Artykuły w czasopismach: „Mouse papillary muscle”

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Widén, C., i C. J. Barclay. "Resting metabolism of mouse papillary muscle". Pflügers Archiv - European Journal of Physiology 450, nr 4 (29.04.2005): 209–16. http://dx.doi.org/10.1007/s00424-005-1408-4.

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Song, Weihua, Petr G. Vikhorev, Mavin N. Kashyap, Christina Rowlands, Michael A. Ferenczi, Roger C. Woledge, Kenneth MacLeod, Steven Marston i Nancy A. Curtin. "Mechanical and energetic properties of papillary muscle from ACTC E99K transgenic mouse models of hypertrophic cardiomyopathy". American Journal of Physiology-Heart and Circulatory Physiology 304, nr 11 (1.06.2013): H1513—H1524. http://dx.doi.org/10.1152/ajpheart.00951.2012.

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We compared the contractile performance of papillary muscle from a mouse model of hypertrophic cardiomyopathy [α-cardiac actin ( ACTC) E99K mutation] with nontransgenic (non-TG) littermates. In isometric twitches, ACTC E99K papillary muscle produced three to four times greater force than non-TG muscle under the same conditions independent of stimulation frequency and temperature, whereas maximum isometric force in myofibrils from these muscles was not significantly different. ACTC E99K muscle relaxed slower than non-TG muscle in both papillary muscle (1.4×) and myofibrils (1.7×), whereas the rate of force development after stimulation was the same as non-TG muscle for both electrical stimulation in intact muscle and after a Ca2+ jump in myofibrils. The EC50 for Ca2+ activation of force in myofibrils was 0.39 ± 0.33 μmol/l in ACTC E99K myofibrils and 0.80 ± 0.11 μmol/l in non-TG myofibrils. There were no significant differences in the amplitude and time course of the Ca2+ transient in myocytes from ACTC E99K and non-TG mice. We conclude that hypercontractility is caused by higher myofibrillar Ca2+ sensitivity in ACTC E99K muscles. Measurement of the energy (work + heat) released in actively cycling heart muscle showed that for both genotypes, the amount of energy turnover increased with work done but with decreasing efficiency as energy turnover increased. Thus, ACTC E99K mouse heart muscle produced on average 3.3-fold more work than non-TG muscle, and the cost in terms of energy turnover was disproportionately higher than in non-TG muscles. Efficiency for ACTC E99K muscle was in the range of 11–16% and for non-TG muscle was 15–18%.

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Liu, Rong, Han-Zhong Feng i J. P. Jin. "Physiological contractility of cardiomyocytes in the wall of mouse and rat azygos vein". American Journal of Physiology-Cell Physiology 306, nr 7 (1.04.2014): C697—C704. http://dx.doi.org/10.1152/ajpcell.00004.2014.

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We recently demonstrated the abundant presence of cardiomyocytes in the wall of thoracic veins of adult mouse and rat. The highly differentiated morphology and myofilament protein contents of the venous cardiomyocytes suggested contractile functions. Here we further investigated the contractility of mouse and rat azygos venous rings compared with that of atrial strips and ventricular papillary muscle. 5-Bromo-4-chloro-indolyl-galactopyranoside (X-gal) staining of transgenic mouse vessels expressing lacZ under a cloned cardiac troponin T promoter demonstrated that the venous cardiomyocytes are discontinuous from atrial myocardium and aligned in the wall of thoracic veins perpendicular to the vessel axis. Histological sections displayed sarcomeric striations in the venous cardiomyocytes, which indicate an encirclement orientation of myofibrils in the vessel wall. Mechanical studies found that the rings of mouse and rat azygos vein produce strong cardiac type twitch contractions when stimulated with electrical pacing in contrast to the weak and slow smooth muscle contractions induced using 90 mM KCl. The twitch contraction and relaxation of mouse azygos veins further exhibited a cardiac type of β-adrenergic responses. Quantitative comparison showed that the contractions of venous cardiomyocytes are slightly slower than those of atrium muscle but significantly faster than those of ventricular papillary muscle. These novel findings indicate that the cardiomyocytes abundant in the wall of rodent thoracic veins possess fully differentiated cardiac muscle phenotype despite their anatomical and functional segregations from the heart.

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Fenwick, Axel J., Peter O. Awinda, Jacob A. Yarbrough-Jones, Jennifer A. Eldridge, Buel D. Rodgers i Bertrand C. W. Tanner. "Demembranated skeletal and cardiac fibers produce less force with altered cross-bridge kinetics in a mouse model for limb-girdle muscular dystrophy 2i". American Journal of Physiology-Cell Physiology 317, nr 2 (1.08.2019): C226—C234. http://dx.doi.org/10.1152/ajpcell.00524.2018.

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Limb-girdle muscular dystrophy 2i (LGMD2i) is a dystroglycanopathy that compromises myofiber integrity and primarily reduces power output in limb muscles but can influence cardiac muscle as well. Previous studies of LGMD2i made use of a transgenic mouse model in which a proline-to-leucine (P448L) mutation in fukutin-related protein severely reduces glycosylation of α-dystroglycan. Muscle function is compromised in P448L mice in a manner similar to human patients with LGMD2i. In situ studies reported lower maximal twitch force and depressed force-velocity curves in medial gastrocnemius (MG) muscles from male P448L mice. Here, we measured Ca2+-activated force generation and cross-bridge kinetics in both demembranated MG fibers and papillary muscle strips from P448L mice. Maximal activated tension was 37% lower in MG fibers and 18% lower in papillary strips from P448L mice than controls. We also found slightly faster rates of cross-bridge recruitment and detachment in MG fibers from P448L than control mice. These increases in skeletal cross-bridge cycling could reduce the unitary force output from individual cross bridges by lowering the ratio of time spent in a force-bearing state to total cycle time. This suggests that the decreased force production in LGMD2i may be due (at least in part) to altered cross-bridge kinetics. This finding is notable, as the majority of studies germane to muscular dystrophies have focused on sarcolemma or whole muscle properties, whereas our findings suggest that the disease pathology is also influenced by potential downstream effects on cross-bridge behavior.

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Dou, Ying, Per Arlock i Anders Arner. "Blebbistatin specifically inhibits actin-myosin interaction in mouse cardiac muscle". American Journal of Physiology-Cell Physiology 293, nr 3 (wrzesień 2007): C1148—C1153. http://dx.doi.org/10.1152/ajpcell.00551.2006.

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Blebbistatin is a powerful inhibitor of actin-myosin interaction in isolated contractile proteins. To examine whether blebbistatin acts in a similar manner in the organized contractile system of striated muscle, the effects of blebbistatin on contraction of cardiac tissue from mouse were studied. The contraction of paced intact papillary muscle preparations and shortening of isolated cardiomyocytes were inhibited by blebbistatin with inhibitory constants in the micromolar range (1.3–2.8 μM). The inhibition constants are similar to those previously reported for isolated cardiac myosin subfragments showing that blebbistatin action is similar in filamentous myosin of the cardiac contractile apparatus and isolated proteins. The inhibition was not associated with alterations in action potential duration or decreased influx through L-type Ca2+ channels. Experiments on permeabilized cardiac muscle preparations showed that the inhibition was not due to alterations in Ca2+ sensitivity of the contractile filaments. The maximal shortening velocity was not affected by 1 μM blebbistatin. In conclusion, we show that blebbistatin is an inhibitor of the actin-myosin interaction in the organized contractile system of cardiac muscle and that its action is not due to effects on the Ca2+ influx and activation systems.

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Guo, Jingxu, Shuwei Li, Hongyang Wang, Tinghui Wu, Zhenhui Wu, Lufei Yu i Meiyan Liang. "A Mouse Model for Studying Stem Cell Effects on Regeneration of Hair Follicle Outer Root Sheaths". Open Life Sciences 15, nr 1 (25.03.2020): 41–50. http://dx.doi.org/10.1515/biol-2020-0005.

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AbstractObjectiveStem cells hold promise for treating hair loss. Here an in vitro mouse model was developed using outer root sheaths (ORSs) isolated from hair follicles for studying stem cell-mediated dermal papillary regeneration.MethodsUnder sterile conditions, structurally intact ORSs were isolated from hair follicles of 3-day-old Kunming mice and incubated in growth medium. Samples were collected daily for 5 days. Stem cell distribution, proliferation, differentiation, and migration were monitored during regeneration.ResultsCell proliferation began at the glass membrane periphery then spread gradually toward the membrane center, with the presence of CD34 and CD200 positive stem cells involved in repair initiation. Next, CD34 positive stem cells migrated down the glass membrane, where some participated in ORS formation, while other CD34 cells and CD200 positive cells migrated to hair follicle centers. Within the hair follicle matrix, stem cells divided, grew, differentiated and caused outward expansion of the glass membrane to form a dermal papillary structure containing alpha-smooth muscle actin. Neutrophils attracted to the wound site phagocytosed bacterial and cell debris to protect regenerating tissue from infection.ConclusionIsolated hair follicle ORSs can regenerate new dermal papillary structures in vitro. Stem cells and neutrophils play important roles in the regeneration process.

