Andressa G. Amaral

Universidade de São Paulo

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Luiz F. Onuchic

Universidade de São Paulo

Silvana Bordin

Universidade de São Paulo

Antônio C. Boschero

Universidade Estadual de Campinas (UNICAMP)

Alicia J. Kowaltowski

Universidade de São Paulo

Elieser Hitoshi Watanabe

Universidade de São Paulo

Everardo M. Carneiro

Universidade Estadual de Campinas (UNICAMP)

João Paulo Camporez

Universidade de São Paulo

Gilson Masahiro Murata

Universidade de São Paulo

Thiago M. Batista

Broad Institute

Rosane Aparecida Ribeiro

Universidade Estadual de Ponta Grossa

Cooperative Institutions

Universidade de São Paulo

Universidade Estadual de Campinas (UNICAMP)

Saarland University

Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo

Universidade Estadual Paulista (Unesp)

Universidade Federal de São Paulo

Institute of Biomedical Science

Universidade Brasil

Instituto Butantan

Universidade Federal do Rio de Janeiro

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Ppia is the most stable housekeeping gene for qRT-PCR normalization in kidney tissues of Pkd1 deficient mouse models

Research Square (Research Square) (2021)

Juan José Augusto Moyano Muñoz Ana Carolina Anauate Andressa G. Amaral Frederico Moraes Ferreira Elieser Hitoshi Watanabe

Abstract Autosomal Dominant Polycystic Kidney Disease (ADPKD) is the most common inherited renal disorder, characterized by renal cyst development leading to end-stage renal disease. Although the appropriate choice of suitable reference is critical for quantitative RNA analysis, no comparison of frequently used “housekeeping” genes is available. Here, we determined the validity of 7 candidate housekeeping genes ( Actb , Actg1 , B2m , Gapdh , Hprt , Pgam1 and Ppia ) in kidney tissues from mouse models orthologous to ADPKD, including a cystic mice (CY) 10–12 weeks old ( Pkd1 flox/flox : Nestin cre / Pkd1 flox/- : Nestin cre , n = 10) and non-cystic (NC) controls ( Pkd1 flox / flox / Pkd1 flox / - , n = 10), Pkd1 -haploinsufficient (HT) mice ( Pkd1 +/- , n = 6) and wild-type (WT) controls ( Pkd1 +/+ , n = 6) and a severely cystic (SC) mice 15 days old ( Pkd1 V/V , n = 7) and their controls (CO, n = 5). Gene expression data were analyzed using six distinct statistical softwares. The estimation of the ideal number of genes suggested the use of Ppia alone as sufficient, although not ideal, to analyze groups altogether. Actb , Hprt and Ppia expression profiles were correlated in all samples. Ppia was identified as the most stable housekeeping gene, while Gapdh was the least stable for all kidney samples. Stat3 expression level was consistent with upregulation in SC compared to CO when normalized by Ppia expression. In conclusion, present findings identified Ppia as the best housekeeping gene for CY + NC and SC + CO groups, while Hprt was the best for the HT + WT group.

PKD1

Housekeeping gene

10.21203/rs.3.rs-551245/v1

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Bases moleculares e celulares das nefropatias hereditárias císticas

Revista de Medicina (2015)

Andressa G. Amaral Luiz F. Onuchic

<p>As nefropatias hereditárias císticas (NHCs) são causadas por mutações gênicas determinantes ao desenvolvimento de anormalidades nas células renais epiteliais, alterações que criam as condições biológicas necessárias à formação cística. A identificação de genes mutados nessas enfermidades e a caracterização de seus produtos proteicos vêm permitindo a elucidação de mecanismos envolvidos em sua patogênese. Esta revisão tem como foco as bases genéticas e a patogênese molecular dessas enfermidades, embora também aborde brevemente aspectos clínicos e epidemiológicos das NHCs de maior impacto médico e socioeconômico. Dentro deste conjunto de moléstias, abordaremos a doença renal policística autossômica dominante, doença renal policística autossômica recessiva, nefronoftises, doença renal túbulo-intersticial autossômica dominante, doença de von Hippel-Lindau e complexo esclerose tuberosa. Essas NHCs possuem sobreposição de manifestações clínicas e compartilham vias e defeitos moleculares. Entre suas características comuns, destacaremos o papel central de anormalidades no cílio apical primário e de vias de sinalização intracelular responsáveis por alterações fundamentais do fenótipo celular. Ao apresentar os avanços obtidos na patogênese molecular e celular das NHCs, discutiremos criticamente o estabelecimento, os papeis e as implicações da homeostase defeituosa de cálcio citosólico; resposta celular hiperproliferativa ao AMP cíclico; taxas elevadas de proliferação celular e apoptose; alterações da matriz extracelular; alterações da polaridade celular; e secreção transepitelial de fluido. O conhecimento acumulado nas últimas duas décadas trouxe um novo contexto molecular e celular às NHCs, capaz de criar a plataforma de conhecimento necessária para o desenvolvimento de ensaios pré-clínicos. Tais ensaios, por sua vez, vêm amparando a condução de estudos clínicos robustos, os quais têm aberto perspectivas terapêuticas promissoras.</p>

