Renal ischemia/reperfusion-induced cardiac hypertrophy in mice: Cardiac morphological and morphometric characterization

Abstract

BackgroundTissue remodeling is usually dependent on the deposition of extracellular matrix that may result in tissue stiffness and impaired myocardium contraction.ObjectivesWe had previously demonstrated that renal ischemia/reperfusion (I/R) is able to induce development of cardiac hypertrophy in mice. Therefore, we aimed to characterize renal I/R-induced cardiac hypertrophy.DesignC57BL/6 J mice were subjected to 60 minutes’ unilateral renal pedicle occlusion, followed by reperfusion (I/R) for 5, 8, 12 or 15 days. Gene expression, protein abundance and morphometric analyses were performed in all time points.ResultsLeft ventricle wall thickening was increased after eight days of reperfusion (p < 0.05). An increase in the number of heart ventricle capillaries and diameter after 12 days of reperfusion (p < 0.05) was observed; an increase in the density of capillaries starting at 5 days of reperfusion (p < 0.05) was also observed. Analyses of MMP2 protein levels showed an increase at 15 days compared to sham (p < 0.05). Moreover, TGF-β gene expression was downregulated at 12 days as well TIMP 1 and 2 (p < 0.05). The Fourier-transform infrared spectroscopy analysis showed that collagen content was altered only in the internal section of the heart (p < 0.05); such data were supported by collagen mRNA levels.ConclusionsRenal I/R leads to impactful changes in heart morphology, accompanied by an increase in microvasculature. Although it is clear that I/R is able to induce cardiac remodeling, such morphological changes is present in only a section of the heart tissue.

Characterization of the Oxidative Stress in Renal Ischemia/Reperfusion-Induced Cardiorenal Syndrome Type 3

“…The beta growth transforming factor (TGF- β ) is one of the main regulators of NOX and has a fundamental role in the establishment of fibrosis and disease progression [ 35 , 36 ]. Despite these studies, previous data from our laboratory indicate a reduction in TGF- β gene expression in 12 and 15 days after ischemia [ 37 ]. In this way, we can suppose that the general reduction observed in NOX is due to a reduction mainly in NOX4 as a consequence of the reduction in TGF- β observed in previous studies in our laboratory.…”

Tanshinone IIA Combined with CsA Inhibit Myocardial Cell Apoptosis Induced by Renal Ischemia-Reperfusion Injury by Modulating Mitochondrial Function Through PI3K/Akt/Bad Pathway in Obese Rats

“…1D). Systemic in ammation regulates cardiac tissue structure, as distinct sections of heart tissues have different collagen content [37]. HE staining of rat myocardial tissue revealed that renal IRI induced a disordered structure, edema, and localized necrosis in myocardial cells, particularly in the IR (obese) group, combined with interstitial edema.…”

“…(AMI) induced by renal IR is indeterminate, including kidney dysfunction which results in a hyperin ammatory state and volume overload [6]. Renal IR can lead to impactful changes in heart morphology combined with increased microvasculature [7]. The study has demonstrated that the IR mechanism is closely related with mitochondrial dysfunction in heart [8].…”

Tanshinone IIA&nbsp;Combined With CsA&nbsp;Inhibit Myocardial Cell Apoptosis Induced by Renal Ischemia-reperfusion Injury by Modulating Mitochondrial Function Through PI3K/Akt/Bad Pathway in Obese Rats&nbsp;

“…We used enzyme-linked immunosorbent assays to detect TNF-α and IL-1β, and our results show that renal IRI increased serum levels of TNF-α and IL-1β, particularly in the IR (obese) group, compared with the sham group (p < 0.05), which decreased after the pretreatment with TIIA, CsA, and TIIA+CsA ( Figure 1D). Systemic inflammation regulates cardiac tissue structure, as distinct sections of heart tissues have different collagen content [37].…”

“…The mechanism of acute myocardial injury (AMI) induced by renal IR is indeterminate, including kidney dysfunction which results in a hyperin ammatory state and volume overload [6]. Renal IR can lead to impactful changes in heart morphology combined with increased microvasculature [7]. The study has demonstrated that the IR mechanism is closely related with mitochondrial dysfunction in heart [8].…”