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Guellich, Aziz, Thibaud Damy, Marc Conti, Victor Claes, Jane-Lise Samuel, Thierry Pineau, Yves Lecarpentier i Catherine Coirault. "Tempol prevents cardiac oxidative damage and left ventricular dysfunction in the PPAR-α KO mouse". American Journal of Physiology-Heart and Circulatory Physiology 304, nr 11 (1.06.2013): H1505—H1512. http://dx.doi.org/10.1152/ajpheart.00669.2012.

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Peroxisome proliferator-activated receptor (PPAR)-α deletion induces a profound decrease in MnSOD activity, leading to oxidative stress and left ventricular (LV) dysfunction. We tested the hypothesis that treatment of PPAR-α knockout (KO) mice with the SOD mimetic tempol prevents the heart from pathological remodelling and preserves LV function. Twenty PPAR-α KO mice and 20 age-matched wild-type mice were randomly treated for 8 wk with vehicle or tempol in the drinking water. LV contractile parameters were determined both in vivo using echocardiography and ex vivo using papillary muscle mechanics. Translational and posttranslational modifications of myosin heavy chain protein as well as the expression and activity of major antioxidant enzymes were measured. Tempol treatment did not affect LV function in wild-type mice; however, in PPAR-α KO mice, tempol prevented the decrease in LV ejection fraction and restored the contractile parameters of papillary muscle, including maximum shortening velocity, maximum extent of shortening, and total tension. Moreover, compared with untreated PPAR-α KO mice, myosin heavy chain tyrosine nitration and anion superoxide production were markedly reduced in PPAR-α KO mice after treatment. Tempol also significantly increased glutathione peroxidase and glutathione reductase activities (∼ 50%) in PPAR-α KO mice. In conclusion, these findings demonstrate that treatment with the SOD mimetic tempol can prevent cardiac dysfunction in PPAR-α KO mice by reducing the oxidation of contractile proteins. In addition, we show that the beneficial effects of tempol in PPAR-α KO mice involve activation of the glutathione peroxidase/glutathione reductase system.

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Widén, C., i C. J. Barclay. "ATP splitting by half the cross-bridges can explain the twitch energetics of mouse papillary muscle". Journal of Physiology 573, nr 1 (9.05.2006): 5–15. http://dx.doi.org/10.1113/jphysiol.2006.104992.

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Markandran, Kasturi, Haiyang Yu, Weihua Song, Do Thuy Uyen Ha Lam, Mufeeda Changaramvally Madathummal i Michael A. Ferenczi. "Functional and Molecular Characterisation of Heart Failure Progression in Mice and the Role of Myosin Regulatory Light Chains in the Recovery of Cardiac Muscle Function". International Journal of Molecular Sciences 23, nr 1 (22.12.2021): 88. http://dx.doi.org/10.3390/ijms23010088.

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Heart failure (HF) as a result of myocardial infarction (MI) is a major cause of fatality worldwide. However, the cause of cardiac dysfunction succeeding MI has not been elucidated at a sarcomeric level. Thus, studying the alterations within the sarcomere is necessary to gain insights on the fundamental mechansims leading to HF and potentially uncover appropriate therapeutic targets. Since existing research portrays regulatory light chains (RLC) to be mediators of cardiac muscle contraction in both human and animal models, its role was further explored In this study, a detailed characterisation of the physiological changes (i.e., isometric force, calcium sensitivity and sarcomeric protein phosphorylation) was assessed in an MI mouse model, between 2D (2 days) and 28D post-MI, and the changes were related to the phosphorylation status of RLCs. MI mouse models were created via complete ligation of left anterior descending (LAD) coronary artery. Left ventricular (LV) papillary muscles were isolated and permeabilised for isometric force and Ca2+ sensitivity measurement, while the LV myocardium was used to assay sarcomeric proteins’ (RLC, troponin I (TnI) and myosin binding protein-C (MyBP-C)) phosphorylation levels and enzyme (myosin light chain kinase (MLCK), zipper interacting protein kinase (ZIPK) and myosin phosphatase target subunit 2 (MYPT2)) expression levels. Finally, the potential for improving the contractility of diseased cardiac papillary fibres via the enhancement of RLC phosphorylation levels was investigated by employing RLC exchange methods, in vitro. RLC phosphorylation and isometric force potentiation were enhanced in the compensatory phase and decreased in the decompensatory phase of HF failure progression, respectively. There was no significant time-lag between the changes in RLC phosphorylation and isometric force during HF progression, suggesting that changes in RLC phosphorylation immediately affect force generation. Additionally, the in vitro increase in RLC phosphorylation levels in 14D post-MI muscle segments (decompensatory stage) enhanced its force of isometric contraction, substantiating its potential in HF treatment. Longitudinal observation unveils potential mechanisms involving MyBP-C and key enzymes regulating RLC phosphorylation, such as MLCK and MYPT2 (subunit of MLCP), during HF progression. This study primarily demonstrates that RLC phosphorylation is a key sarcomeric protein modification modulating cardiac function. This substantiates the possibility of using RLCs and their associated enzymes to treat HF.

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Hemptinne, A. de, R. Marrannes i B. Vanheel. "Surface pH and the control of intracellular pH in cardiac and skeletal muscle". Canadian Journal of Physiology and Pharmacology 65, nr 5 (1.05.1987): 970–77. http://dx.doi.org/10.1139/y87-154.

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Both surface pH (pHs) and intracellular pH (pHi) were measured using single- and double-barreled pH-sensitive microelectrodes in isolated sheep cardiac Purkinje strands, rabbit and cat papillary muscle, and mouse and rat soleus muscle. Superfusion of the preparations with a relatively low buffered solution (containing 5 mM HEPES buffered to control pH) causes surface acidosis that correlates with efflux of metabolically produced acids in the unstirred layer of fluid surrounding the tissue. Acidification of the surface layer induces a slower acid change of pHi and depresses the rate of proton extrusion following an imposed intracellular acid load. In cardiac preparations, the lowering of pHi correlates with depression of twitch tension. Transient changes of pHs and pHi are seen when a weak acid or base is suddenly added to, or removed from the superfusion solution. Indirect evidence of the presence of carbonic anhydrase in the extracellular surface layer is obtained from analysis of transient pHs changes in presence and absence of acetazolamide.

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Tani, Y., A. Suttie, G. P. Flake, A. Nyska i R. R. Maronpot. "Epithelial-Stromal Tumor of the Seminal Vesicles in the Transgenic Adenocarcinoma Mouse Prostate Model". Veterinary Pathology 42, nr 3 (maj 2005): 306–14. http://dx.doi.org/10.1354/vp.42-3-306.

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The transgenic adenocarcinoma mouse prostate (TRAMP) model, designed for researching human prostatic cancer, was genetically engineered to harbor a transgene composed of the simian virus 40 Large-T/small-t antigen promoted by the rat probasin gene. In addition to prostatic neoplasms, the TRAMP mouse develops tumors in the seminal vesicles. This study was conducted to evaluate the pathology and histogenesis of TRAMP seminal vesicle neoplasms. Tissues of accessory sex organs harvested from 72 TRAMP mice of various ages (11-40 weeks of age) were fixed in neutral buffered formalin and stained with hematoxylin and eosin, desmin, 5-bromo-2′-deoxyuridine (BrdU, treated animals only), and SV40 Large-T antigen (SV40-Tag). In the seminal vesicles, we found neoplastic stromal cells that emerged multicentrically just beneath the epithelium, densely packed between the epithelium and the smooth muscle layer These stromal cells frequently exhibited mitotic figures and showed BrdU incorporation and SV40-Tag protein expression in the nuclei and immunopositivity for desmin. The proliferative mesenchymal cells were lined by cuboidal to columnar epithelium. Some of the larger papillary, polypoid lesions exhibited a phyllodes pattern resembling that seen in mixed epithelial-stromal tumors of the breast, prostate, and seminal vesicles of humans. Although the epithelium was negative for SV40-Tag and showed only occasional incorporation of BrdU, it clearly participated in the biphasic proliferation, forming papillary, cystic, and tubuloglandular structures. No conclusive evidence of malignancy (invasion or metastasis) was identified. Our recommended diagnosis of this lesion in the seminal vesicles is epithelial-stromal tumor.

