부산대학교 도서관

Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): This work has been funded by "Instituto de Salud Carlos III" and "Fondos Europeos de Desarrollo Regional FEDER" (Exp. PI20/00637) as well as by "Generalitat Valenciana" (Exp. PROMETEO/2021/008). Introduction Caveolae are lipid invaginations present in the membrane of most mammalian cells. They are mainly made up of three proteins: caveolin (Cav)-1, 2, and 3 and are involved in signal transduction and ion channels. Since caveolae regulate different signalling pathways to promote cardiac protection, the aim of this study is to compare the expression of Cav-1, 2, and 3 in the human myocardium of control subjects and in patients with myocardial infarction (MI). Materials Myocardial samples from human autopsies of 4 controls and 4 MI patients with more than 6 months of evolution were isolated. The infarction and control area were identified by haematoxylin-eosin and Masson's trichromic stainings. The presence of Cav-1, 2 and 3 was detected by immunochemistry. Afterwards, 5 photographs were taken for each antibody and sample and the presence of each protein was morphometrically quantified using the image analyzer Image-Pro Plus. These results were also corroborated by immunofluorescence. Results A constitutive presence of Cav-1, 2, and 3 was observed in the myocardium of control patients, being Cav-1 and 3 higher expressed than Cav-2. Cav-2 and 3 were mainly found in cardiomyocytes, while Cav-1 was detected not only in cardiac muscle cells but also in endothelial cells. Comparing caveolae expression between the peri-infarct region of MI patients and controls, a significant reduction in the expression of the three proteins was observed by immunochemistry. Indeed, the decrease in Cav-2 and 3 could be also detected by immunofluorescence. Lastly, Cav-1 was more expressed in cardiomyocytes than in endothelial cells, but unlike muscle cells, its expression was not diminished after MI. Conclusions The presence of caveolin decreases in the myocardial tissue after MI. Further studies are needed to confirm the cardioprotective role of caveolae post-AMI and their use as potential therapeutic target. [ABSTRACT FROM AUTHOR]