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Postnatal lung development under the influence of pulmonary hypoperfusion

ABSTRACT: We reported the RNAseq analyses of lungs tissues in neonatal SD rats with or without reduced pulmonary blood flow. Lung hypoperfution was induced by causing the supravalvular pulmonary stenosis through performing pulmonary artery banding surgery within 24 hours postnatally (P1). RNAseq analyses of the upper lobe of the right lung tissues was generated at P7 from 5 sham-operated rats and 4 pulmonary artery banding rats (1 rat dead before sample collection). The results revealed that there were 2666 differentially expressed genes between PAB and sham group at P7, among which 1255 were upregulated and 1411 were downregulated.

ORGANISM(S): Rattus

PROVIDER: GSE206972 | GEO | 2023/01/18

REPOSITORIES: GEO

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Congenital heart disease associated bronchopulmonary dysplasia and its underlying mechanisms

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CLINICAL SYMPTOMS OF RIGHT VENTRICULAR FAILURE IN EXPERIMENTAL CHRONIC PRESSURE LOAD ARE ASSOCIATED WITH PROGRESSIVE DIASTOLIC DYSFUNCTION

Project description:Right ventricular failure (RVF) due to pressure load is a major cause of death in congenital heart diseases and pulmonary hypertension. The mechanisms of RVF are yet unknown. Research is hampered by the lack of a good RVF model. Our aim was to study the pathophysiology of RVF in a rat model of chronic pressure load. Wistar rats (n=19) were subjected to pulmonary artery banding (PAB, 1.1mm) or sham surgery (CON). All PAB rats developed RVF (reduced cardiac output, RV stroke volume, TAPSE, increased end diastolic pressure, all p<0.05 vs. CON) but clinical symptoms of RVF (inactivity, ruffled fur, dyspnea, ascites) necessitating termination ensued in a subset (5/12) of rats (RVF+) after a period of 52Â±5 days. Rats with RVF+ had significantly worse RV function and pericardial effusion and liver congestion compared to RVF rats without symptoms (all p<0.05), despite similar pressure load (p=NS RVF vs. RVF+). Chronic pulmonary artery banding invariably leads to RV failure in rats, and a subset transitions to advanced clinical RVF. RVF is characterized by enhanced contractility, progressive diastolic dysfunction and derangement of energy metabolism, thus improving diastolic function and targeting RV metabolism may be the keys to treating RVF. Total RNA optainded ( Heart) of 7 Controls ,5 RVF+ and 4 RVF samples where used for this array study

2014-12-08 | E-GEOD-46863 | biostudies-arrayexpress

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Project description:The molecular mechanisms of progressive right heart failure are incompletely understood. We systematically examined transcriptomic changes occurring over months in isolated cardiomyocytes or whole heart tissues from failing right and left ventricles in rat models of pulmonary artery (PAB) or aortic banding (AOB). Detailed bioinformatics analyses resulted in the identification of gene signatures, protein, and transcription factor networks specific to ventricles and compensated or decompensated disease states. Proteomic and RNA-FISH analyses confirmed PAB-mediated regulation of key genes (including proenkephalin) and revealed spatially heterogeneous mRNA expression in the heart. Intersection of rat PAB-specific gene sets with transcriptome data sets from human patients with chronic thromboembolic pulmonary hypertension led to the identification of more than 50 genes whose expression levels correlated with the severity of right heart disease, including multiple matrix-regulating and secreted factors. These data define a conserved, differentially regulated genetic network associated with right heart failure in rats and humans

2024-04-11 | PXD047022 | Pride

RNA-seq to characterize estrogen receptor alpha mutation in the female rat right ventricle with pressure overload

Project description:Purpose: While women are more susceptible to pulmonary arterial hypertension (PAH) than men, their right ventricular (RV) function is better preserved. Experimental studies have identified estrogen receptor alpha (ERα) as a likely mediator for estrogen protection in the RV. However, the role of ERα in preserving RV function and remodeling during pressure overload remains poorly understood. We hypothesized that loss of functional ERα removes female protection from adverse remodeling and is permissive for development of a maladapted RV phenotype. Methods: Male and female rats with a loss-of-function mutation in ERα (ERαMut) and wildtype (WT) littermates, while at their surgical plane of anesthesia, underwent RV pressure overload by pulmonary artery banding (PAB) or a sham surgery. Results: At 10 weeks post-PAB, WT and ERαMut demonstrated RV hypertrophy. Single beat analysis and Tau Weiss calculation from RV pressure waveforms (collected during surgical plane of anesthesia) demonstrated uncoupling of the RV-pulmonary vascular circuit and diastolic dysfunction, respectively, in female, but not male, ERαMut PAB rats. Similarly, female, but not male, ERαMut exhibited increased RV fibrosis, comprised primarily of stiffer collagen type I, suggesting RV stiffening by collagen type I accumulation. RNA-sequencing in female WT and ERαMut RV revealed Kallikrein related-peptidase 10 (Klk10) and Jun Proto-Oncogene (Jun) as possible mediators of female RV protection during PAB. Conclusions: ERα in females is protective against RV-pulmonary vascular uncoupling, diastolic dysfunction, and fibrosis in response to pressure overload. ERα appears to be dispensable for RV adaptation in males. ERα may be a mediator of superior RV adaptation in female patients with PAH.

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