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Sarin, Vandana, Robert D. Gaffin, Gerald A. Meininger i Mariappan Muthuchamy. "Arginine-glycine-aspartic acid (RGD)-containing peptides inhibit the force production of mouse papillary muscle bundles via α5β1integrin". Journal of Physiology 564, nr 2 (kwiecień 2005): 603–17. http://dx.doi.org/10.1113/jphysiol.2005.083238.

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Gaffin, Robert D., Kuppan Gokulan, James C. Sacchettini, Timothy E. Hewett, Raisa Klevitsky, Jeffrey Robbins, Vandana Sarin, David C. Zawieja, Gerald A. Meininger i Mariappan Muthuchamy. "Changes in end-to-end interactions of tropomyosin affect mouse cardiac muscle dynamics". American Journal of Physiology-Heart and Circulatory Physiology 291, nr 2 (sierpień 2006): H552—H563. http://dx.doi.org/10.1152/ajpheart.00688.2005.

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The ends of striated muscle tropomyosin (TM) are integral for thin filament cooperativity, determining the cooperative unit size and regulating the affinity of TM for actin. We hypothesized that altering the α-TM carboxy terminal overlap end to the β-TM counterpart would affect the amino-terminal association, which would alter the end-to-end interactions of TM molecules in the thin filament regulatory strand and affect the mechanisms of cardiac muscle contraction. To test this hypothesis, we generated transgenic (TG) mouse lines that express a mutant form of α-TM in which the first 275 residues are from α-TM and the last nine amino acids are from β-TM (α-TM9aaΔβ). Molecular analyses show that endogenous α-TM mRNA and protein are nearly completely replaced with α-TM9aaΔβ. Working heart preparations data show that the rates of contraction and relaxation are reduced in α-TM9aaΔβ hearts. Left ventricular pressure and time to peak pressure are also reduced (−12% and −13%, respectively). The ratio of maximum to minimum first derivatives of change in left ventricular systolic pressure with respect to time (ratio of +dP/d t to −dP/d t, respectively) is increased, but τ is not changed significantly. Force-intracellular calcium concentration ([Ca2+]i) measurements from intact papillary fibers demonstrate that α-TM9aaΔβ TG fibers produce less force per given [Ca2+]icompared with nontransgenic fibers. Taken together, the data demonstrate that the rate of contraction is primarily affected in TM TG hearts. Protein docking studies show that in the mutant molecule, the overall carbon backbone is perturbed about 1.5 Å, indicating that end-to-end interactions are altered. These results demonstrate that the localized flexibility present in the coiled-coil structures of TM isoforms is different, and that plays an important role in interacting with neighboring thin filament regulatory proteins and with differentially modulating the myofilament activation processes.

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Ahmad, I. "The role of WNT signalling in urothelial cell carcinoma". Annals of The Royal College of Surgeons of England 97, nr 7 (1.10.2015): 481–86. http://dx.doi.org/10.1308/rcsann.2015.0008.

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Urothelial cell carcinoma (UCC) of the bladder is one of the most common malignancies, causing considerable morbidity and mortality worldwide. It is unique among the epithelial carcinomas as two distinct pathways to tumourigenesis appear to exist: low grade, recurring papillary tumours usually contain oncogenic mutations in FGFR3 or HRAS whereas high grade, muscle invasive tumours with metastatic potential generally have defects in the pathways controlled by the tumour suppressors p53 and retinoblastoma. Over the last two decades, a number of transgenic mouse models of UCC, containing deletions or mutations of key tumour suppressor genes or oncogenes, have helped us understand the mechanisms behind tumour development. In this summary, I present my work investigating the role of the WNT signalling cascade in UCC.

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Redel, Andreas, Werner Baumgartner, Klaus Golenhofen, Detlev Drenckhahn i Nikola Golenhofen. "Mechanical activity and force-frequency relationship of isolated mouse papillary muscle: effects of extracellular calcium concentration, temperature and contraction type". Pfl�gers Archiv European Journal of Physiology 445, nr 2 (1.11.2002): 297–304. http://dx.doi.org/10.1007/s00424-002-0931-9.

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Forbes, Michael S., Barbara A. Thornhill, Carolina I. Galarreta, Jordan J. Minor, Katherine A. Gordon i Robert L. Chevalier. "Chronic unilateral ureteral obstruction in the neonatal mouse delays maturation of both kidneys and leads to late formation of atubular glomeruli". American Journal of Physiology-Renal Physiology 305, nr 12 (15.12.2013): F1736—F1746. http://dx.doi.org/10.1152/ajprenal.00152.2013.

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Unilateral ureteral obstruction (UUO) in the adult mouse is the most widely used model of progressive renal disease: the proximal tubule is the nephron segment most severely affected and atubular glomeruli are formed after only 7 days of UUO. To determine the proximal nephron response to UUO in the maturing kidney, neonatal mice were examined 7 to 28 days following complete UUO under general anesthesia. Proximal tubular mass and maturation were determined by staining with Lotus tetragolonobus lectin. Superoxide was localized by nitroblue tetrazolium and collagen by Sirius red. Cell proliferation, cell death, PAX-2, megalin, α-smooth muscle actin (α-SMA), renin, and fibronectin were identified by immunohistochemistry. During the first 14 days of ipsilateral UUO, despite oxidative stress (4-hydroxynonenal staining), glomerulotubular continuity was maintained and mitochondrial superoxide production persisted. However, from 14 to 28 days, papillary growth was impaired and proximal tubules collapsed with increased apoptosis, autophagy, mitochondrial loss, and formation of atubular glomeruli. Fibronectin, α-SMA, and collagen increased in the obstructed kidney. Oxidative stress was present also in the contralateral kidney: renin was decreased, glomerulotubular maturation and papillary growth were delayed, followed by increased cortical and medullary growth. We conclude that neonatal UUO initially delays renal maturation and results in oxidative stress in both kidneys. In contrast to the adult, proximal tubular injury in the neonatal obstructed kidney is delayed at 14 days, followed only later by the formation of atubular glomeruli. Antioxidant therapies directed at proximal tubular mitochondria during early renal maturation may slow progression of congenital obstructive nephropathy.

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Vanheel, B., A. de Hemptinne i I. Leusen. "Influence of surface pH on intracellular pH regulation in cardiac and skeletal muscle". American Journal of Physiology-Cell Physiology 250, nr 5 (1.05.1986): C748—C760. http://dx.doi.org/10.1152/ajpcell.1986.250.5.c748.

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The influence of the surface pH (pHs) on the intracellular pH (pHi) and the recovery of pHi after an imposed intracellular acid load was investigated in isolated sheep cardiac Purkinje fiber, rabbit papillary muscle, and mouse and rat soleus muscle. pHs and pHi, respectively, were continuously measured by use of single- and double-barreled pH-sensitive glass microelectrodes. Surface acidosis, usually obtained by superfusion with solutions of acid pH, was also produced with low buffered (5 mM N-2-hydroxyethylpiperazine-N'-2-ethane-sulfonic acid) solutions at control pH. The pHs decrease (delta pHs) induced by low buffering was smallest (-0.08 pH unit) in Purkinje fiber and largest (-0.31 pH unit) in rat soleus muscle, which already had a more acid surface in control conditions. delta pHs was somewhat dependent on the superfusion rate. Higher superfusion rates decreased but did not abolish delta pHs. Surface acidosis was associated with a small intracellular acidification. Intracellular acid loads were produced by adding and subsequently withdrawing 20 meq/l NH4+ from the superfusate. In all preparations, the rate of recovery of pHi after NH4+ withdrawal was notably decreased at acidified pHs. This effect was amiloride sensitive. It is concluded that, in superfused multi-cellular preparations, pHs and therefore the buffer concentration of a superfusate can considerably influence steady-state pHi and pHi recovery from an imposed intracellular acid load.

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Wang, Ju-Feng, Xinhua Yan, Jiangyong Min, Matthew F. Sullivan, Thomas G. Hampton i James P. Morgan. "Cocaine downregulates cardiac SERCA2a and depresses myocardial function in the murine model". Canadian Journal of Physiology and Pharmacology 80, nr 10 (1.10.2002): 1015–21. http://dx.doi.org/10.1139/y02-128.

