JOSE EDUARDO KRIEGER

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Departamento de Cardio-Pneumologia, Faculdade de Medicina - Docente
Instituto do Coração, Hospital das Clínicas, Faculdade de Medicina
LIM/13 - Laboratório de Genética e Cardiologia Molecular, Hospital das Clínicas, Faculdade de Medicina - Líder

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Autor e Coautores FMUSP-HC Normalizados: AYUMI AUREA MIYAKAWA YAMAGUCHI ×

Resultados de Busca

Agora exibindo 1 - 10 de 21
  • article 1 Citação(ões) na Scopus
    Temporal Change of Extracellular Matrix during Vein Arterialization Remodeling in Rats
    (2019) MIYAKAWA, Ayumi Aurea; BASSANEZE, Vinicius; DUARTE, Nubia Esteban; GIRAO-SILVA, Thais; BIZERRA, Monica Nunes; CAMPOS, Julliana Carvalho; KRIEGER, Jose Eduardo
    The global expression profile of the arterialized rat jugular vein was established to identify candidate genes and cellular pathways underlying the remodeling process. The arterialized jugular vein was analyzed on days 3 and 28 post-surgery and compared with the normal jugular vein and carotid artery. A gene array platform detected 9846 genes in all samples. A heatmap analysis uncovered patterns of gene expression showing that the arterialized vein underwent a partial transition from vein to artery from day 3 to 28 post-surgery. The same pattern was verified for 1845 key differentially expressed genes by performing a pairwise comparison of the jugular vein with the other groups. Interestingly, hierarchical clustering of 60 genes with altered expression on day 3 and day 28 displayed an expression pattern similar to that of the carotid artery. Enrichment analysis results and the network relationship among genes modulated during vein arterialization showed that collagen might play a role in the early remodeling process. Indeed, the total collagen content was increased, with the augmented expression of collagen I, collagen IV, and collagen V in arterialized veins. Additionally, there was an increase in the expression of versican and Thy-1 and a decrease in the expression of biglycan and beta 1-integrin. Overall, we provide evidence that vein arterialization remodeling is accompanied by consistent patterns of gene expression and that collagen may be an essential element underlying extracellular matrix changes that support the increased vascular wall stress of the new hemodynamic environment.
  • article 18 Citação(ões) na Scopus
    Focal adhesion signaling: Vascular smooth muscle cell contractility beyond calcium mechanisms
    (2021) RIBEIRO-SILVA, J. C.; MIYAKAWA, A. A.; KRIEGER, J. E.
    Smooth muscle cell (SMC) contractility is essential to vessel tone maintenance and blood pressure regulation. In response to vasoconstrictors, calcium-dependent mechanisms promote the activation of the regulatory myosin light chain, leading to increased cytoskeleton tension that favors cell shortening. In contrast, SMC maintain an intrinsic level of a contractile force independent of vasoconstrictor stimulation and sustained SMC contraction beyond the timescale of calcium-dependent mechanisms suggesting the involvement of additional players in the contractile response. Focal adhesions (FAs) are conceivable candidates that may influence SMC contraction. They are required for actin-based traction employed by cells to sense and respond to environmental cues in a process termed mechanotransduction. Depletion of FA proteins impairs SMC contractility, producing arteries that are prone to dissection because of a lack of mechanical stability. Here, we discuss the role of calcium-independent FA signaling mechanisms in SMC contractility. We speculate that FA signaling contributes to the genesis of a variety of SMC phenotypes and discuss the potential implications for mechanical homeostasis in normal and diseased states. ©2021 The Author(s).
