Ceauşu Zenaida, Popa Manuela, Socea Bogdan, Gorecki Gabriel Petre, Costache Mariana, Ceauşu Mihai
Pathology Department, 'Carol Davila' University of Medicine and Pharmacy, 020021 Bucharest, Romania.
Pathology Department, 'Sf. Pantelimon' Emergency Hospital, 021659 Bucharest, Romania.
Exp Ther Med. 2022 Mar;23(3):199. doi: 10.3892/etm.2022.11122. Epub 2022 Jan 5.
The extracellular matrix (ECM) consists of fibrillary and non-fibrillary components in the extracellular zone, and fulfills structural and signaling roles. Cardiac insult can lead to cardiomyocyte death, which subsequently determines dynamic changes of ECM composition and regulates cellular responses, ultimately contributing to cardiac repair. The present retrospective study on a small batch selected from the database of the Pathology Department of 'Sf. Pantelimon' Hospital aimed to determine which molecules may have a role in the dynamics of ECM using histopathology and immunohistochemistry methods. The study batch was composed of cases with cardiac ischemic conditions who died at various ages of myocardial infarcts. Tissue samples were taken from the myocardium of the left ventricle (anterior and lateral walls), and multiple series of histological sections were produced and analyzed using immunohistochemistry for collagen type I (Col-1), tenascin C (Tn-C), matrix metalloproteinase 9, CD34, and CD68. Col-1 and Tn-C showed variable patterns of fibrillar plexiform network, associated with a high micro-vascular density of newly formed capillaries revealed by CD34, and an interstitial infiltrate with histiocytes demonstrated by CD68 presence. The ECM represents therefore a polymorphic microenvironment with its own dynamics that is in continuous change, involving a large spectrum of heterogenous molecules, which play different roles in myocardium remodeling under hypoxic ischemic conditions.
细胞外基质（ECM）由细胞外区域的纤维状和非纤维状成分组成，并发挥结构和信号传导作用。心脏损伤可导致心肌细胞死亡，进而决定ECM组成的动态变化并调节细胞反应，最终促进心脏修复。本回顾性研究从“Sf. Pantelimon”医院病理科数据库中选取一小批病例，旨在使用组织病理学和免疫组织化学方法确定哪些分子可能在ECM动态变化中发挥作用。研究批次由死于不同年龄心肌梗死的心脏缺血性疾病病例组成。从左心室心肌（前壁和侧壁）获取组织样本，并制作多系列组织学切片，使用免疫组织化学方法分析I型胶原（Col-1）、腱生蛋白C（Tn-C）、基质金属蛋白酶9、CD34和CD68。Col-1和Tn-C呈现出不同的纤维状网状模式，与CD34显示的新形成毛细血管的高微血管密度相关，且CD68显示存在组织细胞的间质浸润。因此，ECM代表了一个多态性的微环境，其自身动态处于持续变化中，涉及大量异质分子，这些分子在缺氧缺血条件下的心肌重塑中发挥不同作用。