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Cocaine has been shown to depress myocardial function, which may be linked to abnormal Ca2+ handling by the sarcoplasmic reticulum (SR). To examine whether cocaine affects Ca2+-handling proteins and myocardial performance, we injected BALB/c mice with cocaine daily (30 mg/kg, i.p.) for 14 d. Sarcoplasmic reticulum Ca2+-ATPase (SERCA2a) levels, phospholamban (PLB) protein levels, and hemodynamic parameters were measured. After cocaine exposure, myocardial function was significantly decreased both in vivo and in vitro. Also, SERCA2a protein levels were significantly decreased in all cocaine-treated hearts (p < 0.05 compared with saline control). Normalized SERCA2a levels were 1.2 ± 0.2 (densitometric units) in the cocaine groups (p < 0.05 compared with saline control). However, there was no statistical difference in PLB protein levels between the cocaine and the saline groups. In isolated papillary muscle studies, cocaine did not block the response to extracellular Ca2+ but it did prolong the relaxation time of the muscle. These results indicate that cocaine does not block extracellular Ca2+ entrance across the cell membrane, but that it decreases SERCA2a protein levels. In conclusion, our study demonstrates that cocaine decreases SERCA2a protein levels and depresses myocardial function.Key words: cocaine, SERCA2a, phospholamban, ventricular function, mouse.

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Mizuno, J., M. Otsuji, H. Arita, K. Hanaoka i S. Morita. "New index of velocity with half-logistic time constant for inotropism and lusitropism of isometric tension curve in mouse papillary muscle". European Journal of Anaesthesiology 25, Sup 44 (maj 2008): 48. http://dx.doi.org/10.1097/00003643-200805001-00149.

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Wilkinson, Ross, Weihua Song, Natalia Smoktunowicz i Steven Marston. "A dilated cardiomyopathy mutation blunts adrenergic response and induces contractile dysfunction under chronic angiotensin II stress". American Journal of Physiology-Heart and Circulatory Physiology 309, nr 11 (1.12.2015): H1936—H1946. http://dx.doi.org/10.1152/ajpheart.00327.2015.

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We investigated cardiac contractility in the ACTC E361G transgenic mouse model of dilated cardiomyopathy (DCM). No differences in cardiac dimensions or systolic function were observed in young mice, whereas young adult mice exhibited only mild diastolic abnormalities. Dobutamine had an inotropic and lusitropic effect on the mouse heart. In papillary muscle at 37°C, dobutamine increased relaxation rates [∼50% increase of peak rate of force decline normalized to force (dF/dtmin/F), 25% reduction of time to 90% relaxation (t90) in nontransgenic (NTG) mice], but in the ACTC E361G mouse, dF/dtmin/F was increased 20–30%, and t90 was only reduced 10% at 10 Hz. Pressure-volume measurements showed increases in maximum rate of pressure decline and decreases in time constant of left ventricular pressure decay in the ACTC E361G mouse that were 25–30% of the changes in the NTG mouse, consistent with blunting of the lusitropic response. The inotropic effect of dobutamine was also blunted in ACTC E361G mice, and the dobutamine-stimulated increase in cardiac output (CO) was reduced from 2,100 to 900 μl/min. Mice were treated with high doses of ANG II for 4 wk. The chronic stress treatment evoked systolic dysfunction in ACTC E361G mice but not in NTG. There was a significant reduction in rates of pressure increase and decrease, as well as reduced end-systolic pressure and increased volume. Ejection fraction and CO were reduced in the ACTC E361G mouse, indicating DCM. In vitro DCM-causing mutations uncouple the relationship between Ca2+ sensitivity and troponin I phosphorylation. We conclude that this leads to the observed, reduced response to β1 agonists and reduced cardiac reserve that predisposes the heart to DCM under conditions of chronic stress.

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Palmbos, Phillip Lee, Lidong Wang, Huibin Yang, Taylor Detzler, Gina Ney, Yair Lotan, J. E. Wilkerson i in. "ATDC as a novel oncogene in bladder cancer." Journal of Clinical Oncology 30, nr 5_suppl (10.02.2012): 269. http://dx.doi.org/10.1200/jco.2012.30.5_suppl.269.

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269 Background: Bladder cancer is a common and deadly disease, but the molecular events leading to its initiation and progression are incompletely understood. We recently identified Ataxia-Telangiectasia Group D Associated (ATDC) as a novel oncogene which drives tumor proliferation and invasion in pancreatic carcinoma (Cancer Cell, 2009). In this study, we describe the role of ATDC as an oncogene in bladder cancer. Methods: To further determine the oncogenic role of ATDC, we generated ATDC transgenic (tg) mice in which ATDC expression was driven by a CMV promoter and characterized the resulting tumors. Results: The dominant phenotype in these mice was the development of both papillary and invasive urothelial carcinomas (9% and 20% respectively, average age of onset 10-12 months of age). Histologically, these tumors were indistinguishable from human urothelial carcinomas. Gene expression profiling of invasive tumors derived from ATDC tg mice demonstrated a marked overlap with gene signatures of human invasive bladder cancers. Analysis of a human bladder cancer tissue microarray (311 samples) showed elevated expression in 70% (173/252) of muscle-invasive carcinomas, whereas normal bladder had no expression. 22% (5/23) of papillary tumors also expressed elevated levels of ATDC. ATDC was the 11th most highly up-regulated gene in bladder cancers represented in the Oncomine gene expression database. ATDC tg mouse bladder tumors demonstrated loss of p53 signaling and down-regulation of PTEN expression, which was determined to be due to ATDC abrogation of p53 function by cytoplasmic sequestration and ATDC-mediated methylation of the PTEN promoter. Furthermore, ATDC knock-down in invasive cancer cell lines resulted in decreased proliferation, invasion and reactivation of p53-mediated signaling and PTEN expression. Conclusions: ATDC is a novel oncogene that is highly expressed in human bladder cancers and is sufficient to drive the development of invasive bladder tumors in tg mice. The mechanism by which ATDC drives bladder cancer formation involves alterations in p53 and PTEN pathways known to be important in bladder tumorigenesis.

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Kawai, Masataka, Tarek Karam i Jose R. Pinto. "Ca2+-Sensitivity and Elementary Steps of the Cross-Bridge Cycle in Papillary Muscle Fibers from the Troponin C (TnC)-A8V Knock-In Mouse, which Exhibits Hypertrophic Cardiomyopathy (HCM)". Biophysical Journal 110, nr 3 (luty 2016): 464a—465a. http://dx.doi.org/10.1016/j.bpj.2015.11.2486.

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Feng, Hanzhong, i J. P. Jin. "A Method to Study Contractility of Skinned Frozen Sections of Mouse Ventricular Papillary Muscle and the Effect of the Restrictive Truncation of the N-Terminal Extension of Cardiac Troponin I". Biophysical Journal 118, nr 3 (luty 2020): 592a. http://dx.doi.org/10.1016/j.bpj.2019.11.3206.

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Endo, Toyoshi, i Tetsuro Kobayashi. "Concurrent overexpression of RET/PTC1 and TTF1 confers tumorigenicity to thyrocytes". Endocrine-Related Cancer 20, nr 6 (4.09.2013): 767–76. http://dx.doi.org/10.1530/erc-13-0310.

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A variant located on 14q13.3 nearest to thyroid transcription factor-1 (TTF1) predisposes individuals to thyroid cancer, but whether this variant is related to the RET/PTC rearrangement associated with human papillary thyroid carcinomas (PTCs) is unknown. The aims of this study were to investigate the effects of RET/PTC1 on the expression of thyroid-specific genes in thyrocytes and their relationship with malignant transformation of the thyrocytes. In the absence or presence of TSH, an extracellular signal-regulated kinase was phosphorylated in FRTL5 cells that stably expressed RET/PTC1, and these cells grew independently of TSH. FRTL (RET/PTC1) cells produced 566% more thyroglobulin mRNA and 474% more Na+/I− symporter mRNA than did the control FRTL (pcDNA) cells. FRTL (RET/PTC1) cells expressed 468% more Ttf1 mRNA than did FRTL (pcDNA) cells, but these two cell types did not differ significantly with respect to Pax8 or Ttf2 mRNA levels. When FRTL (RET/PTC1) cells and FRTL (pcDNA), cells were injected into each of nine nude mice, each mouse developed a single tumor at the site of FRTL (RET/PTC1) cell injection; in contrast, tumor formation never occurred at sites of FRTL (cDNA) cells injection. Tumors resulting from FRTL (RET/PTC1) cells retained 125I-uptake activity; moreover, the cells invaded into surrounding skeletal muscle. When overexpression of Ttf1 in FRTL (RET/PTC1) cells was silenced, the cells completely lost their tumorigenic potential. Exogenous TTF1 cDNA enhanced the tumorigenicity of BHP18-21v cells, human PTC cells that express RET/PTC1, in nude mice. These results indicated that concurrent overexpression of RET/PTC1 and TTF1 confers tumorigenicity to FRTL5 and BHP18-21v cells in nude mice.

