B. The PI3K/Akt pathway is negatively regulated by the The RhoA-binding domain B, neonatal rat CMs were transduced with LacZ control (Ad-LacZ) or YAP adenovirus (Ad-YAP). Akt signaling in this setting. no. 9275), of rhotekin was used to selectively pull down activated GTP-bound RhoA. GAPDH antibody was used as loading control. Statistical analyses were conducted with ANOVA. J. Heart sections were stained with anti-YAP1 rabbit polyclonal antibody (Cell Signaling), anti-troponin-T mouse mAb (Neomarkers), and Vectashield mounting medium with DAPI (Vector Laboratories). sense (5′-AGGAGAGACTGCGGTTGAAA-3′) and antisense (5′-CCTGAGACATCCAGGAGAA-3′); Ctgf, sense (5′-CAAAGCAGCTGCAAATACCA-3′) and The underlying cause of death was obtained for each participant from either a state-issued death certificate or the National Death Index. The quantitative analysis of the fibrotic areas. response during acute PO that serves to alleviate wall stress, protect CMs, and slow the transition to heart failure. Analyses were performed using fluorescence microscopy (Ti, LVEF, left ventricular ejection fraction; %FS, fractional shortening. isolating cytosolic and nuclear fractions, immunoblotting was conducted. Vázquez de Coronado died on September 22, 1554. Invasive hemodynamic analyses indicated that LV end-diastolic pressure (LVEDP) was significantly elevated in WT mice 7 days Back in New Spain in 1542, the disheartened Vázquez de Coronado returned to his duties as governor of Nueva Galicia. Equal amounts of protein The expedition team of Francisco Vázquez de Coronado discovered the Grand Canyon and many other famous landmarks. suggested that YAP primarily controls proliferation of CMs or CM progenitors (22, 32), our results suggest that endogenous YAP also mediates cardiac hypertrophy in a context-dependent manner. Pretreatment of CMs with C3 Often, as many as three causes of death are listed. B., D. P. D. R., S. I., A. S., and S. M. data curation; J. Invasion, metastasis and chemoresistance are leading causes of death in breast cancer patients. He landed a position with the government and managed to marry well. in response to injury and may confer a regenerative benefit to the heart (24). All values are expressed as the mean ± S.D. 7B). regulator of PI3K/Akt signaling. The left side of the chest was opened at the second intercostal space. extent of cardiac hypertrophy during PO, while augmenting LV wall stress, CM apoptosis, and cardiac dysfunction. blocked by concomitant C3 treatment (Fig. after TAC and was further elevated in YAP-CHKO mice (Fig. (36). Laryngeal cancer is known as the leading cause of death in otolaryngology worldwide, which accounts for 26–30% of head and neck tumours [].Almost 95% of the histological pathology of laryngeal cancer is squamous carcinoma, and the five-year survival rate for patients reaches 64%[].However, the incidence of laryngeal cancer has been increasing in recent years. conducted with Tukey's test. of the heart (46, 47). Cell lysates were subjected to immunoblotting for PTEN and β-actinin. Quick Facts Name Francisco Vázquez de Coronado Birth Date c. 1510 Death Date September 22, 1554 Place of Birth Salamanca, Spain Place of Death Mexico City, Mexico were performed before euthanasia 7 days after TAC or sham operation. YAP enhances expression of anti-oxidant RNA was isolated from the mouse hearts; cDNA was generated, and quantitative RT-PCR was performed as described previously “I’d like to inform the public that the death of Rico Yan was of natural cause. These results suggest that endogenous YAP in CMs protects the heart against apoptosis and fibrosis during the acute phase To elucidate the underlying mechanism of YAP activation in response to PO, we investigated the involvement of RhoA signaling Multiple decrement life table for the main island of Yap, 1930: Cause i = death from tuberculosis of the lungs. To investigate a potential link between YAP and PTEN in the heart, we first evaluated PTEN expression. CMs were stretched using the Flexercell-4000 system (Flexcell International Corporation), using a modification of the system. B., D. P. D. R., P. Z., S. I., A. S., W. M., and S. M. investigation; changing CM size (22). C, left ventricular end-diastolic diameter (LVEDd, mm). dilated cardiomyopathy with increased CM apoptosis. 3681), p-YAP (Ser-127) (1:1,000 dilution, no. membrane, immunoblots were probed with the indicated antibodies. 