  • article 24 Citação(ões) na Scopus
    Adipose Tissue-Derived Stem Cells from Humans and Mice Differ in Proliferative Capacity and Genome Stability in Long-Term Cultures
    (2011) DANOVIZ, Maria Elena; BASSANEZE, Vinicius; NAKAMUTA, Juliana Sanajotti; SANTOS-JUNIOR, Gabriel Ribeiro dos; SAINT-CLAIR, Danilo; BAJGELMAN, Marcio Chaim; FAE, Kellen Cristhina; KALIL, Jorge; MIYAKAWA, Ayumi Aurea; KRIEGER, Jose Eduardo
    Adipose tissue-derived stem cells (ASCs) are among the more attractive adult stem cell options for potential therapeutic applications. Here, we studied and compared the basic biological characteristics of ASCs isolated from humans (hASCs) and mice (mASCs) and maintained in identical culture conditions, which must be examined prior to considering further potential clinical applications. hASCs and mASCs were compared for immunophenotype, differentiation potential, cell growth characteristics, senescence, nuclear morphology, and DNA content. Although both strains of ASCs displayed a similar immunophenotype, the percentage of CD73(+) cells was markedly lower and CD31(+) was higher in mASC than in hASC cultures. The mean population doubling time was 98.08 +/- 6.15 h for hASCs and 52.58 +/- 3.74 h for mASCs. The frequency of nuclear aberrations was noticeably lower in hASCs than in mASCs regardless of the passage number. Moreover, as the cells went through several in vitro passages, mASCs showed changes in DNA content and cell cycle kinetics (frequency of hypodiploid, G0/G1, G2/M, and hyperdiploid cells), whereas all of these parameters remained constant in hASCs. Collectively, these results suggest that mASCs display higher proliferative capacity and are more unstable than hASCs in long-term cultures. These results underscore the need to consider specificities among model systems that may influence outcomes when designing potential human applications.
  • article 41 Citação(ões) na Scopus
    Thioredoxin interacting protein genetic variation is associated with diabetes and hypertension in the Brazilian general population
    (2012) FERREIRA, Noely E.; OMAE, Samantha; PEREIRA, Abel; RODRIGUES, Mariliza V.; MIYAKAWA, Ayumi A.; CAMPOS, Luciene C. G.; SANTOS, Paulo C. J. L.; DALLAN, Luiz A.; MARTINEZ, Tania L.; SANTOS, Raul D.; MILL, Jose G.; KRIEGER, Jose E.; PEREIRA, Alexandre C.
    Objective: To investigate the relationship between TXNIP polymorphisms, diabetes and hypertension phenotypes in the Brazilian general population. Methods: Five hundred seventy-six individuals randomly selected from the general urban population according to the MONICA-WHO project guidelines were phenotyped for cardiovascular risk factors. A second, independent, sample composed of 487 family-trios from a different site was also selected. Nine TXNIP polymorphisms were studied. The potential association between TXNIP variability and glucose-phenotypes in children was also explored. TXNIP expression was quantified by real-time PCR in 53 samples from human smooth muscle cells primary culture. Results: TXNIP rs7211 and rs7212 polymorphisms were significantly associated with glucose and blood pressure related phenotypes. In multivariate logistic regression models the studied markers remained associated with diabetes even after adjustment for covariates. TXNIP rs7211 T/rs7212 G haplotype (present in approximately 17% of individuals) was significantly associated to diabetes in both samples. In children, the TXNIP rs7211 T/rs7212 G haplotype was associated with fasting insulin concentrations. Finally, cells harboring TXNIP rs7212 G allele presented higher TXNIP expression levels compared with carriers of TXNIP rs7212 CC genotype (p = 0.02). Conclusion: Carriers of TXNIP genetic variants presented higher TXNIP expression, early signs of glucose homeostasis derangement and increased susceptibility to chronic metabolic conditions such as diabetes and hypertension. Our data suggest that genetic variation in the TXNIP gene may act as a ""common ground"" modulator of both traits: diabetes and hypertension.
  • article 19 Citação(ões) na Scopus
    Short-term mechanical stretch fails to differentiate human adipose-derived stem cells into cardiovascular cell phenotypes
    (2014) GIRAO-SILVA, Thais; BASSANEZE, Vinicius; CAMPOS, Luciene Cristina Gastalho; BARAUNA, Valerio Garrone; DALLAN, Luis Alberto Oliveira; KRIEGER, Jose Eduardo; MIYAKAWA, Ayumi Aurea
    Background: We and others have previously demonstrated that adipose-derived stem cells (ASCs) transplantation improve cardiac dysfunction post-myocardium infarction (MI) under hemodynamic stress in rats. The beneficial effects appear to be associated with pleiotropic factors due to a complex interplay between the transplanted ASCs and the microenvironment in the absence of cell transdifferentiation. In the present work, we tested the hypothesis that mechanical stretch per se could change human ASCs (hASCs) into cardiovascular cell phenotypes that might influence post-MI outcomes. Methods: Human ASCs were obtained from patients undergoing liposuction procedures. These cells were stretched 12%, 1Hz up to 96 hours by using Flexercell 4000 system. Protein and gene expression were evaluated to identify cardiovascular cell markers. Culture medium was analyzed to determine cell releasing factors, and contraction potential was also evaluated. Results: Mechanical stretch, which is associated with extracellular signal-regulated kinase (ERK) phosphorylation, failed to induce the expression of cardiovascular cell markers in human ASCs, and mesenchymal cell surface markers (CD29; CD90) remained unchanged. hASCs and smooth muscle cells (SMCs) displayed comparable contraction ability. In addition, these cells demonstrated a profound ability to secrete an array of cytokines. These two properties of human ASCs were not influenced by mechanical stretch. Conclusions: Altogether, our findings demonstrate that hASCs secrete an array of cytokines and display contraction ability even in the absence of induction of cardiovascular cell markers or the loss of mesenchymal surface markers when exposed to mechanical stretch. These properties may contribute to beneficial post-MI cardiovascular outcomes and deserve to be further explored under the controlled influence of other microenvironment components associated with myocardial infarction, such as tissue hypoxia.