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Palmbos, Phillip Lee, Lidong Wang, Huibin Yang, Taylor Detzler, Gina Ney, Yair Lotan, Patrick N. Healy i in. "Novel oncogenic function of ATDC in bladder cancer." Journal of Clinical Oncology 30, nr 15_suppl (20.05.2012): 4591. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.4591.

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4591 Background: Bladder cancer is a common and deadly disease, but the molecular events leading to its initiation and progression are incompletely understood. We recently identified Ataxia-Telangiectasia Group D Associated (ATDC) as a novel oncogene which drives tumor proliferation and invasion in pancreatic carcinoma (Cancer Cell, 2009). In this study, we describe the role of ATDC as an oncogene in bladder cancer. Methods: To further determine the oncogenic role of ATDC, we generated ATDC transgenic (tg) mice in which ATDC expression was driven by a CMV promoter and characterized the resulting tumors. Results: Interestingly, the dominant phenotype in these mice was the development of both non-invasive and invasive urothelial carcinomas (9% and 20% respectively, average age of onset 10-12 months of age). Histologically, these tumors were indistinguishable from human urothelial carcinomas. Gene expression profiling of invasive tumors derived from ATDC tg mice demonstrated a marked overlap with gene signatures of human invasive bladder cancers. ATDC was the 11th most highly up-regulated gene in bladder cancers represented in the Oncomine gene expression database. Analysis of a human bladder cancer tissue microarray (311 samples) by IHC showed elevated expression in 70% (173/252) of muscle-invasive carcinomas, 22% (5/23) of papillary tumors and little or no expression in normal bladder urothelium. ATDC tg mouse bladder tumors demonstrated loss of p53 signaling and down-regulation of PTEN expression, which correlated with ATDC induced methylation of the PTEN promoter by DNMT3A. Furthermore, ATDC knock-down in invasive cancer cell lines resulted in decreased proliferation, invasion and reactivation of p53-mediated signaling and PTEN expression. Conclusions: ATDC is a novel oncogene that is highly expressed in human bladder cancers and is sufficient to drive the development of invasive bladder tumors in tg mice. The mechanism by which ATDC drives bladder cancer formation involves alterations in p53 and PTEN pathways known to be important in bladder tumorigenesis.

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Min, Jiang-Yong, Matthew F. Sullivan, Xinhua Yan, Xin Feng, Victor Chu, Ju-Feng Wang, Ivo Amende, James P. Morgan, Kenneth D. Philipson i Thomas G. Hampton. "Overexpression of Na+/Ca2+ exchanger gene attenuates postinfarction myocardial dysfunction". American Journal of Physiology-Heart and Circulatory Physiology 283, nr 6 (1.12.2002): H2466—H2471. http://dx.doi.org/10.1152/ajpheart.01062.2001.

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We monitored myocardial function in postinfarcted wild-type (WT) and transgenic (TG) mouse hearts with overexpression of the cardiac Na+/Ca2+ exchanger. Five weeks after infarction, cardiac function was better maintained in TG than WT mice [left ventricular (LV) systolic pressure: WT, 41 ± 2; TG, 58 ± 3 mmHg; P < 0.05; maximum rising rate of LV pressure (+dP/d t max): WT, 3,750 ± 346; TG, 5,075 ± 334 mmHg/s; P < 0.05]. The isometric contractile response to β-adrenergic stimulation was greater in papillary muscles from TG than WT mice (WT, 13.2 ± 0.9; TG, 16.3 ± 1.0 mN/mm2 at 10−4 M isoproterenol). The sarcoplasmic reticulum (SR) Ca2+content investigated by rapid cooling contractures in papillary muscles was greater in TG than WT mouse hearts. We conclude that myocardial function is better preserved in TG mice 5 wk after infarction, which results from enhanced SR Ca2+ content via overexpression of the Na+/Ca2+ exchanger.

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Montgomery, David E., Beata M. Wolska, W. Glen Pyle, Brian B. Roman, Jasmine C. Dowell, Peter M. Buttrick, Alan P. Koretsky, Pedro Del Nido i R. John Solaro. "α-Adrenergic response and myofilament activity in mouse hearts lacking PKC phosphorylation sites on cardiac TnI". American Journal of Physiology-Heart and Circulatory Physiology 282, nr 6 (1.06.2002): H2397—H2405. http://dx.doi.org/10.1152/ajpheart.00714.2001.

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Protein kinase C (PKC)-mediated phosphorylation of cardiac myofilament (MF) proteins has been shown to depress the actomyosin interaction and may be important during heart failure. Biochemical studies indicate that phosphorylation of Ser43 and Ser45 of cardiac troponin I (cTnI) plays a substantial role in the PKC-mediated depression. We studied intact and detergent-extracted papillary muscles from nontransgenic (NTG) and transgenic (TG) mouse hearts that express a mutant cTnI (Ser43Ala, Ser45Ala) that lacks specific PKC-dependent phosphorylation sites. Treatment of NTG papillary muscles with phenylephrine (PE) resulted in a transient increase and a subsequent 62% reduction in peak twitch force. TG muscles showed no transient increase and only a 45% reduction in force. There was a similar difference in maximum tension between NTG and TG fiber bundles that had been treated with a phorbol ester and had received subsequent detergent extraction. Although levels of cTnI phosphorylation correlated with these differences, the TG fibers also demonstrated a decrease in phosphorylation of cardiac troponin T. The PKC-specific inhibitor chelerythrine inhibited these responses. Our data provide evidence that specific PKC-mediated phosphorylation of Ser43 and Ser45 of cTnI plays an important role in regulating force development in the intact myocardium.

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Kennedy, Murray J., Murray W. Lankester i J. Barry Snider. "Paramphistomum cervi and Paramphistomum liorchis (Digenea: Paramphistomatidae) in moose, Alces alces, from Ontario, Canada". Canadian Journal of Zoology 63, nr 5 (1.05.1985): 1207–10. http://dx.doi.org/10.1139/z85-180.

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Two species of Paramphistomum were found in moose in Ontario. Paramphistomum liorchis Fischoeder, 1901 can be distinguished from P. cervi (Zeder, 1790) by the presence of cuticular papillae, in having longer papillae lining the anterior one-quarter of the inner surface of the pharynx, and having more median external circular muscle bundles.

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Wu, Xin, Sanjukta Chakraborty, Cristine L. Heaps, Michael J. Davis, Gerald A. Meininger i Mariappan Muthuchamy. "Fibronectin increases the force production of mouse papillary muscles via α5β1 integrin". Journal of Molecular and Cellular Cardiology 50, nr 1 (styczeń 2011): 203–13. http://dx.doi.org/10.1016/j.yjmcc.2010.10.003.

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Song, Weihua, Stteven B. Marston, Roger C. Woledge i Nancy Curtin. "Reduced Efficiency of Intact Papillary Muscles in ACTC E99K Transgenic Mouse Heart". Biophysical Journal 102, nr 3 (styczeń 2012): 355a. http://dx.doi.org/10.1016/j.bpj.2011.11.1942.

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Sasaki, Bianca Ribeiro de Souza, Ianny Brum Reis, Gabriela Oliveira, Nelson Duran i Wagner José Fávaro. "Modulation of the RANK/RANKL/OPG system and FOXP3+ regulatory T cells in the tumor microenvironment of noninvasive bladder cancer after intravesical oncotherad immunotherapy associated with platelet-rich plasma." Journal of Clinical Oncology 39, nr 6_suppl (20.02.2021): 462. http://dx.doi.org/10.1200/jco.2021.39.6_suppl.462.