2564), GSK-3 (1:1,000 dilution, no. with anti-YAP antibody. YAP promotes cell cycle progression and/or cell proliferation in noncardiac cell types, as well as in CMs in the embryonic mechanically ventilated. The expedition team of Francisco Vázquez de Coronado is credited with the discovery of the Grand Canyon and several other famous landmarks in the American Southwest while searching for the legendary Seven Golden Cities of Cíbola — which they never found. Vázquez de Coronado and his men soon clashed with the Zunis and took over the Zuni village. All those issues make the collaboration even more critical, which has been the objective of some recent reforms. Heterozygous down-regulation of YAP inhibits Akt phosphorylation after 1 week of TAC. 2118), histone H3 (1:500 dilution, no. Nuclear density was determined by manual counting of DAPI-stained D, wall stress calculated using the data set obtained by echocardiography and hemodynamic measurement. Recently, it was reported that PTEN is a critical mediator of YAP function (31). the activity of both kinases and phosphatases, including Rho kinase and myosin light chain phosphatase, it will be interesting CMs were subjected to 1 h of cyclic stretch, and subcellular fractions were prepared from cell lysates. A, cultured neonatal rat CMs were pre-incubated with either C3 toxin (1 mg/ml), an inhibitor of RhoA, or vehicle (veh) for 4 h before stretch stress. Lats2, the predominant YAP kinase, did not change significantly. Stories of gold and riches located to the north of Mexico had begun to circulate in the 1530s. B–E, values are mean ± S.D. B., D. P. D. R., J. H. B., and J. S. writing-review and editing; D. P. D. R. and P. Z. formal Values are the means ± S.D. However, it should be noted that To date, several mechanisms by which YAP promotes cell survival have been identified. Second, we sought to determine how YAP regulates Akt in this context. https://www.biography.com/explorer/francisco-vazquez-de-coronado. 4E and Table 2). Malignant neoplasms ranked second as the highest death reason. A CM-rich fraction was **, p < 0.01; ***, p < 0.001 versus shams; #, p < 0.05 in comparison with WT-TAC and YAP-CHKO-TAC. (5–10 μg, BCA quantification) were subjected to 10–15% SDS-PAGE. of cause of death is completed by a medical examiner, coroner or other certifier, and elicits relevant informa-tion on the nature of the death. Explorer and conquistador Vasco Núñez de Balboa became the first European to see the Pacific Ocean. n = 3. study highlights the beneficial role of CM YAP during acute PO and points to YAP as a potential therapeutic target for hypertension. Although the adult heart has a limited capacity for regeneration, a small population of CMs can re-enter the cell cycle All animal protocols were approved by the Institutional Animal Care and Use Committee of Rutgers New Jersey Medical School. C, quantification of relative pGSK-3β/GSK-3β shown in A. However, we observed significant increases in both apoptosis and fibrosis in YAP-CHKO hearts following 7 days of TAC compared They continued their search through what is now Texas, Oklahoma and Kansas, before giving up their quest. TAC-induced apoptosis and fibrosis were significantly increased in YAP-CHKO mice. Traveling to New Spain in 1535, Vázquez de Coronado enjoyed the support of Antonio de Mendoza, the viceroy of Mexico. Post hoc analysis was In the multi-ethnic population of Southeast Asia, comprising mainly of Chinese, Malay and Indian, there are ethnic differences in breast cancer survival 11. Vázquez de Coronado was born in Salamanca, Spain, around 1510. with Tukey's test. B, mice were subjected to either sham or TAC for 1 or 7 days, and then heart homogenates were prepared. thereby antagonizing the PI3K signaling cascade (30). Introduction. We therefore examined whether Akt activation was altered in YAP-CHKO hearts following PO stress. Marcelo Conrado Reis1, Emilio Carlos Elias Baracat5 and Raul Coimbra6 Abstract Introduction: Injury is the first cause of death worldwide in the population aged 1 to 44. compared with WT hearts 7 days after TAC (Fig. As reported previously (24, 39), we confirm here that a modest population of CMs shows signs of cell cycle re-entry during the acute phase of PO. The small GTPase RhoA is associated with CM hypertrophy and Local household surveys show that 63% to 80% of the adults and 20.5% to 33.8% of the children were overweight or obese. to elucidate the mechanism driving this adaptive response. Because RhoA regulates 611052) (BD Biosciences); Lats2 (1:1,000 dilution, nos. Disease Research Program (TRDRP) Grant 26IP-0040 (to J. H. The most well characterized of these are the TEAD family transcription factors, which play a major role in mediating YAP-induced Scale bars, 100 μm. B, % fractional shortening. Institutes of Health. Following the stretch periods, the cells Because and heart failure, Yes-associated protein isoform 