Ask about this productRelated genes to: Pde2a antibody
- Gene:
- PDE2A NIH gene
- Name:
- phosphodiesterase 2A
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 11q13.4
- Locus Type:
- gene with protein product
- Date approved:
- 1997-11-10
- Date modifiied:
- 2016-10-05
Related products to: Pde2a antibody
Related articles to: Pde2a antibody
- Endothelial dysfunction is an early event in atherosclerosis development and is centrally linked with insufficient endothelial NO production. However, chronically increased NO levels, including NO from other cellular sources, may induce endothelial dysfunction. Here, we studied how chronically elevated NO production from erythrocytes, achieved by genetic deletion of ARG1 (arginase-1), impacts smooth muscle cell (SMC) lipid accumulation and atherosclerosis progression. - Source: PubMed
Publication date: 2026/05/01
Sun BeichenGogiraju RajinikanthGreulich FranziskaKumi FrankGhasemi ImanBochenek Magdalena LPagel Svenvan der Vorst Emiel P CKhuu My PhungMoiko KaterynaRenner LuisaGuliani PayalRuf WolframPorubsky StefanReinhardt ChristophFleming IngridBindila LauraLurz PhilippSchäfer Katrin - Diabetic cardiomyopathy (DCM) results in high mortality with surprisingly rare therapeutic approaches. Anacardic acid (AA) shows broad pharmacological properties, but its effect on DCM was unknown. This study aims to investigate the effect and molecular action of AA on DCM. KKAy mice, a model of spontaneous type 2 diabetes, were fed a high-fat diet, and were subsequently administered with AA by gavage at 5 mg/kg for 14 weeks. AA attenuated cardiac dysfunction, pathological injuries, inflammation, fibrosis, oxidative stress, and apoptosis. Mechanistically, AA was enriched in the colon, but not serum and heart, improving colonic histopathological scores, enhancing colonic tight junction protein expression and reducing serum lipopolysaccharide level, suggesting colonic epithelial barrier integrity (CEBI) as a key target of AA. In vitro experiment employed high glucose and palmitic acid-challenged colonic epithelial cells as a cell model of CEBI, showing that AA at 5 µmol/L reversed the impaired expression of tight junction proteins. RNA-sequencing identified Pde2a gene to be significantly inhibited by AA. Lentivirus-induced Pde2a overexpression in colonic epithelial cells abolished the protective effect of AA on CEBI. The present study reports that AA enhances CEBI to attenuate DCM, possibly through inhibiting colonic epithelial expression of Pde2a. - Source: PubMed
Ge RuiYin JialinMeng HualiHuang XiaoliSun LeiZheng YanYang JianjunWu Hao - - Source: PubMed
Publication date: 2026/04/02
Wen YuanZhao YuboBai Minghan - BackgroundPhysical exercise shows neuroprotective and anti-inflammatory effects in Alzheimer's disease (AD) models, but whether it modulates neuroinflammation through regulation of peripheral T-cell activity is still unresolved.ObjectiveThe present study aimed to explore the mechanisms by which aerobic exercise regulates peripheral T cell-mediated immune responses and their potential contribution to neuroinflammation in AD.MethodsMale wild-type mice and APP/PS1 transgenic mice were divided into four groups: wild-type sedentary mice (WT-SE) group, wild-type exercise group (WT-EX), APP/PS1 transgenic AD sedentary mice (AD-SE) group, and APP/PS1 transgenic AD exercise mice (AD-EX) group. The sedentary groups received no exercise training, while the exercise groups underwent a 3-month treadmill aerobic exercise intervention. At the end of the intervention, T lymphocytes were isolated from spleens. Label-free proteomics combined with LC-MS/MS was used to identify differentially expressed proteins (DEPs) and perform functional and pathway enrichment analyses. Differentially expressed protein-coding genes were validated at the mRNA level using RT-qPCR.ResultsA total of 3399 proteins were quantified across the four groups. Applying a threshold of |log fold change| > 0.67 and < 0.05, 913 DEPs were identified. These DEPs were significantly enriched in biological processes including immune system processes, protein-containing complexes, and structural molecule activity, as well as signaling pathways including AD, TGF-β, and apoptosis.ConclusionsOverall, HSP90AB1, HSP90AA1, BAG5, DNAJC8, CTSD, and ANXA1 may play a role in peripheral T-cell immune dysregulation in AD, with potential implications for central neuroinflammation. Furthermore, the beneficial effects of aerobic exercise on AD-related peripheral immune alterations, and its potential modulation of neuroinflammation, may be associated with expression changes in DEPs including Ppp2r1b, Pde2a, Casp8, Apaf-1, Dnajb11, and Dnajc13. - Source: PubMed
Publication date: 2026/03/30
Ye XingHu KaiLiu Renyi - Colorectal cancer (CRC) remains a major cause of cancer-related morbidity and mortality, with high recurrence rates and limited treatment options for metastatic disease. The tumor microenvironment (TME) and metabolic reprogramming are critical drivers of CRC progression, influencing immune responses, therapeutic resistance, and patient outcomes. - Source: PubMed
Publication date: 2026/03/09
Fu YuxiangLai JianboHuang KaibinLiu LipingLiao Guixiang