Cholecystokinin Expression in the Development of Myocardial Hypertrophy

Abstract

Background. Expression of cholecystokinin is found in myocardial tissues as a gastrointestinal hormone and may be involved in cardiovascular regulation. However, it is unclear whether there is an increase in cholecystokinin expression in myocardial hypertrophy progression induced by abdominal aortic constriction. The study is aimed at exploring the relationship between cholecystokinin expression and myocardial hypertrophy. Methods. We randomly divided the 70 Sprague-Dawley rats into two groups: the sham operation group and the abdominal aortic constriction group. The hearts of rats were measured by echocardiography, and myocardial tissues and blood were collected at 4 weeks, 8 weeks, and 12 weeks after surgery. Morphological changes were assessed by microscopy. The cholecystokinin expression was evaluated by immunochemistry, Western blotting, quantitative real-time polymerase chain reaction, and enzyme-linked immunosorbent assay. Results. The relative protein levels of cholecystokinin were significantly increased in the abdominal aortic constriction groups compared with the corresponding sham operation groups at 8 weeks and 12 weeks. The cholecystokinin mRNA in the abdominal aortic constriction groups was significantly higher than the time-matched sham operation groups. Changes in the left ventricular wall thickness were positively correlated with the relative protein levels of cholecystokinin and the mRNA of cholecystokinin. Conclusions. The development of myocardial hypertrophy can affect the cholecystokinin expression of myocardial tissues.

Bioinformatic analysis and validation of cardiac hypertrophy-related genes

“…MH animal can be established in several mammal species (Roth et al 2017;Fu et al 2020;Han et al 2021), but mice are widely used because of their complete genetic background information, abundant commercial reagents, economical maintenance and easy feeding. Mice models of transverse aortic constriction (TAC) respond to post-load stress by initiating a series of altered gene expressions and activating complex crosstalk between signal pathways (Zhao et al 2004).…”

Cholecystokinin Octapeptide Promotes ANP Secretion through Activation of NOX4–PGC-1α–PPARα/PPARγ Signaling in Isolated Beating Rat Atria

“…Cholecystokinin (CCK) is a classical gut hormone and a potent stimulator of gallbladder contraction that was found in extracts of small intestinal mucosa in the 1920s [ 8 , 9 ]. Subsequently, CCK has also been found in neurons [ 10 ], immune cells [ 11 ], kidney cells, and lung cells [ 12 ]. Pro-CCK is processed into several molecular forms such as CCK-58, CCK-33, CCK-22, CCK-8, and CCK-4; however, sulfated carboxyl-terminal CCK octapeptide (CCK-8) is the major biological active fragment of CCK, which retains most of the bioactivities of CCK.…”

“…Pro-CCK is processed into several molecular forms such as CCK-58, CCK-33, CCK-22, CCK-8, and CCK-4; however, sulfated carboxyl-terminal CCK octapeptide (CCK-8) is the major biological active fragment of CCK, which retains most of the bioactivities of CCK. Two types of receptors for CCK (CCK 1 receptor (CCK 1 R) and CCK 2 receptor (CCK 2 R)) have been classified as belonging to the G protein-coupled receptor superfamily (GPCRs) and its distribution is tissue-dependent [ 12 – 14 ]. Recently, it has been demonstrated that pro-CCK, CCK, and its receptors are expressed in mammalian cardiomyocytes [ 15 , 16 ].…”

“…Nevertheless, the development of postinfarction heart failure is associated with the upregulation of CCK levels in relation to cardiac functional parameters and brain natriuretic peptide levels [ 20 ]. Furthermore, mRNA and protein levels of CCK are increased in the hypertrophic myocardial tissue of rats, which was positively correlated with changes in the left ventricular wall thickness [ 12 ]. In clinical studies of heart failure patients, an increase in plasma CCK is associated with mortality in elderly females [ 21 ].…”