  • article 8 Citação(ões) na Scopus
    Endothelial, platelet, and macrophage microparticle levels do not change acutely following transcatheter aortic valve replacement
    (2016) MARCHINI, Julio F.; MIYAKAWA, Ayumi Aurea; TARASOUTCHI, Flavio; KRIEGER, Jose Eduardo; LEMOS, Pedro; CROCE, Kevin
    Background: Patients with severe aortic stenosis have increased levels of prothrombotic and proinflammatory microparticles (MP), and MPs actively regulate pathological processes that lead to atherothrombotic cardiovascular events. Shear stress is a validated stimulus of MP production, and abnormal shear stress in aortic stenosis increases MP release in ex-vivo studies. We hypothesized that in patients with severe aortic stenosis, percutaneous replacement of the aortic valve (TAVR) would reduce abnormal shear stress and would decrease levels of circulating MPs. Findings: The experimental protocol utilized flow cytometry (FC) and nanoparticle tracking analysis (NTA) to quantify circulating plasma MP levels in aortic stenosis patients at baseline and 5 days after TAVR. The baseline and 5 day MP counts measured by FC were 6.10.10(5) +/- 1.21.10(5) MP/mu L and 5.74.10(5) +/- 9.54.10(4) MP/mu L, respectively (p = 0.91). The baseline and 5 day MP counts measured by NTA were 9.29.10(13) +/- 1.66.10(13) MP/mu L and 3.95.10(14) +/- 3.11.10(14) MP/mu L, respectively (p = 0.91). When MPs were stratified by cell source, there was no difference in pre/post TAVR endothelial, platelet, or leukocyte MP levels. Conclusion: Levels of circulating MPs do not change acutely following TAVR therapy for aortic stenosis. Trial registered at clinicaltrials. gov NCT02193035 on July 11, 2014.
  • conferenceObject
    Stretch induces CRP3 expression in vein grafts
    (2012) CAMPOS, Luciene Cristina Gastalho; MIYAKAWA, Ayumi Aurea; BARAUNA, Valerio Garrone; BORIN, Thaiz Ferraz; DALLAN, Luis Alberto de Oliveira; KRIEGER, Jose Eduardo
    Cysteine- and glycine- rich protein 3 (CRP3) can act as structural protein and potent transcriptional cofactor during muscle differentiation and vascular remodeling. In this context, we have demonstrated, by real time RT–PCR, that CRP3 expression is 10 times higher in smooth muscle cells (SMCs) from human mammary artery vs. saphenous vein (h-SV) and that CRP3 expression can be induced in arterialized h-SV using an ex vivo flow through system that mimics arterial condition. The upregulation of CRP3 was primarily dependent on stretch stimulus in SMCs, rather than shear stress in ECs. Here, we assessed the induction and localization of CRP3 in SMCs during arterialization. Using a rat vein arterializations model in vivo, 1–14 days after surgery, CRP3 immunostaining was observed predominantly in the inner layer and 28–90 days it appears more scattered in the vessel. Confocal microscopy and western blot analysis showed that CRP3 is expressed in cytoplasm and nucleous of SMCs under stretch and in early stages of rat arterialization model. Later, the localization was restricted to the cytoplasm. Our data provide evidence that CRP3 is primarily expressed in arterial SMCs but upon stretching there is early expression of CRP3 induction in vein SMC cytoplasm and nucleous. These finding support to the idea that CRP3 may influence vascular adaptation to stress via cytoskeleton rearrangement and gene expression reprogramming.
