ArticleInternational journal of clinical and experimental medicine2015
ANP/NPRA signaling preferentially mediates Th2 responses in favor of pathological processes during the course of acute allergic asthma.
Article in International journal of clinical and experimental medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- Deterioration of diabetic nephropathy via stimulating secretion of cytokines by atrial natriuretic peptide.BMC endocrine disorders · 2021Article
- (Biological psychiatry global open science · 2021Article
- Upregulation of Phosphodiesterase 2A Augments T Cell Activation by Changing cGMP/cAMP Cross-Talk.Frontiers in pharmacology · 2021Article
- Helicobacter Pylori Induces GATA3-Dependent Chitinase 3 Like 1 (CHI3L1) Upregulation and Contributes to Vascular Endothelial Injuries.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Rheb1 deletion in myeloid cells aggravates OVA-induced allergic inflammation in mice.Scientific reports · 2017Article
- Effect of miR-503 Down-Regulation on Growth and Invasion of Esophagus Carcinoma and Related Immune Function.Medical science monitor : international medical journal of experimental and clinical research · 2015Article
- High mobility group box 1: a novel mediator of Th2-type response-induced airway inflammation of acute allergic asthma.Journal of thoracic disease · 2015Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although atrial natriuretic peptide (ANP) has been well recognized for its role in the regulation of volume-pressure homeostasis in cardiovascular system, its impact on respiratory system, particularly on the pathogenesis of acute allergic asthma, is yet to be elucidated. In the present report, we induced mice with OVA for onset of acute allergic asthma along with the administration of recombinant ANP or A71915 (an antagonist for ANP/natriuretic peptide receptor A, NPRA). It was noted that treatment of mice with ANP significantly promoted inflammatory infiltration in the airway and the production of inflammatory cytokines in the bronchoalveolar lavage fluid (BALF) and lung homogenates, and the number of inflammatory cells in the BALF was significantly higher as compared with that of PBS treated asthmatic mice. Moreover, blockade of ANP/NPRA signaling by A71915 almost completely attenuated the effect of ANP administration. Mechanistic studies revealed that ANP repressed the expression of Th1 transcription factor T-bet, but enhanced Th2 transcription GATA3 expression. Together, our data provided feasible evidence suggesting that ANP/NPRA signaling predominantly induces a Th2-type response in favor of pathological processes during the course of acute allergic asthma.
Indexed as
Identifiers
26131085PMC4483987W2398166702What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.