The conserved role of the AKT/GSK3 axis in cell survival and glycogen metabolism in Rhipicephalus (Boophilus) microplus embryo tick cell line BME26

Abreu, Leonardo; Calixto, Christiano; Waltero, Camila Fernanda; Noce, Bárbara Della; Githaka, Naftaly; Seixas, Adriana; Parizi, Luís Fernando; Konnai, Satoru; Vaz, Itabajara da Silva; Ohashi, Kazuhiko; Logullo, Carlos

doi:10.1016/j.bbagen.2012.12.016

Cited by 18 publications

(37 citation statements)

References 66 publications

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“…Cell treatments with small molecules such as lithium chloride, alsterpaullone [54][55][56], 6-bromoindirubin-3 0 -oxime, and insulin [27,40,50,57] are common pharmacological and physiological means of inhibiting GSK3 and are also used to study its role in different cell types. However, GSK3 inhibitors frequently compete with ATP, have limited specificity, and can cause inhibition of other kinases [58].…”

Section: Discussionmentioning

confidence: 99%

Loss of Glycogen Synthase Kinase 3 Isoforms During Murine Oocyte Growth Induces Offspring Cardiac Dysfunction1

Rocha

Ding

Slawny

et al. 2015

Biology of Reproduction

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Glycogen synthase kinase-3 (GSK3) is a constitutively active serine threonine kinase with 1) two isoforms (GSK3A and GSK3B) that have unique and overlapping functions, 2) multiple molecular intracellular mechanisms that involve phosphorylation of diverse substrates, and 3) implications in pathogenesis of many diseases. Insulin causes phosphorylation and inactivation of GSK3 and mammalian oocytes have a functional insulin-signaling pathway whereby prolonged elevated insulin during follicle/oocyte development causes GSK3 hyperphosphorylation, reduced GSK3 activity, and altered oocyte chromatin remodeling. Periconceptional diabetes and chronic hyperinsulinemia are associated with congenital malformations and onset of adult diseases of cardiovascular origin. Objectives were to produce transgenic mice with individual or concomitant loss of GSK3A and/or GSK3B and investigate the in vivo role of oocyte GSK3 on fertility, fetal development, and offspring health. Wild-type males bred to females with individual or concomitant loss of oocyte GSK3 isoforms did not have reduced fertility. However, concomitant loss of GSK3A and GSK3B in the oocyte significantly increased neonatal death rate due to congestive heart failure secondary to ventricular hyperplasia. Individual loss of oocyte GSK3A or GSK3B did not induce this lethal phenotype. In conclusion, absence of oocyte GSK3 in the periconceptional period does not alter fertility yet causes offspring cardiac hyperplasia, cardiovascular defects, and significant neonatal death. These results support a developmental mechanism by which periconceptional hyperinsulinemia associated with maternal metabolic syndrome, obesity, and/or diabetes can act on the oocyte and affect offspring cardiovascular development, function, and congenital heart malformation.

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Section: Discussionmentioning

confidence: 99%

Loss of Glycogen Synthase Kinase 3 Isoforms During Murine Oocyte Growth Induces Offspring Cardiac Dysfunction1

Rocha

Ding

Slawny

et al. 2015

Biology of Reproduction

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“…Tick cell lines have also played a valuable role in the study of tick cell metabolism which can help in developing novel control methods. De Abreu et al (2013) investigated the role of protein kinase B (AKT) and glycogen synthase kinase 3 (GSK3) in glycogen metabolism and cell viability using the R. microplus cell line BME26, and the results revealed an antagonistic role for AKT and GSK3. A reduction in AKT caused a decrease in glycogen content, cell viability and altered cell membrane permeability, whereas the inhibition of GSK3 promoted an increase in glycogen content.…”

Section: Tick Cell Lines Elucidate Novel Aspects Of Tick Cell Metabolmentioning

confidence: 99%

Tick Cell Lines in Research on Tick Control

Al-Rofaai

Bell‐Sakyi

2020

Front. Physiol.

