ArticleJournal of neuroinflammation2017
Arginine vasopressin altered the expression of monocarboxylate transporters in cultured astrocytes isolated from stroke-prone spontaneously hypertensive rats and congenic SHRpch1_18 rats.
Article in Journal of neuroinflammation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 6 citations in OpenAlex.
- Astrocyte-Neuron Crosstalk in Hypertension: Mechanisms and Therapeutic Significance.Reviews in cardiovascular medicine · 2026Review
- Expression of TNFR1, VEGFA, CD147 and MCT1 as early biomarkers of diabetes complications and the impact of aging on this profile.Scientific reports · 2023Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAstrocytes support a range of brain functions as well as neuronal survival, but their detailed relationship with stroke-related edema is not well understood. We previously demonstrated that the release of lactate from astrocytes isolated from stroke-prone spontaneously hypertensive rats (SHRSP/Izm) was attenuated under stroke conditions. The supply of lactate to neurons is regulated by astrocytic monocarboxylate transporters (MCTs). The purpose of this study was to examine the contributions of arginine vasopressin (AVP) and/or hypoxia and reoxygenation (H/R) to the regulation of MCTs and neurotrophic factor in astrocytes obtained from SHRSP/Izm and congenic SHRpch1_18 rats.
methodsWe compared AVP-induced lactate levels, MCTs, and brain-derived neurotrophic factor (BDNF) in astrocytes isolated from SHRSP/Izm, SHRpch1_18, and Wistar Kyoto rats (WKY/Izm). The expression levels of genes and proteins were determined by PCR and Western blotting (WB).
resultsThe production of lactate induced by AVP was increased in astrocytes from all three strains. However, the levels of lactate were lower in SHRSP/Izm and SHRpch1_18 animals compared with the WKY/Izm strain. Gene expression levels of Slc16a1, Slc16a4, and Bdnf were lowered by AVP in SHRSP/Izm and SHRpch1_18 rats compared with WKY/Izm. The increase of MCT4 that was induced by AVP was blocked by the addition of a specific nitric oxide (NO) chelator, 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (CPTIO). Furthermore, AVP increased the expression of iNOS and eNOS proteins in WKY/Izm and SHRSP/Izm rat astrocytes. However, the iNOS expression levels in SHRSP astrocytes differed from those of WKY/Izm astrocytes. The increase of MCT4 protein expression during AVP treatment was blocked by the addition of a specific NF-kB inhibitor, pyrrolidine dithiocarbamate (PDTC). The induction of MCT4 by AVP may be regulated by NO through NF-kB.
conclusionsThese results suggest that the expression of MCTs mediated by AVP may be regulated by NO. The data suggest that AVP attenuated the expression of MCTs in SHRSP/Izm and SHRpch1_18 astrocytes. Reduced expression of MCTs may be associated with decreased lactate production in SHRSP.
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