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462 Background: The activity of the receptor activator of nuclear factor-kβ RANK/RANKL in cancer cells has been correlated with tumor progression and poor prognosis in solid tumors including bladder cancer. Regulatory T cells (Tregs), often identified by FOXP3 biomarker, suppress the anti-tumor response and allow immune tolerance through suppression of T cells. Immunomodulator OncoTherad is an inorganic phosphate nanocomplex associated with glycosidic protein, developed by the University of Campinas/Brazil, with antitumor effects. Previous reports have demonstrated immune activation and antitumor effects of Platelet Rich Plasma (PRP). We evaluated the effects of OncoTherad associated with PRP in the RANK/RANKL system and Tregs in a mouse model of non-muscle invasive bladder cancer (NMIBC). Methods: C57BL/6J mice were assigned to groups (n = 42): Control; Cancer (N-ethyl-N-nitrosourea carcinogen, 50 mg/ml); PRP (0.1 ml); OncoTherad (20 mg/ml); OncoTherad+PRP 10 mg/ml and OncoTherad+PRP 20 mg/ml. The intravesical doses (0.1 ml) were instilled once a week for 6 consecutive weeks after induction. Results: After NMIBC induction, all animals in the Cancer group showed flat carcinoma in situ (pTis) and both percentages of RANK, RANKL, OPG, and FOXP3 positive cells and the intensity of immunoreaction for these antigens were significantly higher in comparison with healthy animals. In addition to ensuring this NMIBC model, these results indicated the involvement of RANK/RANKL in urothelial carcinogenesis and the presence of Tregs in a suppressed immune tumor microenvironment. Mice treated with PRP only showed a 28.6% rate of tumor progression inhibition (TPI) and exhibited papillary urothelial carcinoma (pTa) and pTis. In this group, the intensity of the RANKL and FOXP3 immunoreaction was weaker when compared to the Cancer group. Thus, PRP showed immunomodulatory effects, reducing Tregs that are sources of RANKL. Oncotherad immunotherapy led to an TPI of 85.7%, and benign flat hyperplasia was the most frequent diagnosis. Oncotherad reduced the total RANK and RANKL immunoreactivities and decreased the intensity of RANKL immunostaining in comparison to the Cancer. In the OncoTherad+PRP 10 mg/ml or 20 mg/ml group, TPI was 71.4%, with a predominance of non-malignant lesions such as flat hyperplasia, low-grade intraurothelial neoplasia, and reactive atypia. Treatments with Oncotherad and Oncotherad plus PRP decreased the percentage of FOXP3+ cells and reduced the intensity of FOXP3 immunoreaction compared to the Cancer and PRP groups. Conclusions: The tumor inhibition obtained with Oncotherad plus PRP was related to the alteration of the immune profile of the tumor microenvironment by decreasing RANK/RANKL expression and Tregs, resulting in an effective immune response against the tumor.

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BLUHM, WOLFGANG F., MARKUS MEYER, ERIC A. SWANSON i WOLFGANG H. DILLMAN. "Postrest Potentiation of Active Force in Mouse Papillary Muscles Is Greatly Accelerated by Increased Stimulus Frequency". Annals of the New York Academy of Sciences 853, nr 1 CARDIAC SARCO (wrzesień 1998): 304–7. http://dx.doi.org/10.1111/j.1749-6632.1998.tb08285.x.

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Kawai, Masataka, Jamie R. Johnston, Tarek Karam, Li Wang, Rakesh K. Singh i Jose R. Pinto. "Myosin Rod Hypophosphorylation and CB Kinetics in Papillary Muscles from a TnC-A8V KI Mouse Model". Biophysical Journal 112, nr 8 (kwiecień 2017): 1726–36. http://dx.doi.org/10.1016/j.bpj.2017.02.045.

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Hongo, Kenichi, Satoshi Morimoto, Makoto Kawai, Kimiaki Komukai, Jin O-Uchi, Sachio Morimoto i Satoshi Kurihara. "Changes in Ca2+ transient and contraction of left ventricular papillary muscles in mouse model of dilated cardiomyopathy". Journal of Molecular and Cellular Cardiology 44, nr 2 (luty 2008): 441. http://dx.doi.org/10.1016/j.yjmcc.2007.07.022.

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Slominski, Andrzej, Alexander Pisarchik, Desmond J. Tobin, Joseph E. Mazurkiewicz i Jacobo Wortsman. "Differential Expression of a Cutaneous Corticotropin-Releasing Hormone System". Endocrinology 145, nr 2 (1.02.2004): 941–50. http://dx.doi.org/10.1210/en.2003-0851.

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Abstract We completed the mapping of a cutaneous CRH signaling system in two species with widely different determinants of skin functions, humans and mice. In human skin, the CRH receptor (CRH-R) 1 was expressed in all major cellular populations of epidermis, dermis, and subcutis with CRH-R1α being the most prevalent isoform. The CRH-R2 gene was expressed solely in hair follicle keratinocytes and papilla fibroblasts, whereas CRH-R2 antigen was localized predominantly in hair follicles, sebaceous and eccrine glands, muscle and blood vessels. In mouse skin, the CRH-R2 gene and protein were widely expressed in all cutaneous compartments and in cultured normal and malignant melanocytes. CRH-binding protein mRNA was present in dermal fibroblasts, melanoma cells, and sc fat of human skin and undetectable in mouse skin. The urocortin II gene was expressed equally in mouse and human skin. Taken together with our previous investigations, the present studies document the preferential expression of CRH-R1 in human skin, which mirrors CRH-R2 expression patterns in human and mouse skin. They are likely reflecting different functional activities of human and mouse skin. The adnexal location of CRH-R2 suggests a role for the receptor in hair growth. The differential interspecies CRH signaling expression pattern probably reflects adaptation to species-specific skin function determinants.

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Mizuno, Ju, Mikiya Otsuji, Hideko Arita, Kazuo Hanaoka, Shigeho Morita, Robert Akins, Shuta Hirano, Yoichiro Kusakari i Satoshi Kurihara. "Characterization of Intracellular Ca2+ Transient by the Hybrid Logistic Function in Aequorin-Injected Rabbit and Mouse Papillary Muscles". Journal of Physiological Sciences 57, nr 6 (2007): 349–59. http://dx.doi.org/10.2170/physiolsci.rp013107.

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Mizuno, Ju, Mikiya Otsuji, Kenji Takeda, Yoshitsugu Yamada, Hideko Arita, Kazuo Hanaoka, Shuta Hirano, Yoichiro Kusakari i Satoshi Kurihara. "Superior Logistic Model for Decay of Ca2+ Transient and Isometric Relaxation Force Curve in Rabbit and Mouse Papillary Muscles". International Heart Journal 48, nr 2 (2007): 215–32. http://dx.doi.org/10.1536/ihj.48.215.

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Detombe, Sarah A., Fu-Li Xiang, Joy Dunmore-Buyze, James A. White, Qingping Feng i Maria Drangova. "Rapid microcomputed tomography suggests cardiac enlargement occurs during conductance catheter measurements in mice". Journal of Applied Physiology 113, nr 1 (1.07.2012): 142–48. http://dx.doi.org/10.1152/japplphysiol.00831.2011.

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Conductance catheters (CC) represent an established method of determining cardiac function in mice; however, the potentially detrimental effects a catheter may have on the mouse heart have never been evaluated. The present study takes advantage of rapid three-dimensional (3D) microcomputed tomography (CT) to compare simultaneously acquired micro-CT and CC measurements of left ventricular (LV) volumes in healthy and infarcted mice and to determine changes in LV volume and function associated with CC insertion. LV volumes were measured in C57BL/6 mice (10 healthy, 10 infarcted, 2% isoflurane anesthesia) using a 1.4-Fr Millar CC. 3D micro-CT images of each mouse were acquired before CC insertion as well as during catheterization. Each CT scan produced high-resolution images throughout the entire cardiac cycle in <1 min, enabling accurate volume measurements as well as direct visualization of the CC within the LV. Bland-Altman analysis demonstrated that CC measurements underestimate volume compared with CT measurements in both healthy [bias of −18.4 and −28.9 μl for end-systolic (ESV) and end-diastolic volume (EDV), respectively] and infarcted mice (ESV = −51.6 μl and EDV = −71.7 μl); underestimation was attributed to the off-center placement of the catheter. Individual evaluation of each heart revealed LV dilation following CC insertion in 40% of mice in each group. No change in ejection fraction was observed, suggesting the enlargement was caused by volume overload associated with disruption of the papillary muscles or chords. The enlargement witnessed was not significant; however, the results suggest the potential for CC insertion to detrimentally affect mouse myocardium, necessitating further investigation.

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Maxwell, Krista, Jason Scott, Alexander Omelchenko, Anton Lukas, Liyan Lu, Yujuan Lu, Mark Hnatowich, Kenneth D. Philipson i Larry V. Hryshko. "Functional role of ionic regulation of Na+/Ca2+ exchange assessed in transgenic mouse hearts". American Journal of Physiology-Heart and Circulatory Physiology 277, nr 6 (1.12.1999): H2212—H2221. http://dx.doi.org/10.1152/ajpheart.1999.277.6.h2212.

