The role of TCPTP on leptin effects on astrocyte morphology

Debarba, Lucas Kniess; Vechiato, Fernanda Maria Veanholi; Veida-Silva, Hellen; Borges, Beatriz de Carvalho; Jamur, Maria Célia; Antunes‐Rodrigues, José; Elias, Lucila Leico Kagohara

doi:10.1016/j.mce.2018.12.010

Cited by 7 publications

(4 citation statements)

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“…Homogeneous T-cell protein tyrosine phosphatase (TCPTP) inhibitory activities were investigated simultaneously by the same method. 47–49 Compounds 6a and 6c exhibited 4.34-fold and 3.43-fold greater selectivity for PTP1B than for TCPTP respectively. Besides TCPTP, we tested the inhibitory activity of 6a and 6c against SHP2, both of them showed similar activities against PTP1B.…”

Section: Resultsmentioning

confidence: 94%

Synthesis of 2-ethoxycarbonylthieno[2,3-b]quinolines in biomass-derived solvent γ-valerolactone and their biological evaluation against protein tyrosine phosphatase 1B

Wang

Feng

et al. 2021

RSC Adv.

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Section: Resultsmentioning

confidence: 94%

Synthesis of 2-ethoxycarbonylthieno[2,3-b]quinolines in biomass-derived solvent γ-valerolactone and their biological evaluation against protein tyrosine phosphatase 1B

Wang

Feng

et al. 2021

RSC Adv.

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“…Knockdown of Cx43 was performed by using an HVJ envelope (HVJ-E) transfection kit (GenomONE™, Cosmo Bio Co., Ltd., Tokyo, Japan), which is widely used for in vivo siRNA transfer [32, 33]. Cx43 siRNA (siGENOME SMARTpool, mouse GJA1, Thermo Scientific) [34, 35] was incorporated into the HVJ-E according to the manufacturer’s instructions. Two days prior to SAH induction, siRNA (5 pg in 10 μl sterile saline) was slowly injected into the cisterna magna as pretreatment, similar to the induction of SAH described above.…”

Section: Methodsmentioning

confidence: 99%

The important role of connexin 43 in subarachnoid hemorrhage-induced cerebral vasospasm

et al. 2019

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Background: Gap junctions are involved in the development of cerebral vasospasm (CVS) after subarachnoid hemorrhage (SAH). However, the specific roles and regulatory functions of related connexin isoforms remain unknown. The aim of this study was to investigate the importance of connexin 43 (Cx43) in CVS and determine whether Cx43 alterations are modulated via the protein kinase C (PKC) signaling transduction pathway.Methods: Oxyhemoglobin (OxyHb)-induced smooth muscle cells of basilar arterial and second-injection model in rat were used as CVS models in vitro and in vivo. In addition, dye transfer assays were used for gap junction-mediated intercellular communication (GJIC) observation in vitro and delayed cerebral ischemia (DCI) was observed in vivo by perfusion-weighted imaging (PWI) and intravital fluorescence microscopy.Results: Increase in Cx43 mediated the development of SAH-induced CVS was found in both in vitro and in vivo CVS models. Enhanced GJIC was observed in vitro CVS model, this effect and increased Cx43 were reversed by preincubation with specific PKC inhibitors (chelerythrine or GF 109203X). DCI was observed in vivo on day 7 after SAH. However, DCI was attenuated by pretreatment with Cx43 siRNA or PKC inhibitors, and the increased Cx43 expression in vivo was also reversed by Cx43 siRNA or PKC inhibitors. Conclusions:These data provide strong evidence that Cx43 plays an important role in CVS and indicate that changes in Cx43 expression may be mediated by the PKC pathway. The current findings suggest that Cx43 and the PKC pathway are novel targets for developing treatments for SAH-induced CVS. Ethics approval and consent to participateAll animal procedures were carried out in accordance with the Guide for the Care and Use of Laboratory Animals published by the US National Institutes of Health (NIH publication no. 86-23, revised 1985); animal use and welfare followed a protocol reviewed and approved by the First Affiliated Hospital of Nanchang University. Consent for publicationNot applicable.

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“…LepR is expressed in hypothalamic astrocytes [ 192 , 193 ], and hypothalamic astrocytes participate in the mediation of leptin signaling [ 194 , 195 ]. Absence of LepR in astrocytes weakens pSTAT3 signaling and increases TCPTP level, leading to altered glial morphology, reduced astrocytic coverage of melanocortin cells, and augmented synaptic inputs onto hypothalamic neurons [ 195 , 196 ]. These alterations of astrocytes promote the development of diet-induced obesity [ 194 , 195 ].…”

Section: Cellular Mechanism Underlying Leptin Functionmentioning

confidence: 99%

Leptin signaling and leptin resistance

et al. 2022

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With the prevalence of obesity and associated comorbidities, studies aimed at revealing mechanisms that regulate energy homeostasis have gained increasing interest. In 1994, the cloning of leptin was a milestone in metabolic research. As an adipocytokine, leptin governs food intake and energy homeostasis through leptin receptors (LepR) in the brain. The failure of increased leptin levels to suppress feeding and elevate energy expenditure is referred to as leptin resistance, which encompasses complex pathophysiological processes. Within the brain, LepR-expressing neurons are distributed in hypothalamus and other brain areas, and each population of the LepR-expressing neurons may mediate particular aspects of leptin effects. In LepR-expressing neurons, the binding of leptin to LepR initiates multiple signaling cascades including janus kinase (JAK)–signal transducers and activators of transcription (STAT) phosphatidylinositol 3-kinase (PI3K)-protein kinase B (AKT), extracellular regulated protein kinase (ERK), and AMP-activated protein kinase (AMPK) signaling, etc., mediating leptin actions. These findings place leptin at the intersection of metabolic and neuroendocrine regulations, and render leptin a key target for treating obesity and associated comorbidities. This review highlights the main discoveries that shaped the field of leptin for better understanding of the mechanism governing metabolic homeostasis, and guides the development of safe and effective interventions to treat obesity and associated diseases.

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The role of TCPTP on leptin effects on astrocyte morphology

Cited by 7 publications

References 56 publications

Synthesis of 2-ethoxycarbonylthieno[2,3-b]quinolines in biomass-derived solvent γ-valerolactone and their biological evaluation against protein tyrosine phosphatase 1B

Synthesis of 2-ethoxycarbonylthieno[2,3-b]quinolines in biomass-derived solvent γ-valerolactone and their biological evaluation against protein tyrosine phosphatase 1B

The important role of connexin 43 in subarachnoid hemorrhage-induced cerebral vasospasm

Leptin signaling and leptin resistance

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