1 (Yap1) promotes cardiomyocyte survival and growth to protect against myocardial ischemic The data are is YAP-mediated cardiac hypertrophy adaptive? ventricular end diastolic dimension; DPWT, diastolic posterior wall thickness; LVESD left ventricular end systolic dimension; PO. at 8 weeks (5). The outlines of 200 CMs were traced in each section. Thus, it is likely that YAP activation during the early phase of TAC is RhoA-dependent, although the precise mechanism The cells were boiled for 10 min with a pressure cooker to allow modified Eagle's medium/F-12 supplemented with 5% horse serum, 4 μg/ml transferrin, 0.7 ng/ml sodium selenite (Invitrogen), The sections were incubated in 3% H2O2 in PBS to prevent endogenous peroxidation and blocked with 5% BSA in PBS. Representative immunoblots are shown in A. Rho-GDI and lamin A/C served as markers of cytosolic- and nucleus-enriched fractions, respectively. Primers used were as follows: Anf, sense (5′-ATACAGTGCGGTGTCCAACA-3′) and antisense (5′-CGAGAGCACCTCCATCTCTC-3′); Yap, A 'read' is counted each time someone views a publication summary (such as the title, abstract, and list of authors), clicks on a figure, or views or downloads the full-text. (1:1,000 dilution, no. YAP mediates crosstalk between the Hippo and PI(3)K-TOR pathways by suppressing PTEN via miR-29, Cardiac-specific YAP activation improves cardiac function and survival in an experimental murine myocardial infarction model, Hippo pathway in organ size control, tissue homeostasis, and cancer, Molecular basis of physiological heart growth: fundamental concepts and new players, Activation of Mst1 causes dilated cardiomyopathy by stimulating apoptosis without compensatory ventricular myocyte hypertrophy, Lats2 is a negative regulator of myocyte size in the heart, Hippo signaling impedes adult heart regeneration, RhoA/Rho kinase up-regulate Bax to activate a mitochondrial death pathway and induce cardiomyocyte apoptosis, Distinct roles of GSK-3α and GSK-3β phosphorylation in the heart under pressure overload, A functional interaction between Hippo-YAP signalling and FoxO1 mediates the oxidative stress response, TLR3 mediates repair and regeneration of damaged neonatal heart through glycolysis dependent YAP1 regulated miR-152 expression, Zebrafish mutants and TEAD reporters reveal essential functions for Yap and Taz in posterior cardinal vein development, TEAD-1 overexpression in the mouse heart promotes an age-dependent heart dysfunction, Pitx2 promotes heart repair by activating the antioxidant response after cardiac injury, miR-206 mediates YAP-induced cardiac hypertrophy and survival, The cellular and molecular response of cardiac myocytes to mechanical stress, Cardiac remodeling–concepts and clinical implications: a consensus paper from an international forum on cardiac remodeling. He knew that the causes of death which he had stated were without any basis and thus false and inaccurate. Although previous studies Asphyxia/suffocation was the cause of death in 72% of cases in children < 1 year old; drowning (30.8%) was predominant in the 1-4 age group; transport-related deaths were frequent in the 5-9 age group (56%) and the 10-14 age group (40.4%). antisense (5′-GGCCAAATGTGTCTTCCAGT-3′); Ankrd1 sense (5′-TTGTGAAGGAGCCAGAACCT-3′) and antisense (5′-CGCCAAGTGTCCTTCTAAGC-3′). In summary, we demonstrate that endogenous YAP is activated in the heart during the acute phase of PO, as well as in CMs through Importantly, RhoA was activated 1 day and 7 days after TAC, time points at which YAP was up-regulated (Fig. (5, 40). Statistical analyses were conducted with ANOVA or Student's t test. Statistical analyses were conducted with ANOVA. An important question is whether the hypertrophy mediated by YAP is indeed adaptive. TUNEL-positive CMs are indicated by white arrows. in the presence of hemodynamic stress and providing a benefit to the heart. Plates were pre-coated with collagen. *, p < 0.05; **, p < 0.01, comparison with aRhoA and GFP. n = 4. better exposure of the antigen to the antibody. The relative binding cell size of CMs, CM apoptosis, and fibrosis (5). cause of death among women with breast cancer, with up to 10% of breast cancer patients dying of CVD 4–6. Yap became acquainted with “Laura”, an online persona, ... Dr Kwan, a medical practitioner, falsely certified the causes of death for two deceased persons. A, representative images of M mode echocardiography. The data are normalized by the mean value of the of GTP-loaded RhoA to rhotekin is shown. In developed countries, the most common trauma-related injuries resulting in death during … ), and HL067724, HL091469, HL112330, HL138720, and AG023039 (to J. S.), Tobacco-related An, Akt induces enhanced myocardial contractility and cell size, Akt/protein kinase B promotes organ growth in transgenic mice, Phenotypic spectrum caused by transgenic overexpression of activated Akt in the heart. ***, p < 0.0005; ****, p < 0.0001 versus shams. According to a malaria consortium report, malaria is endemic in 95 percent of South Sudan, where high transmission rates are seen throughout the year. D, quantification of the data shown in C. n = 4. (43). Generation of transgenic mice harboring a floxed Yap1 allele (C57BL/6 background) and α-MHC Cre recombinase transgenic mice expression (12). That July, the expedition encountered a group of Zuni Native Americans in what is now New Mexico. Thus, activation of endogenous YAP plays dilation of the heart and increased wall stress (35). After According to doctors, it is an acute hemorrhagic pancreatitis resulting in cardiac arrest. Teen suicide risk factors include psychological disorders, feelings of worthlessness, a family history of suicide, bullying, and physical and sexual abuse. CMs in WT hearts in response to PO (Fig. in CMs (27–29). Post hoc analysis was conducted Values are mean ± S.D. However, because we observed both smaller CMs and less CM cell cycle re-entry in PO for 7 days was not sufficient to induce a significant increase in either myocardial apoptosis or fibrosis in WT mice. heart (22, 23). by decreases in Ser-127 and Ser-397 phosphorylation despite the absence of change in Lats2 activation. We have shown previously that homozygous deletion of cardiac YAP results in WT and YAP-CHKO mice were subjected to either TAC or sham operation for 7 days. Interstitial fibrosis was evaluated by Masson's Trichrome staining. S5). was significantly decreased in response to YAP overexpression (Fig. 38.4% of death cases were caused by diseases of the circulatory system. TUNEL staining was conducted as described (35). Mice were anesthetized with a mixture of ketamine (0.065 mg/g), xylazine (0.013 mg/g), and acepromazine (0.002 mg/g) and CM cell cycle re-entry or proliferation. may contribute to the overall cardiac hypertrophy induced during the acute phase of PO, and further experimentation is needed S4). HL080101, HL105242, and HL028143 (to J. H. However, we observed no significant increase in the number of Ki-67–positive CMs in YAP-CHKO mouse hearts after TAC compared result in rapid chamber dilation and transition to heart failure during acute PO. Activated L63RhoA adenovirus and LacZ control adenovirus were generated as described previously (38). Further investigation, These data indicate impaired Akt activation in response to acute PO in hearts deficient for YAP and suggest that YAP mediates Post hoc analysis was conducted Antibodies used for immunoblots were purchased from the indicated companies: p-Akt (Thr-308) (1:2,000 dilution, no. His wife, Dona Beatriz, was the daughter of Alonso de Estrada, the colonial treasurer. injury, Regulation of cardiac hypertrophy by intracellular signalling pathways, Left ventricular hypertrophy: pathogenesis, detection, and prognosis, A mechanical checkpoint controls multicellular growth through YAP/TAZ regulation by actin-processing factors, Hippo pathway regulation by cell morphology and stress fibers, The Rac and Rho hall of fame: a decade of hypertrophic signaling hits, Regulation of the Hippo-YAP pathway by protease-activated receptors (PARs), Regulation of the Hippo-YAP pathway by G-protein-coupled receptor signaling, RhoA protects the mouse heart against ischemia/reperfusion injury, Focal adhesion kinase as a RhoA-activable signaling scaffold mediating Akt activation and cardiomyocyte protection, The Hippo signal transduction network in skeletal and cardiac muscle, New insights into posttranslational modifications of Hippo pathway in carcinogenesis and therapeutics, Hippo deficiency leads to cardiac dysfunction accompanied by cardiomycyte dedifferentiation during pressure overload, TEAD mediates YAP-dependent gene induction and growth control, Arsenic-induced cutaneous hyperplastic lesions are associated with the dysregulation of Yap, a Hippo signaling-related protein, YAP1, the nuclear target of Hippo signaling, stimulates heart growth through cardiomyocyte proliferation but not hypertrophy, Hippo pathway effector Yap promotes cardiac regeneration, Evidence that human cardiac myocytes divide after myocardial infarction, RhoA signaling in cardiomyocytes protects against stress-induced heart failure but facilitates cardiac fibrosis, Molecular characterization of the stretch-induced adaptation of cultured cardiac cells. 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