ArticleFrontiers in physiology2018
Substance P Receptor in the Rat Heart and Regulation of Its Expression in Long-Term Diabetes.
Article in Frontiers in physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 13 citations in OpenAlex.
- Autophagy and mitophagy as potential therapeutic targets in diabetic heart condition: Harnessing the power of nanotheranostics.Asian journal of pharmaceutical sciences · 2024Review
- Regulation of Prepro-NeuropeptideW/B and Its Receptor in the Heart of ZDF Rats: An Animal Model of Type II DM.International journal of molecular sciences · 2022Article
- Laser Capture Microdissection Coupled Capillary Immunoassay to Study the Expression of PCK-2 on Spatially-Resolved Islets of Rat Langerhans.Pharmaceutics · 2021Article
- Neuropeptides: Roles and Activities as Metal Chelators in Neurodegenerative Diseases.The journal of physical chemistry. B · 2021Review
- Identification of NPB, NPW and Their Receptor in the Rat Heart.International journal of molecular sciences · 2020Article
- Substance P enhances the local activation of NKBMC molecular and cell biology · 2020Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Substance P (SP) is a neuropeptide engaged in the signal transmission of neural C fibers afferents in the myocardium. The actions of SP in the heart are extensive and they are mediated by the neurokinin 1 receptor (NK1R), a member of the tachykinin subfamily of G-protein coupled receptors. The receptors have been found in the heart, but to our knowledge, their exact localization in the heart has not been described yet. Here, we investigated the presence of NK1R protein in separate rat heart compartments by means of western blot and its tissue distribution by means of immunofluorescence. Specificity of NK1R immunolabeling was controlled by preabsorption of the antiserum with its corresponding peptide. Additionally, we investigated abundance of gene for NK1R in separated heart chambers by means of quantitative real-time PCR (RT-PCR). Relative abundance of NK1R mRNA was expressed as a ratio of target gene Cq value to Cq value of control gene - beta-actin. Finally, we studied abundance of NK1R mRNA in different cell types of heart isolated by laser capture microdissection. Immunofluorescence showed NK1R immunoreactivity on the surface of some intracardiac neurons and smooth muscle cells of coronary vessels. The results of quantitative RT-PCR indicate abundance of mRNA for NK1R in all heart chambers with highest level in the left atrium. The presence of NK1R mRNA was detected in some samples of dissected intracardiac neurons, but not in cardiomyocytes or smooth muscle cells of coronary vessels. In the course of long-term diabetes, a significant downregulation of the NK1R mRNA was seen in the right atrium and upregulation in the right ventricle 53 weeks after the induction of diabetes. Our results indicate localization of NK1R in some intracardiac neurons and smooth muscle cells. Impaired transcription of the NK1R gene in the diabetic heart may be induced by unidentified genes or factors involved in the development of diabetic cardiomyopathy.
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