10.11606/issn.1679-9836.v94i4p263-281

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Taurine supplementation enhances nutrient‐induced insulin secretion in pancreatic mice islets

Diabetes/Metabolism Research and Reviews (2009)

Rosane Aparecida Ribeiro Maria Lúcia Bonfleur Andressa G. Amaral Emerielle C. Vanzela Silvana A. Rocco

Abstract Background Taurine (TAU), a naturally occurring sulfur‐containing amino acid, is found at high concentrations in plasma and mammalian tissues and regulates osmolarity, ion channel activity, and glucose homeostasis. Several reports have shown that physiological plasma TAU levels seem to be important for adequate beta (β)‐cell function and insulin action, since low concentrations of TAU in the plasma have been reported in the pre‐diabetic and diabetic states. Methods Glucose tolerance and insulin sensitivity were investigated in mice supplemented with 2% (w/v) TAU in their drinking water for 30 days, as well as the insulin secretion from isolated islets stimulated by glucose or L‐leucine. Results TAU‐supplemented mice demonstrated improved glucose tolerance and higher insulin sensitivity, compared to controls (CTL). In addition, their islets secreted more insulin in response to high concentrations of glucose and L‐leucine. L‐[U‐ 14 C]leucine oxidation was higher in TAU than in CTL islets, whereas D‐[U‐ 14 C]glucose oxidation, ATP levels, glucose transporter (GLUT) 2 and glucokinase (GCK) protein expressions were similar in both types of islets. The L‐type β 2 subunit voltage‐sensitive Ca 2+ channel protein, as well as 45 Ca uptake, were significantly higher in TAU‐supplemented than CTL islets. In addition, islets from TAU‐supplemented mice secreted more glucagon than CTL islets at low glucose. Conclusions TAU supplementation improves glucose tolerance and insulin sensitivity in mice, as well as insulin secretion from isolated islets. The latter effect seems to be, at least in part, dependent on a better Ca 2+ handling by the islets. Copyright © 2009 John Wiley & Sons, Ltd.

Glucokinase

Pancreatic Islets

GLUT2

10.1002/dmrr.959

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Citations (73)

Response of Apoptosis Related Proteins to Running in Fluoride-Exposed Mice

Mary Canning Fatemeh Vida Zohoori Ruth A. Valentine Zohaib N. Khan Aesar A. Ahmed

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Abdominal pain, arthritis, and nephrotic syndrome in a Syrian patient

Clinics (2012)

Bruno Eduardo Pedroso Balbo André Albuquerque Silva Andressa G. Amaral Denise Maria Avancini Costa Malheiros Luiz F. Onuchic

Familial Mediterranean fever (FMF) is an autosomal recessive disorder that is characterized by sporadic paroxysmal attacks of fever and serosal inflammation. Although it occurs primarily in ethnic groups originating in the Mediterranean region, FMF is not restricted to these groups and is still underdiagnosed in nephrology settings in non-Mediterranean countries (1). The disease morbidity is largely associated with recurrent attacks of pain and fever, and mortality is mainly associated with amyloidosis and kidney disease (1). The discovery of colchicine in 1972 led to an effective treatment for FMF in the prevention of acute attacks and secondary amyloidosis, significantly increasing the importance of an accurate and early diagnosis (2). The clinical criteria proposed by Livneh et al. (3) in 1997 continue to be the gold standard for diagnosis. However, limitations arise in atypical cases and in patients of non-Mediterranean origin. The gene mutated in FMF, MEFV (Mediterranean fever), was cloned in 1997, shedding light on the disease pathogenesis and improving the tools for diagnosis (4). In this scenario, genotype-phenotype correlation studies revealed specific alleles that were associated with amyloidosis and kidney disease, and mutation-based analysis, particularly directed toward hot spots, emerged as an essential approach for diagnosis in atypical cases (5).