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Na+/Ca2+exchange is the primary mechanism mediating Ca2+ efflux from cardiac myocytes during diastole and, thus, can prominently influence contractile force. In addition to transporting Na+and Ca2+, the exchanger is also regulated by these ions. Although structure-function studies have identified protein regions of the exchanger subserving these regulatory processes, their physiological importance is unknown. In this study, we examined the electrophysiological and mechanical consequences of cardiospecific overexpression of the canine cardiac exchanger NCX1.1 and a deletion mutant of NCX1.1 (Δ680–685), devoid of intracellular Na+([Formula: see text])- and Ca2+([Formula: see text])- dependent regulatory properties, in transgenic mice. Using the giant excised patch-clamp technique, normal ionic regulation was observed in membrane patches from cardiomyocytes isolated from control and transgenic mice overexpressing NCX1.1. In contrast, ionic regulation was nearly abolished in mice overexpressing Δ680–685, indicating that the native regulatory processes could be overwhelmed by expression of the transgene. To address the physiological consequences of ionic regulation of the Na+/Ca2+exchanger, we examined postrest force development in papillary muscles from NCX1.1 and Δ680–685 transgenic mice. Postrest potentiation was found to be substantially greater in Δ680–685 than in NCX1.1 transgenic mice, supporting the notion that ionic regulation of Na+/Ca2+exchange plays a significant functional role in cardiac contractile properties.

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Powers, Joseph D., Natalie J. Kirkland, Canzhao Liu, Swithin S. Razu, Xi Fang, Adam J. Engler, Ju Chen i Andrew D. McCulloch. "Subcellular Remodeling in Filamin C Deficient Mouse Hearts Impairs Myocyte Tension Development during Progression of Dilated Cardiomyopathy". International Journal of Molecular Sciences 23, nr 2 (14.01.2022): 871. http://dx.doi.org/10.3390/ijms23020871.

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Dilated cardiomyopathy (DCM) is a life-threatening form of heart disease that is typically characterized by progressive thinning of the ventricular walls, chamber dilation, and systolic dysfunction. Multiple mutations in the gene encoding filamin C (FLNC), an actin-binding cytoskeletal protein in cardiomyocytes, have been found in patients with DCM. However, the mechanisms that lead to contractile impairment and DCM in patients with FLNC variants are poorly understood. To determine how FLNC regulates systolic force transmission and DCM remodeling, we used an inducible, cardiac-specific FLNC-knockout (icKO) model to produce a rapid onset of DCM in adult mice. Loss of FLNC reduced systolic force development in single cardiomyocytes and isolated papillary muscles but did not affect twitch kinetics or calcium transients. Electron and immunofluorescence microscopy showed significant defects in Z-disk alignment in icKO mice and altered myofilament lattice geometry. Moreover, a loss of FLNC induces a softening myocyte cortex and structural adaptations at the subcellular level that contribute to disrupted longitudinal force production during contraction. Spatially explicit computational models showed that these structural defects could be explained by a loss of inter-myofibril elastic coupling at the Z-disk. Our work identifies FLNC as a key regulator of the multiscale ultrastructure of cardiomyocytes and therefore plays an important role in maintaining systolic mechanotransmission pathways, the dysfunction of which may be key in driving progressive DCM.

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Dutt, Mriga, Yaan-Kit Ng, Jeffrey Molendijk, Hamzeh Karimkhanloo, Luoping Liao, Ronnie Blazev, Magdalene K. Montgomery, Matthew J. Watt i Benjamin L. Parker. "Western Diet Induced Remodelling of the Tongue Proteome". Proteomes 9, nr 2 (12.05.2021): 22. http://dx.doi.org/10.3390/proteomes9020022.

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The tongue is a heavily innervated and vascularized striated muscle that plays an important role in vocalization, swallowing and digestion. The surface of the tongue is lined with papillae which contain gustatory cells expressing various taste receptors. There is growing evidence to suggest that our perceptions of taste and food preference are remodelled following chronic consumption of Western diets rich in carbohydrate and fats. Our sensitivity to taste and also to metabolising Western diets may be a key factor in the rising prevalence of obesity; however, a systems-wide analysis of the tongue is lacking. Here, we defined the proteomic landscape of the mouse tongue and quantified changes following chronic consumption of a chow or Western diet enriched in lipid, fructose and cholesterol for 7 months. We observed a dramatic remodelling of the tongue proteome including proteins that regulate fatty acid and mitochondrial metabolism. Furthermore, the expressions of several receptors, metabolic enzymes and hormones were differentially regulated, and are likely to provide novel therapeutic targets to alter taste perception and food preference to combat obesity.

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Mizuno, Ju, Shigeho Morita, Mikiya Otsuji, Hideko Arita, Kazuo Hanaoka, Robert E. Akins, Shuta Hirano, Yoichiro Kusakari i Satoshi Kurihara. "Half-Logistic Time Constants as Inotropic and Lusitropic Indices for Four Sequential Phases of Isometric Tension Curves in Isolated Rabbit and Mouse Papillary Muscles". International Heart Journal 50, nr 3 (2009): 389–404. http://dx.doi.org/10.1536/ihj.50.389.

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Yoo, Kee Hwan, Barbara A. Thornhill, Michael S. Forbes i Robert L. Chevalier. "Inducible nitric oxide synthase modulates hydronephrosis following partial or complete unilateral ureteral obstruction in the neonatal mouse". American Journal of Physiology-Renal Physiology 298, nr 1 (styczeń 2010): F62—F71. http://dx.doi.org/10.1152/ajprenal.00234.2009.

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To investigate the role of endogenous inducible nitric oxide synthase (iNOS) in the response of the developing kidney to unilateral ureteral obstruction (UUO), neonatal iNOS null mutant (−/−) and wild-type (WT) mice were subjected to partial or complete UUO. At 7 and 21 days of age, apoptosis, renin, vascular endothelial growth factor (VEGF), fibroblasts (anti-fibroblast-specific peptide 1), myofibroblasts (α-smooth muscle actin), macrophages (F4/80), and collagen were measured in kidney tissue. Compared with WT, renal parenchymal thickness was increased, with preservation of the papilla, in −/− mice with partial UUO, but decreased in −/− mice with complete UUO. Ureteral peristalsis increased with severity of pelvic dilatation in WT, and increased further in −/− mice with partial UUO. Apoptosis, fibroblasts, and macrophages were increased in −/− mice with complete UUO, but there was no effect of iNOS on other histological parameters following complete UUO. Renin was decreased in −/− mice with partial UUO. There was no effect of iNOS genotype on renal collagen accumulation at either 7 or 21 days of age. These results are consistent with an injurious role for endogenous iNOS following partial UUO by inhibiting ureteral peristalsis and increasing renal renin although renal fibrosis is not affected. In contrast, in mice with complete UUO, iNOS attenuates apoptosis and enhances renal parenchymal thickness. Alterations in the severity of ureteral obstruction may therefore influence the effect of iNOS on long-term renal injury.

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Morgan, Patricio E., María V. Correa, Irene L. Ennis, Ariel A. Diez, Néstor G. Pérez i Horacio E. Cingolani. "Silencing of sodium/hydrogen exchanger in the heart by direct injection of naked siRNA". Journal of Applied Physiology 111, nr 2 (sierpień 2011): 566–72. http://dx.doi.org/10.1152/japplphysiol.00200.2011.

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Cardiac Na+/H+ exchanger (NHE1) hyperactivity is a central factor in cardiac remodeling following hypertension, myocardial infarction, ischemia-reperfusion injury, and heart failure. Treatment of these pathologies by inhibiting NHE1 is challenging because specific drugs that have been beneficial in experimental models were associated with undesired side effects in clinical practice. In the present work, small interference RNA (siRNA) produced in vitro to specifically silence NHE1 (siRNANHE1) was injected once in vivo into the apex of the left ventricular wall of mouse myocardium. After 48 h, left ventricular NHE1 protein expression was reduced in siRNANHE1-injected mice compared with scrambled siRNA by 33.2 ± 3.4% ( n = 5; P < 0.05). Similarly, NHE1 mRNA levels were reduced by 20 ± 2.0% ( n = 4). At 72 h, siRNANHE1 spreading was evident from the decrease in NHE1 expression in three portions of the myocardium (apex, medium, base). NHE1 function was assessed based on maximal velocity of intracellular pH (pHi) recovery (dpHi/d t) after an ammonium prepulse-induced acidic load. Maximal dpHi/d t was reduced to 14% in siRNANHE1-isolated left ventricular papillary muscles compared with scrambled siRNA. In conclusion, only one injection of naked siRNANHE1 successfully reduced NHE1 expression and activity in the left ventricle. As has been previously suggested, extensive NHE1 expression reduction may indicate myocardial spread of siRNA molecules from the injection site through gap junctions, providing a valid technique not only for further research into NHE1 function, but also for consideration as a potential therapeutic strategy.

