fibroblasts throughout the experimental phases (24, 48, and 72 hours) in comparison to the control groups. MRC-5 cells exposed to T and LDL resulted in increased proliferation rates and remarkable cellular damage. In contrast, E exposure induced decreased levels of MDA compared to T exposure. Results from this investigation suggest the development of collagen matrix post cardiovascular necrosis can be attributed to the presence of T. This response could be triggered directly at the fibroblast level or by altering the physiochemical characteristics of LDL.
越来越多的证据表明,低密度脂蛋白(LDL)和性别是心血管疾病(CVD)发生发展的重要风险因素。本研究的长期目标是确定性激素、LDL与CVD发生之间的可能关系。本研究的具体目标包括:(1)评估雌激素(E)和睾酮(T)对MRC - 5细胞增殖的影响;(2)研究E和T对暴露于生理和超生理水平LDL的MRC - 5细胞活力的作用;(3)评估单独或联合使用E、T和LDL对MRC - 5细胞形态变化的影响。按照标准实验室程序进行增殖率、生化标志物分析和形态学评估。研究结果表明,与对照组相比,生理和超生理水平的LDL单独或与E和T联合使用,在整个实验阶段(24、48和72小时)均能诱导MRC - 5成纤维细胞的功能和结构能力发生显著变化。暴露于T和LDL的MRC - 5细胞导致增殖率增加和明显的细胞损伤。相比之下,与暴露于T相比,暴露于E导致丙二醛水平降低。本研究结果表明,心血管坏死后置胶原基质的形成可能归因于T的存在。这种反应可能直接在成纤维细胞水平触发,或通过改变LDL的理化特性引发。