10.6061/clinics/2012(06)24

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Camundongos deficientes em Pkd1 apresentam disfunção cardíaca associada a reprogramação metabólica e aumento de inflamação e apoptose

Andressa G. Amaral

10.11606/t.5.2020.tde-29062020-111929

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Regulation of Mitochondrial Calcium Transport by Caloric Restriction in Rat Kidney

The FASEB Journal (2022)

Julian C. Serna Andressa G. Amaral Camille Caldeira da Silva Ana Cláudia Munhoz Alicia J. Kowaltowski

Caloric restriction (CR) in laboratory rodents prevents obesity, promotes healthy aging, and increases resilience against several pathological stimuli. At the mitochondrial level, protection promoted by CR in the brain and liver is related to higher calcium uptake rates and retention capacity, preventing Ca2+ -induced mitochondrial permeability transition. Dietary restriction has been demonstrated to increase kidney resistance against damaging stimuli such as ischemia/reperfusion, but if these effects are related to similar mitochondrial adaptations had not yet been uncovered. Here, we characterized changes in mitochondrial function in response to six months of CR in rats, measuring oxidative phosphorylation, redox balance and calcium homeostasis. CR promoted an increase in mitochondrial oxygen consumption rates under non-phosphorylating (state 4) and uncoupled (state 3U) conditions. While CR prevents mitochondrial reactive oxygen species production in many tissues, in kidney we found that mitochondrial H2 O2 release was enhanced in CR rats, although levels of carbonylated proteins and methionine sulfoxide were unchanged. Surprisingly, and opposite to the effects observed in brain and liver, mitochondria from CR animals are more prone to Ca2+ -induced mitochondrial permeability transition. CR mitochondria also displayed higher calcium uptake rates, which were not accompanied by changes in calcium efflux rates, nor related to altered inner mitochondrial membrane potentials, or the amounts of the Mitochondrial Calcium Uniporter (MCU). Instead, increased mitochondrial calcium uptake rates correlate with a loss of Mitochondrial Calcium Uptake 2 (MICU2), an MCU modulator, in CR kidneys. Interestingly, MICU2 is also modulated by CR in liver, suggesting it has a broader diet-sensitive regulatory role determining mitochondrial calcium homeostasis. Together, our results remark the highly organ-specific bioenergetic, redox, and ionic transport effects of CR. Specifically, we describe the regulation of the expression of MICU2, and its effects on mitochondrial calcium transport, as a novel and interesting aspect of the metabolic responses to dietary interventions.

Uniporter

Mitochondrial ROS

10.1096/fasebj.2022.36.s1.r4470

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Ppia is the most stable housekeeping gene for qRT-PCR normalization in kidneys of three Pkd1-deficient mouse models

Scientific Reports (2021)

Juan José Augusto Moyano Muñoz Ana Carolina Anauate Andressa G. Amaral Frederico Moraes Ferreira Elieser Hitoshi Watanabe

Abstract Autosomal Dominant Polycystic Kidney Disease (ADPKD) is the most common inherited renal disorder, characterized by renal cyst development leading to end-stage renal disease. Although the appropriate choice of suitable reference is critical for quantitative RNA analysis, no comparison of frequently used “housekeeping” genes is available. Here, we determined the validity of 7 candidate housekeeping genes ( Actb , Actg1 , B2m , Gapdh , Hprt , Pgam1 and Ppia ) in kidney tissues from mouse models orthologous to ADPKD, including a cystic mice (CY) 10–12 weeks old ( Pkd1 flox/flox : Nestin cre / Pkd1 flox/− : Nestin cre , n = 10) and non-cystic (NC) controls ( Pkd1 flox / flox / Pkd1 flox / - , n = 10), Pkd1 -haploinsufficient (HT) mice ( Pkd1 +/− , n = 6) and wild-type (WT) controls ( Pkd1 +/+ , n = 6) and a severely cystic (SC) mice 15 days old ( Pkd1 V/V , n = 7) and their controls (CO, n = 5). Gene expression data were analyzed using six distinct statistical softwares. The estimation of the ideal number of genes suggested the use of Ppia alone as sufficient, although not ideal, to analyze groups altogether. Actb , Hprt and Ppia expression profiles were correlated in all samples. Ppia was identified as the most stable housekeeping gene, while Gapdh was the least stable for all kidney samples. Stat3 expression level was consistent with upregulation in SC compared to CO when normalized by Ppia expression. In conclusion, present findings identified Ppia as the best housekeeping gene for CY + NC and SC + CO groups, while Hprt was the best for the HT + WT group.

