scholarly journals The Fly Homologue of MFSD11 Is Possibly Linked to Nutrient Homeostasis and Has a Potential Role in Locomotion: A First Characterization of the Atypical Solute Carrier CG18549 in Drosophila Melanogaster

Insects ◽  
2021 ◽  
Vol 12 (11) ◽  
pp. 1024
Author(s):  
Mikaela M. Ceder ◽  
Frida A. Lindberg ◽  
Emelie Perland ◽  
Michael J. Williams ◽  
Robert Fredriksson
Keyword(s):  
Gene Expression ◽  
The Body ◽  
Adult Brain ◽  
Receptor Expression ◽  
Cellular Transport ◽  
Adipokinetic Hormone ◽  
Hormone Receptor Expression ◽  
And Function ◽  
And Behavior

Cellular transport and function are dependent on substrate influx and efflux of various compounds. In humans, the largest superfamily of transporters is the SoLute Carriers (SLCs). Many transporters are orphans and little to nothing is known about their expression and/or function, yet they have been assigned to a cluster called atypical SLCs. One of these atypical SLCs is MFSD11. Here we present a first in-depth characterization of the MFSD11, CG18549. By gene expression and behavior analysis on ubiquitous and brain-specific knockdown flies. CG18549 knockdown flies were found to have altered adipokinetic hormone and adipokinteic hormone receptor expression as well as reduced vesicular monoamine transporter expression; to exhibit an altered locomotor behavior, and to have an altered reaction to stress stimuli. Furthermore, the gene expression of CG18549 in the brain was visualized and abundant expression in both the larvae and adult brain was observed, a result that is coherent with the FlyAtlas Anatomy microarray. The exact mechanism behind the observed behaviors is not fully understood, but this study provides new insights into the expression and function of CG18549. Clearly, these results provide a strong example as to why it is vital to fully characterize orphan transporters and through that gain knowledge about the body during normal condition and disease.

Characterization of DREADD receptor expression and function in rhesus macaques trained to discriminate ethanol

2021 ◽  
Author(s):  
Daicia C. Allen ◽  
Vanessa A. Jimenez ◽  
Timothy L. Carlson ◽  
Nicole A. Walter ◽  
Kathleen A. Grant ◽  
...  
Keyword(s):  
Rhesus Macaques ◽  
Receptor Expression ◽  
And Function

scholarly journals Liraglutide, a GLP-1 Receptor Agonist, Which Decreases Hypothalamic 5-HT2A Receptor Expression, Reduces Appetite and Body Weight Independently of Serotonin Synthesis in Mice

2018 ◽  
Vol 2018 ◽  
pp. 1-6 ◽  
Author(s):  
Katsunori Nonogaki ◽  
Takao Kaji
Keyword(s):  
Gene Expression ◽  
Weight Loss ◽  
Body Weight ◽  
Receptor Agonist ◽  
Tryptophan Hydroxylase ◽  
Intraperitoneal Administration ◽  
Body Weight Loss ◽  
Receptor Activation ◽  
The Body ◽  
Receptor Expression

A recent report suggested that brain-derived serotonin (5-HT) is critical for maintaining weight loss induced by glucagon-like peptide-1 (GLP-1) receptor activation in rats and that 5-HT2A receptors mediate the feeding suppression and weight loss induced by GLP-1 receptor activation. Here, we show that changes in daily food intake and body weight induced by intraperitoneal administration of liraglutide, a GLP-1 receptor agonist, over 4 days did not differ between mice treated with the tryptophan hydroxylase (Tph) inhibitor p-chlorophenylalanine (PCPA) for 3 days and mice without PCPA treatment. Treatment with PCPA did not affect hypothalamic 5-HT2A receptor expression. Despite the anorexic effect of liraglutide disappearing after the first day of treatment, the body weight loss induced by liraglutide persisted for 4 days in mice treated with or without PCPA. Intraperitoneal administration of liraglutide significantly decreased the gene expression of hypothalamic 5-HT2A receptors 1 h after injection. Moreover, the acute anorexic effects of liraglutide were blunted in mice treated with the high-affinity 5-HT2A agonist (4-bromo-3,6-dimethoxybenzocyclobuten-1-yl) methylamine hydrobromide 14 h or 24 h before liraglutide injection. These findings suggest that liraglutide reduces appetite and body weight independently of 5-HT synthesis in mice, whereas GLP-1 receptor activation downregulates the gene expression of hypothalamic 5-HT2A receptors.