  • article 16 Citação(ões) na Scopus
    High stretch induces endothelial dysfunction accompanied by oxidative stress and actin remodeling in human saphenous vein endothelial cells
    (2021) GIRAO-SILVA, T.; FONSECA-ALANIZ, M. H.; RIBEIRO-SILVA, J. C.; LEE, J.; PATIL, N. P.; DALLAN, L. A.; BAKER, A. B.; HARMSEN, M. C.; KRIEGER, J. E.; MIYAKAWA, A. A.
    The rate of the remodeling of the arterialized saphenous vein conduit limits the outcomes of coronary artery bypass graft surgery (CABG), which may be influenced by endothelial dysfunction. We tested the hypothesis that high stretch (HS) induces human saphenous vein endothelial cell (hSVEC) dysfunction and examined candidate underlying mechanisms. Our results showed that in vitro HS reduces NO bioavailability, increases inflammatory adhesion molecule expression (E-selectin and VCAM1) and THP-1 cell adhesion. HS decreases F-actin in hSVECs, but not in human arterial endothelial cells, and is accompanied by G-actin and cofilin's nuclear shuttling and increased reactive oxidative species (ROS). Pre-treatment with the broad-acting antioxidant N-acetylcysteine (NAC) supported this observation and diminished stretch-induced actin remodeling and inflammatory adhesive molecule expression. Altogether, we provide evidence that increased oxidative stress and actin cytoskeleton remodeling play a role in HS-induced saphenous vein endothelial cell dysfunction, which may contribute to predisposing saphenous vein graft to failure.
  • article 2 Citação(ões) na Scopus
    Activation of Interleukin-1 Beta in Arterialized Vein Grafts and the Influence of the -511C/T IL-1 beta Gene Polymorphism
    (2019) MIYAKAWA, Ayumi Aurea; BONIN, Thaiz Ferraz; CAMPOS, Luciene Cristina Gastalho; GIRAO-SILVA, Thais; RIBEIRO-SILVA, Joao Carlos; DALLAN, Luis Alberto Oliveira; KRIEGER, Jose Eduardo
    The interleukin-1 family is associated with innate immunity and inflammation. The latter has been linked to the genesis of cardiovascular diseases. We, therefore, investigated whether interleukin-1 beta (IL-1 beta) is activated during arterialization of vein grafts. First, we examined the activation of IL-1 beta using the rat arterialized jugular vein serially sampled for up to 90 days. IL-1 beta expression increased 18 times on day 1 in the arterialized rat jugular vein and remained five times above nonarterialized vein levels for up to 90 days. Similarly, IL-1 beta expression increased early (1-5 days) in human vein graft autopsy samples compared with late phases (1-4 years). Activation was also detected in ex vivo arterialized human saphenous veins. Upon stratification of the results, we uncovered a T allele promoter attenuating effect in IL-1 beta activation in response to hemodynamic stress. Altogether, the results show that IL-1 beta is activated during arterialization of vein grafts in rats and humans, and this response is modulated by -511C/T IL-1 beta gene polymorphism. It is tempting to speculate that the activation of IL-1 beta, and consequently local inflammation, modulates early vascular remodeling and that the gene polymorphism may be useful in predicting outcomes or assisting in interventions.
  • article 10 Citação(ões) na Scopus
    beta-arrestin is critical for early shear stress-induced Akt/eNOS activation in human vascular endothelial cells
    (2017) CARNEIRO, Ana Paula; FONSECA-ALANIZ, Miriam Helena; DALLAN, Luis Alberto Oliveira; MIYAKAWA, Ayumi Aurea; KRIEGER, Jose Eduardo
    Recent evidence suggests that beta-arrestins, which are involved in G protein-coupled receptors desensitization, may influence mechanotransduction. Here, we observed that nitric oxide (NO) production was abrogated in human saphenous vein endothelial cells (SVECs) transfected with siRNA against beta-arrestin 1 and 2 subjected to shear stress (SS, 15 dynes/cm2, 10 min). The downregulation of beta-arrestins 1/2 in SVECs cells also prevented the SS-induced rise in levels of phosphorylation of Akt and endothelial nitric oxide synthase (eNOS, Serine 1177). Interestingly, immunoprecipitation revealed that beta-arrestin interacts with Akt, eNOS and caveolin-1 and these interactions are not influenced by SS. Our data indicate that barrestins and Akt/eNOS downstream signaling are required for early SS-induced NO production in SVECs, which is consistent with the idea that beta-arrestins and caveolin-1 are part of a pre-assembled complex associated with the cellular mechanotransduction machinery.