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Ticks and the diseases they transmit are of huge veterinary, medical and economic importance worldwide. Control of ticks attacking livestock and companion animals is achieved primarily by application of chemical or plant-based acaricides. However, ticks can rapidly develop resistance to any new product brought onto the market, necessitating an ongoing search for novel active compounds and alternative approaches to tick control. Many aspects of tick and tick-borne pathogen research have been facilitated by the application of continuous cell lines derived from some of the most economically important tick species. These include cell lines derived from acaricide-susceptible and resistant ticks, cell sub-lines with in vitro-generated acaricide resistance, and genetically modified tick cells. Although not a replacement for the whole organism, tick cell lines enable studies at the cellular and molecular level and provide a more accessible, more ethical and less expensive in vitro alternative to in vivo tick feeding experiments. Here we review the role played by tick cell lines in studies on acaricide resistance, mode-of-action of acaricides, identification of potential novel control targets through better understanding of tick metabolism, and anti-tick vaccine development, that may lead to new approaches to control ticks and tick-borne diseases.

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“…Our results have provided insights into the dynamics of nutrient utilization during tick embryogenesis. Information generated from our studies may help finding candidate antigens for the development of vaccines against ticks (MORAES et al, 2007;LOGULLO et al, 2009;FABRES et al, 2010;ABREU et al, 2013).…”

Section: Energy Metabolism In the Arthropod Embryomentioning

confidence: 99%

“…Furthermore, the investigation of key components of these metabolic pathways has provided invaluable information for the development and improvement of vaccines and drugs to control important disease vectors. Although these events are primarily studied in embryonic cells or during embryogenesis (ABREU et al, 2013;AN et al, 2014), some of the aspects of glucose metabolism have also been investigated in adult arthropod tissues and organs before or after a blood meal (VITAL et al, 2010).…”

Section: Energy Metabolism In the Arthropod Embryomentioning

confidence: 99%

The dynamics of energy metabolism in the tick embryo

Martins

Ruiz

Fonseca

et al. 2018

Rev. Bras. Parasitol. Vet.

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The cattle tick Rhipicephalus (Boophilus) microplus is an ectoparasite capable of transmitting a large number of pathogens, causing considerable losses in the cattle industry, with substantial damage to livestock. Over the years, important stages of its life cycle, such as the embryo, have been largely ignored by researchers. Tick embryogenesis has been typically described as an energy-consuming process, sustaining cell proliferation, differentiation, and growth. During the embryonic stage of arthropods, there is mobilization of metabolites of maternal origin for the development of organs and tissues of the embryo. Glycogen resynthesis in late embryogenesis is considered as an effective indicator of embryonic integrity. In the cattle tick R.(B. (B.) microplus, glycogen resynthesis is sustained by protein degradation through the gluconeogenesis pathway at the end of the embryonic period. Despite recent advancements in research on tick energy metabolism at the molecular level, the dynamics of nutrient utilization during R. (B.) microplus embryogenesis is still poorly understood. The present review aims to describe the regulatory mechanisms of carbohydrate metabolism during maternal-zygotic transition and identify possible new targets for the development of novel drugs and other control measures against R. (B.) microplus infestations.

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The conserved role of the AKT/GSK3 axis in cell survival and glycogen metabolism in Rhipicephalus (Boophilus) microplus embryo tick cell line BME26

Abstract: The AKT/GSK3 axis is conserved in tick in a way that integrates glycogen metabolism and cell survival, and exhibits phylogenic differences that could be important for the development of novel control methods.

Cited by 18 publications

References 66 publications

Loss of Glycogen Synthase Kinase 3 Isoforms During Murine Oocyte Growth Induces Offspring Cardiac Dysfunction1

Loss of Glycogen Synthase Kinase 3 Isoforms During Murine Oocyte Growth Induces Offspring Cardiac Dysfunction1

Tick Cell Lines in Research on Tick Control

The dynamics of energy metabolism in the tick embryo

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