2016
DOI: 10.1152/ajpheart.00842.2015
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Renin overexpression leads to increased titin-based stiffness contributing to diastolic dysfunction in hypertensive mRen2 rats

Abstract: A. Renin overexpression leads to increased titin-based stiffness contributing to diastolic dysfunction in hypertensive mRen2 rats. Am J Physiol Heart Circ Physiol 310: H1671-H1682, 2016. First published April 8, 2016; doi:10.1152/ajpheart.00842.2015.-Hypertension (HTN) is a major risk factor for heart failure. We investigated the influence of HTN on cardiac contraction and relaxation in transgenic renin overexpressing rats (carrying mouse Ren-2 renin gene, mRen2, n ϭ 6). Blood pressure (BP) was measured. Cardi… Show more

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Cited by 23 publications
(22 citation statements)
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“…A 5-mm tissue sampling volume was obtained at the mitral annulus from both septal and lateral walls. From the acquired images, the following functional parameters were measured: S’, E’/A’ wave velocities, E/E’ (early diastolic mitral inflow velocity divided by average value of lateral and septal tissue Doppler early diastolic velocities) and E’/A’ (tissue Doppler early and late diastolic velocity ratio) [48]. …”
Section: Experimental Section (Methodology)mentioning
confidence: 99%
“…A 5-mm tissue sampling volume was obtained at the mitral annulus from both septal and lateral walls. From the acquired images, the following functional parameters were measured: S’, E’/A’ wave velocities, E/E’ (early diastolic mitral inflow velocity divided by average value of lateral and septal tissue Doppler early diastolic velocities) and E’/A’ (tissue Doppler early and late diastolic velocity ratio) [48]. …”
Section: Experimental Section (Methodology)mentioning
confidence: 99%
“…Thus, at least S12884 (mouse)/S12022 (human) can be phosphorylated by both CaMKIIδ and PKCα. The phospho-specific antibodies against p-S11878 and p-S12022 (p-S12742 and p-S12884 in mouse titin) have been used repeatedly to quantify PEVK phosphorylation by western blot in mouse, rat, dog, or human hearts (Hamdani et al 2013a, b, c; Hidalgo et al 2014; Hudson et al 2011; Hutchinson et al 2015; Kötter et al 2013, 2016; Kovács et al 2016; Mohamed et al 2016; Rain et al 2014; Tschöpe et al 2016; Zile et al 2015). …”
Section: Phosphorylation Sites Of the Pevk Domainmentioning
confidence: 99%
“…In a metabolic risk-induced animal model of HFpEF, the obese Zucker spontaneously hypertensive fatty-1 (ZSF1) rat, N2Bus phosphorylation at S4010 (S3991 in rat) was lower, but PEVK phosphorylation at S12022 (S12884 in rat) was higher than in healthy rat hearts, whereas PEVK phosphorylation at S11878 (S12742 in rat) was unaltered (Hamdani et al 2013b). The hearts of renin-overexpressing, hypertensive rats showed increased phosphorylation at PEVK site S12742 and unaltered phosphorylation at S12884, while N2Bus phosphosites were not studied (Kovács et al 2016). In mouse hearts stressed by pressure overload due to transverse aortic constriction surgery, PEVK site p-S11878 (PKCα) was hyper-phosphorylated and PEVK site p-S12022 (CaMKIIδ/PKCα) hypo-phosphorylated, whereas N2Bus phosphosites were again not studied (Hudson et al 2011).…”
Section: Alterations Of Titin Phosphorylation In Heart Failurementioning
confidence: 99%
“…For further analysis of the samples, titin was separated by SDS-PAGE on 2% agarose-strengthened gels as detailed elsewhere [25]. Protein bands with apparent molecular mass of 3000–3300 kDa were visualized using Coomassie brilliant blue (Reanal, Ltd., Budapest, Hungary).…”
Section: Methodsmentioning
confidence: 99%