目的:探讨细胞表面抗原4F2重链(4F2 heavy chain,4F2hc)在人脑胶质瘤组织中的表达水平及其与胶质瘤病理学特征、细胞增殖以及血管形成的关系。方法:采用免疫组化方法检测4F2hc、Ki-67和CD34在62例人脑胶质瘤组织中的表达,计数Ki-67标记...目的:探讨细胞表面抗原4F2重链(4F2 heavy chain,4F2hc)在人脑胶质瘤组织中的表达水平及其与胶质瘤病理学特征、细胞增殖以及血管形成的关系。方法:采用免疫组化方法检测4F2hc、Ki-67和CD34在62例人脑胶质瘤组织中的表达,计数Ki-67标记指数(Ki-67 LI)和微血管密度(MVD)。结果:4F2hc在胶质瘤中高表达,其免疫阳性染色既定位于瘤细胞也定位于血管内皮;4F2hc表达随胶质瘤病理级别升高而明显增强(P=0.001),在高度恶性胶质瘤中4F2hc表达明显强于低度恶性胶质瘤(P=0.002);4F2hc表达与胶质瘤Ki-67标记指数存在明显正相关(P=0.003),但与微血管密度无明显相关性(P=0.214)。结论:4F2hc与胶质瘤的发生和发展关系密切,可能在胶质瘤的恶性增殖过程中具有重要作用。展开更多
Background: Extracellular matrix (ECM) participates in heart growth and influences cardiac stem-cell differentiation and migration. The modification of ECM associated with cardiomyopathies is a complex process involvi...Background: Extracellular matrix (ECM) participates in heart growth and influences cardiac stem-cell differentiation and migration. The modification of ECM associated with cardiomyopathies is a complex process involving a cohort of proteins. ECM proteins are involved in the regulation of neoangiogenesis in physiological and pathological conditions through their interaction with some angiogenic factors. Our aim was to investigate the role of some angiogenesis-related ECM proteins in the remodeling heart. Methods: We examined cardiac tissue samples from 21 explanted human hearts and 10 non-failing hearts before transplantation. Each specimen was submitted to morphological and biomolecular analysis. Results: We demonstrated a reduced expression of α2-chain laminin mRNA in pathological samples that could play an important role in the progression of cardiac failure by contributing to sarcolemma modifications. Reduced expression of tenascin cytotactin (TN-C) and TN-X in explanted hearts indicated chronic cardiac damage and an impaired capacity to stimulate new vessel development. The observed type IV collagen increase was not related to neoangiogenesis, as reflected by the decreased expression of vascular endothelial growth factor (VEGF)-A and VEGF receptor-2. The inverse correlation between heart dimension and VEGF-A immunopositivity seems particularly interesting. Conclusions: Our findings suggest that ECM reacts strongly to ischemic damage in failing hearts through some important modifications of its protein composition. Nevertheless, this reaction cannot completely restore myocardium structure if it is not supported by adequate neoangiogenesis. The decrease in some ECM proteins related to vessel development has a negative effect on postischemic neoangiogenesis and clinical outcome.展开更多
文摘目的:探讨细胞表面抗原4F2重链(4F2 heavy chain,4F2hc)在人脑胶质瘤组织中的表达水平及其与胶质瘤病理学特征、细胞增殖以及血管形成的关系。方法:采用免疫组化方法检测4F2hc、Ki-67和CD34在62例人脑胶质瘤组织中的表达,计数Ki-67标记指数(Ki-67 LI)和微血管密度(MVD)。结果:4F2hc在胶质瘤中高表达,其免疫阳性染色既定位于瘤细胞也定位于血管内皮;4F2hc表达随胶质瘤病理级别升高而明显增强(P=0.001),在高度恶性胶质瘤中4F2hc表达明显强于低度恶性胶质瘤(P=0.002);4F2hc表达与胶质瘤Ki-67标记指数存在明显正相关(P=0.003),但与微血管密度无明显相关性(P=0.214)。结论:4F2hc与胶质瘤的发生和发展关系密切,可能在胶质瘤的恶性增殖过程中具有重要作用。
文摘Background: Extracellular matrix (ECM) participates in heart growth and influences cardiac stem-cell differentiation and migration. The modification of ECM associated with cardiomyopathies is a complex process involving a cohort of proteins. ECM proteins are involved in the regulation of neoangiogenesis in physiological and pathological conditions through their interaction with some angiogenic factors. Our aim was to investigate the role of some angiogenesis-related ECM proteins in the remodeling heart. Methods: We examined cardiac tissue samples from 21 explanted human hearts and 10 non-failing hearts before transplantation. Each specimen was submitted to morphological and biomolecular analysis. Results: We demonstrated a reduced expression of α2-chain laminin mRNA in pathological samples that could play an important role in the progression of cardiac failure by contributing to sarcolemma modifications. Reduced expression of tenascin cytotactin (TN-C) and TN-X in explanted hearts indicated chronic cardiac damage and an impaired capacity to stimulate new vessel development. The observed type IV collagen increase was not related to neoangiogenesis, as reflected by the decreased expression of vascular endothelial growth factor (VEGF)-A and VEGF receptor-2. The inverse correlation between heart dimension and VEGF-A immunopositivity seems particularly interesting. Conclusions: Our findings suggest that ECM reacts strongly to ischemic damage in failing hearts through some important modifications of its protein composition. Nevertheless, this reaction cannot completely restore myocardium structure if it is not supported by adequate neoangiogenesis. The decrease in some ECM proteins related to vessel development has a negative effect on postischemic neoangiogenesis and clinical outcome.