scholarly journals The semantics of microglia activation: neuroinflammation, homeostasis, and stress

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Samuel C. Woodburn ◽  
Justin L. Bollinger ◽  
Eric S. Wohleb
Keyword(s):  
Microglia Activation ◽  
Immune Functions ◽  
Neuronal Function ◽  
Stress Effects ◽  
Pathological Conditions ◽  
Microglial Phenotype ◽  
And Function ◽  
And Behavior

AbstractMicroglia are emerging as critical regulators of neuronal function and behavior in nearly every area of neuroscience. Initial reports focused on classical immune functions of microglia in pathological contexts, however, immunological concepts from these studies have been applied to describe neuro-immune interactions in the absence of disease, injury, or infection. Indeed, terms such as ‘microglia activation’ or ‘neuroinflammation’ are used ubiquitously to describe changes in neuro-immune function in disparate contexts; particularly in stress research, where these terms prompt undue comparisons to pathological conditions. This creates a barrier for investigators new to neuro-immunology and ultimately hinders our understanding of stress effects on microglia. As more studies seek to understand the role of microglia in neurobiology and behavior, it is increasingly important to develop standard methods to study and define microglial phenotype and function. In this review, we summarize primary research on the role of microglia in pathological and physiological contexts. Further, we propose a framework to better describe changes in microglia1 phenotype and function in chronic stress. This approach will enable more precise characterization of microglia in different contexts, which should facilitate development of microglia-directed therapeutics in psychiatric and neurological disease.

scholarly journals Makna Stimulasi Pertumbuhan Dan Perkembangan Anak Usia Dini Dalam Perspektif Fisik Dan Mental

2019 ◽  
Vol 1 (1) ◽  
pp. 9-20
Author(s):  
Jauharotur Rihlah
Keyword(s):  
Psychological Health ◽  
Growth And Development ◽  
Optimal Growth ◽  
The Body ◽  
State Behavior ◽  
Childhood Growth ◽  
Children Nutrition ◽  
Content Analysis Method ◽  
And Function ◽  
And Behavior

Growth (growth) is an increase in the size of various organs that can be measured by the size of weight (grams, kilograms) or length (centimeters, meters). Development (development) is the increase in the ability or expertise in the structure and function of the body more complex, in an orderly pattern, as a result of the process of maturation. Keep in mind that the growth and development of each individual is unique. This is caused by several factors including genetic factors (heredity), environment (whether biological or psychological) and behavior (state / behavior in the family). For optimal growth and development of children, the environment must be considered, it must support the biological and psychological health of children, nutrition, must be sufficient and balanced, regularity to health services includes, providing immunization, rest and sleep must be sufficient and avoid fatigue. By using the content analysis method and documentary study, this research seeks to describe the meaning of early childhood growth and development stimulation in physical and mental perspectives. Appropriate stimulation will further optimize multi aspects in children, especially in terms of physical and mental.

Characterization of liver X receptor expression and function in human skin and the pilosebaceous unit

2007 ◽  
Vol 16 (10) ◽  
pp. 844-852 ◽  
Author(s):  
Louise E. Russell ◽  
Wesley J. Harrison ◽  
Adiam W. Bahta ◽  
Christos C. Zouboulis ◽  
Jacky M. Burrin ◽  
...  
Keyword(s):  
Human Skin ◽  
Liver X Receptor ◽  
Receptor Expression ◽  
Pilosebaceous Unit ◽  
And Function

scholarly journals The corticosterone-glucocorticoid receptor-AP1/CREB axis inhibits luteinizing hormone receptor expression in mouse granulosa cells

2020 ◽  
Author(s):  
Yinghui Wei ◽  
Ming Shen
Keyword(s):  
Luteinizing Hormone ◽  
Glucocorticoid Receptor ◽  
Granulosa Cells ◽  
Hormone Receptor ◽  
Follicular Development ◽  
The Body ◽  
Receptor Expression ◽  
Luteinizing Hormone Receptor ◽  
Control Group ◽  
Hormone Receptor Expression

