Fontana Estevez Florencia S, Miksztowicz Verónica, Seropián Ignacio M, Cassaglia Pablo, Bustos Romina, Touceda Vanessa, Cianciulli Tomas, Cassanova Verónica, Morales Celina, González Germán E
Laboratorio de Patología Cardiovascular Experimental e Hipertensión Arterial, Instituto de Investigaciones Biomédicas, Universidad Católica Argentina-CONICET.
Laboratorio de Patología Cardiovascular Experimental e Hipertensión Arterial, Instituto de Investigaciones Biomédicas, Universidad Católica Argentina-CONICET; Servicio de Hemodinamia y Cardiología Intervencionista, Hospital Italiano de Buenos Aires.
J Vis Exp. 2023 Jul 14(197). doi: 10.3791/64143.
Cardiovascular disease is the most prevalent cause of death in Western countries, with acute myocardial infarction (MI) being the most prevalent form. This paper describes a protocol for studying the role of galectin 3 (Gal-3) in the temporal evolution of cardiac healing and remodeling in an experimental animal model of MI. The procedures described include an experimental model of MI with a permanent coronary ligature in male C57BL/6J (control) and Gal-3 knockout (KO) mice, an echocardiography procedure to study cardiac remodeling and systolic function in vivo, a histological evaluation of interstitial myocardial fibrosis with picrosirius red-stained and rhodamine-conjugated lectin-stained sections for studying myocyte hypertrophy by the cross-sectional area (MCSA), and the quantification of infarct size and cardiac remodeling (scar thinning, septum thickness, and expansion index) by planimetry in slices stained with Masson's trichrome and triphenyl tetrazolium chloride. Gal-3 KO mice with MI showed disrupted cardiac remodeling and an increase in the scar thinning ratio and the expansion index. At the onset of MI, myocardial function and cardiac remodeling were also severely affected. At 4 weeks post MI, the natural evolution of fibrosis in infarcted Gal-3 KO mice was also affected. In summary, the experimental model of MI is a suitable model for studying the temporal evolution of cardiac repair and remodeling in mice with the genetic deletion of Gal-3 and other animal models. The lack of Gal-3 affects the dynamics of cardiac repair and disrupts the evolution of cardiac remodeling and function after MI.
心血管疾病是西方国家最常见的死亡原因，急性心肌梗死（MI）是最常见的形式。本文描述了一种在MI实验动物模型中研究半乳糖凝集素3（Gal-3）在心脏愈合和重塑时间演变中作用的方案。所描述的程序包括在雄性C57BL/6J（对照）和Gal-3基因敲除（KO）小鼠中进行永久性冠状动脉结扎的MI实验模型、用于研究体内心脏重塑和收缩功能的超声心动图程序、用苦味酸天狼星红染色和罗丹明偶联凝集素染色切片对心肌间质纤维化进行组织学评估以通过横截面积（MCSA）研究心肌细胞肥大，以及通过对用Masson三色染色和氯化三苯基四氮唑染色的切片进行平面测量来量化梗死面积和心脏重塑（瘢痕变薄、室间隔厚度和扩张指数）。患有MI的Gal-3 KO小鼠表现出心脏重塑紊乱，瘢痕变薄率和扩张指数增加。在MI发作时，心肌功能和心脏重塑也受到严重影响。在MI后4周，梗死的Gal-3 KO小鼠中纤维化的自然演变也受到影响。总之，MI实验模型是研究Gal-3基因缺失小鼠及其他动物模型中心脏修复和重塑时间演变的合适模型。Gal-3的缺乏影响心脏修复的动力学，并破坏MI后心脏重塑和功能的演变。