PKD1

Housekeeping gene

10.1038/s41598-021-99366-x

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Citations (17)

1602-P: Galectin-3 Inhibition Protects ApoE Knockout Mice against Western Diet–Induced Nonalcoholic Steatohepatitis and Glucose Intolerance

Diabetes (2023)

Layanne Cabral da Cunha Araujo FELIPE SUCUPIRA Carolina Castilho Dias Andressa G. Amaral João Paulo Camporez

Nonalcoholic Fatty Liver Disease represents a broad spectrum of histological abnormalities ranging from simple steatosis to nonalcoholic steatohepatitis (NASH), which may progress to cirrhosis or hepatocellular carcinoma. NASH is characterized by steatosis, hepatic inflammation, hepatocellular ballooning, and fibrosis. Therefore, the aim of this work was to evaluate the effect of modified citrus pectin (MCP), inhibitor of galectin-3, in ApoE KO mice fed a western diet (WD). ApoE KO mice were divided into 3 groups: standard diet-fed (SD) group, WD-fed group, and WD-fed + MCP-treated group (WD+MCP). WD-fed mice displayed increased hepatic triacylglycerides (TAG-290%), and plasma ALT (115%) and AST (130%) compared with SD group. MCP treatment decreased hepatic TAG (30%) in WD-fed mice, plasma ALT and AST were reverted. WD-fed mice also displayed increased hepatic collagen deposition (18%), and MCP treatment inhibited this increase. These results were similar with hydroxyproline concentration in liver. WD-fed mice showed an impaired glucose tolerance compared with SD-fed mice, while MCP treatment improved glucose tolerance in WD-fed mice. Also, WD-fed mice presented increased fasting insulin (140%) compared with SD-fed mice, and MCP treatment reverted this increase by 100%. Gene expression of F4/80 was increased by 76% in the WD group compared with SD group, however had not significant difference between WD+MCP and SD group. Gene expression of matrix metalloproteinase 2 was increased by 5-fold in WD group compared with SD group, while this increase was inhibited with MCP treatment. Also, it was observed an increase in JNK phosphorylation by 3-fold in WD group, and MCP treatment inhibited this increase. Taken together, we confirm WD-fed ApoE KO mice as a suitable experimental model of NASH, and the inhibition of galectin-3 by the treatment with MCP protects ApoE KO mice against the development of NASH and glucose intolerance. Disclosure L. Araujo: None. F. Sucupira: None. C.C.B. Dias: None. A. Amaral: None. J. Camporez: None. Funding São Paulo Research Foundation (FAPESP)

Steatosis

Steatohepatitis

Apolipoprotein E

10.2337/db23-1602-p

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Citations (1)

Regulation of kidney mitochondrial function by caloric restriction

AJP Renal Physiology (2022)

Julian D. C. Serna Andressa G. Amaral Camille C. Caldeira da Silva Ana Cláudia Munhoz Eloisa Aparecida Vilas‐Boas

Prevention of obesity through caloric restriction (CR) is well known to protect many tissues but has been poorly studied in kidneys. Here, we determined the effects of long-term CR in rat kidney mitochondria, which are central players in energy metabolism and aging. Surprisingly, we found that the diet increased mitochondrial reactive oxygen production and permeability transition. This suggests that the kidneys respond differently to restricted diets and may be more susceptible under CR.

Bioenergetics

Uniporter

Mitochondrial ROS

Homeostasis

Mitochondrial apoptosis-induced channel

10.1152/ajprenal.00461.2021

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Citations (9)