Abstract Background Under stress conditions, luteinizing hormone (LH)-mediated ovulation is inhibited, resulting in insufficient oocyte production and excretion during follicular development. When the body is stressed, a large amount of corticosterone (CORT) is generated, which will lead to disorder of the body's endocrine system and damage to the body. Our previous work showed that corticosterone can block follicular development in mice. Since LH acts through binding with the LH receptor (LHR), the present study aimed to investigate whether and how CORT influence luteinizing hormone receptor expression in mouse ovarian granulosa cells (GCs). Methods For this purpose, 3-week-old ICR female mice were injected intraperitoneally with pregnant horse serum gonadotropin (PMSG). Meanwhile, the treatment group were injected with corticosterone corticosterone (1 mg/mouse) at intervals of 8 h; while the control group was injected with same volume of methyl sulfoxide (DMSO). Granulosa cells were collected at 24 h, 48 h, and 55 h after PMSG injection. For in vitro experiments, mice granulosa cells obtained from healthy follicles were treated with corticosterone alone, or together with inhibitors against glucocorticoid receptor (GR). Results The results showed that corticosterone caused down-regulation of luteinizing hormone receptor expression in granulosa cells, which was accompanied by impaired cell viability. Moreover, the effects of corticosterone was mediated by binding to its receptor in granulosa cells. Further investigations revealed that glucocorticoid receptor might regulated the transcription of luteinizing hormone receptor through inhibiting the expression of luteinizing hormone receptor transcription factors, including AP1 and CREB. Conclusions Our findings suggested a possible mechanism of corticosterone-induced anovulation involving the inhibition of luteinizing hormone receptor expression in granulosa cells by corticosterone-glucocorticoid receptor-AP1 / CREB axis.

scholarly journals Regulation of Human Growth Hormone Receptor Expression by MicroRNAs

2014 ◽  
Vol 28 (9) ◽  
pp. 1448-1459 ◽  
Author(s):  
Samar Elzein ◽  
Cynthia Gates Goodyer
Keyword(s):  
Gene Expression ◽  
Growth Hormone Receptor ◽  
Human Growth ◽  
Receptor Expression ◽  
Hek293 Cells ◽  
Luciferase Reporter ◽  
Target Cells ◽  
Protein Levels ◽  
Coding Regions ◽  
Hormone Receptor Expression

Human GH binds to its receptor (GHR) on target cells and activates multiple intracellular pathways, leading to changes in gene expression, differentiation, and metabolism. GHR deficiency is associated with growth and metabolic disorders whereas increased GHR expression has been reported in certain cancers, suggesting that the GHR gene requires tight controls. Several regulatory mechanisms have been found within its 5′-untranslated region (UTR) promoter and coding regions. However, the 3′-UTR has not been previously examined. MicroRNAs (miRNAs) are small (19–22 nucleotides) noncoding RNAs that downregulate gene expression mainly through targeting the 3′-UTR of mRNAs and enhancing their degradation or inhibiting translation. In the present study, we investigated whether miRNAs regulate GHR expression. To define putative miRNA binding sites in the GHR 3′-UTR, we used multiple in silico prediction tools, analyzed conservation across species and the presence of parallel sites in GH/IGF axis-related genes, and searched for reports linking miRNAs to GHR-related physiological or pathophysiological activities. To test prioritized sites, we cotransfected a wild-type GHR 3′-UTR luciferase reporter vector as well as miRNA binding site mutants into HEK293 cells with miRNA mimics. Furthermore, we tested whether the miRNAs altered endogenous GHR mRNA and protein levels in HEK293 cells and in 2 cancer cell lines (MCF7 and LNCaP). Our experiments have identified miRNA (miR)-129–5p, miR-142–3p, miR-202, and miR-16 as potent inhibitors of human GHR expression in normal (HEK293) and cancer (MCF7 and LNCaP) cells. This study paves the way for the development of miRNA inhibitors as therapeutic agents in GH/GHR-related pathophysiologies, including cancer.

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