ArticleInternational journal of clinical and experimental medicine2015
Biological characteristics of tracheal smooth muscle cells regulated by NK-1R in asthmatic rat with airway remodeling.
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 2 papers.
What it found
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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.
The trial behind it
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Who cites it
2 citing papers in PubMed, 4 citations in OpenAlex.
- Shikonin Exerts an Antileukemia Effect against FLT3-ITD Mutated Acute Myeloid Leukemia Cells via Targeting FLT3 and Its Downstream Pathways.Acta haematologica · 2024Article
- Neurokinin 1 receptor promotes rat airway smooth muscle cell migration in asthmatic airway remodelling by enhancing tubulin expression.Journal of thoracic disease · 2018Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study aims to investigate the biological characteristic changes of infant rat tracheal smooth muscle cells in asthma airway remodeling and the impact of NK-1R on the mechanism. Ovalbumin (OVA) was used to excited juvenile SD rats by 8 w. Immunofluorescence, MTT assay, transwell chambers, real time quantitative PCR, Western blot and other methods were used to observe the proliferation, migration, synthesis and secretion changes of infant airway remodeling in rat tracheal smooth muscle cell and the Neurokinin 1 receptor (NK-1R) expression. 1. NK-1R mRNA, protein expression of airway smooth muscle cell (ASMC) of each asthma group were higher than that of the control group, especially the asthma 8 w group had highest expression (P<0.01). 2. The average A value of 8 w asthma group measured by MTT method were significantly higher than that of the control group (P<0.05), WIN62577 10(-8) mol/L group had the strongest inhibition of ASMC proliferation (P<0.01). 3. The number of cell migration in the asthma group significantly increased than that in the control group. The number of migrating cells in the NK-1R antagonist group significantly reduced compared with the asthma 8 w group (P<0.05). 4. The average gray value of type III collagen in each asthma group were higher than that of the control group, and the asthma 8 w group had the highest (P<0.01). After NK-1R blocking, the average gray value of type III collagen was significantly lower (P<0.05). ASMC proliferation, migration, synthesis and secretion function increased in the airway remodeling group, and NK-1R played an important role.
Indexed as
Identifiers
26628953PMC4658842W2183775390What 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.