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Wang, Li, Priya Muthu, Danuta Szczesna-Cordary i Masataka Kawai. "Characterizations of myosin essential light chain’s N-terminal truncation mutant Δ43 in transgenic mouse papillary muscles by using tension transients in response to sinusoidal length alterations". Journal of Muscle Research and Cell Motility 34, nr 2 (9.02.2013): 93–105. http://dx.doi.org/10.1007/s10974-013-9337-x.

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Elnakish, Mohammad T., Leni Moldovan, Mahmood Khan, Hamdy H. Hassanain i Paul M. L. Janssen. "Myocardial Rac1 Exhibits Partial Involvement in Thyroxin-induced Cardiomyocyte Hypertrophy and Its Inhibition Is Not Sufficient to Improve Cardiac Dysfunction or Contractile Abnormalities in Mouse Papillary Muscles". Journal of Cardiovascular Pharmacology 61, nr 6 (czerwiec 2013): 536–44. http://dx.doi.org/10.1097/fjc.0b013e31828d4b9d.

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Hoe, Kwang-Lae, Ines Armando, Gustavo Baiardi, Taduru Sreenath, Ashok Kulkarni, Alfredo Martiánez i Juan M. Saavedra. "Molecular cloning, characterization, and distribution of the gerbil angiotensin II AT2 receptor". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 285, nr 6 (grudzień 2003): R1373—R1383. http://dx.doi.org/10.1152/ajpregu.00008.2003.

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We isolated a cDNA clone encoding the gerbil AT2 receptor (gAT2) gene from a gerbil adrenal gland cDNA library. The full-length cDNA contains a 1,089-bp open reading frame encoding 363 amino acid residues with 90.9, 96.1, and 95.6% identity with the human (hAT2), rat (rAT2), and mouse AT2 (mAT2) receptors, respectively. There are at least seven nonconserved amino acids in the NH2-terminal domain and in positions Val196, Val217, and Met293, important for angiotensin (ANG) II but not for CGP-42112 binding. Displacement studies in adrenal sections revealed that affinity of the gAT2 receptor was 10-20 times lower for ANG II, ANG III, and PD-123319 than was affinity of the rAT2 receptor. The affinity of each receptor remained the same for CGP-42112. When transfected into COS-7 cells, the gAT2 receptor shows affinity for ANG II that is three times lower than that shown by the hAT2 receptor, whereas affinities for ANG III and the AT2 receptor ligands CGP-42112 and PD-123319 were similar. Autoradiography in sections of the gerbil head showed higher binding in muscles, retina, skin, and molars at embryonic day 19 than at 1 wk of age. In situ hybridization and emulsion autoradiography revealed that at embryonic day 19 the gAT2 receptor mRNA was highly localized to the base of the dental papilla of maxillary and mandibular molars. Our results suggest selective growth-related functions in late gestation and early postnatal periods for the gAT2 receptor and provide an essential basis for future mutagenesis studies to further define structural requirements for agonist binding.

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Lian, Hong, Zhuyun Qin, Mengge Wu, Peipei Zuo, Lina Bai, Minjie Lu, Lulu Li i Haitao Zhang. "Contractility detection of isolated mouse papillary muscle using myotronic Myostation‐Intact device". Animal Models and Experimental Medicine, 27.09.2022. http://dx.doi.org/10.1002/ame2.12272.

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Kirk, Jonathan A., Stephen H. Smith, Guy A. MacGowan i Sanjeev G. Shroff. "Abstract 5403: Protein Kinase C-Induced Troponin I Phosphorylation Causes Changes in Cardiac Contractile Function but not the Intracellular Calcium Transient". Circulation 118, suppl_18 (28.10.2008). http://dx.doi.org/10.1161/circ.118.suppl_18.s_544.

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Both intracellular calcium transients ([Ca] i ) and myofilament properties determine cardiac muscle contractile force. Transgenic mouse models created to perturb specific myofilament proteins often cause a compensatory change in [Ca] i , which confounds the assessment of myofilament structure-function relationships. We have created a new transgenic mouse that has all three protein kinase C (PKC) phosphorylation sites on cardiac troponin I (cTnI) mutated to glutamic acid, rendering these sites constitutively pseudo-phosphorylated. Our goal was to determine the effects of this mutation on cardiac muscle contractile function and whether these effects would be concurrent with changes in the [Ca] i . Two sets of studies were conducted: skinned muscle fiber experiments to characterize the steady-state force-pCa relationships at sarcomere lengths of 1.9 and 2.3 μm and right ventricular papillary muscle experiments to characterize the peak developed force (F dev )-muscle length (L) relationships and [Ca] i (fura-5F calcium dye, emission: 510 nm, excitation: 340 and 380 nm, R = [emission fluorescence 340 ]/[emission fluorescence 380 ]). In skinned fibers, there was a significant decrease in maximally activated force (i.e., force at pCa 4.33) in transgenic mice (Wild-Type, WT (n = 7): 64.4± 8.0, Transgenic, TG (n = 6): 42.6±6.8 mN•mm −2 , P = 0.004), without any changes in calcium sensitivity or cooperativity (Hill coefficient). In intact papillary muscles, TG mice showed a decrease in F dev and slowed relaxation for all muscle lengths examined (F dev @ 100% L max , WT (n = 5): 9.3±3.5, TG (n = 6): 4.2±1.6 mN•mm −2 , P = 0.005; dF/dt min @ 100% L max , WT: −136±32, TG: −74±38 mN•mm −2 •s −1 , P = 0.002). In contrast, [Ca] i was unaltered in TG mice at all muscle lengths examined ([Ca] i amplitude as quantified by R systole / R diaastole , WT: 1.62±0.07, TG: 1.48±0.22; [Ca] i relaxation rate d R /dt min , WT: −96±37, TG: −64±30 s −1 ). Thus, PKC-induced TnI phosphorylation affects cardiac muscle contraction (reduced force magnitude and slowed relaxation) via changes in the myofilament properties (activation and/or crossbridge dynamics), and these contractile effects are not related to any changes in the intracellular calcium transient.

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Hou, Luqia, Mohit Kumar, Priti Anand, Yinhong Chen, Nesrine El-Bizri, Chad J. Pickens, W. Michael Seganish, Sakthivel Sadayappan i Gayathri Swaminath. "Modulation of myosin by cardiac myosin binding protein-C peptides improves cardiac contractility in ex-vivo experimental heart failure models". Scientific Reports 12, nr 1 (14.03.2022). http://dx.doi.org/10.1038/s41598-022-08169-1.

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AbstractCardiac myosin binding protein-C (cMyBP-C) is an important regulator of sarcomeric function. Reduced phosphorylation of cMyBP-C has been linked to compromised contractility in heart failure patients. Here, we used previously published cMyBP-C peptides 302A and 302S, surrogates of the regulatory phosphorylation site serine 302, as a tool to determine the effects of modulating the dephosphorylation state of cMyBP-C on cardiac contraction and relaxation in experimental heart failure (HF) models in vitro. Both peptides increased the contractility of papillary muscle fibers isolated from a mouse model expressing cMyBP-C phospho-ablation (cMyBP-CAAA) constitutively. Peptide 302A, in particular, could also improve the force redevelopment rate (ktr) in papillary muscle fibers from cMyBP-CAAA (nonphosphorylated alanines) mice. Consistent with the above findings, both peptides increased ATPase rates in myofibrils isolated from rats with myocardial infarction (MI), but not from sham rats. Furthermore, in the cMyBP-CAAA mouse model, both peptides improved ATPase hydrolysis rates. These changes were not observed in non-transgenic (NTG) mice or sham rats, indicating the specific effects of these peptides in regulating the dephosphorylation state of cMyBP-C under the pathological conditions of HF. Taken together, these studies demonstrate that modulation of cMyBP-C dephosphorylation state can be a therapeutic approach to improve myosin function, sarcomere contractility and relaxation after an adverse cardiac event. Therefore, targeting cMyBP-C could potentially improve overall cardiac performance as a complement to standard-care drugs in HF patients.

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