Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pulmonary hypertension (PH), remains a challenging disease with a large impact on both humans and meat-type chickens. PH is characterized by the onset of idiopathic pulmonary arterial hypertension leading to right ventricular failure. In this experiment relative gene expression of adenosine A1 receptor (ADORA1), serotonin transporter (SERT), phosphodiesterase 5A (PDE5) and troponin T2 were compared in hearts from broilers with acute right ventricular failure and from healthy birds. There were major increases in adenosine A1 receptor (177%) and serotonin transporter (475%), and more modest but significant increases in PDE5 (146%) and troponin T2 (140%) gene expressions in broilers with right ventricular failure compared to healthy birds (P<0.01). This novel report shows that pulmonary hypertension related gene expression in broilers is similar to that in humans. This molecular similarity between PH in broilers and human patients suggests, first, that they will make a suitable animal model for study PH in humans, but also that the literature on PH in humans may be profitably applied to the study of PH in broilers.
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PMID:Upregulation of SERT and ADORA1 in broilers with acute right ventricular failure. 2917 7

Increased synthesis of serotonin and/or activity of serotonin in pulmonary arteries has been implicated in the pathobiology of pulmonary arterial hypertension (PAH). The incidence of PAH associated with diet pills such as aminorex, fenfluramine, and chlorphentermine initially led to the "serotonin hypothesis of pulmonary hypertension." Over the last couple of decades there has been an accumulation of convincing evidence that targeting serotonin synthesis or signaling is a novel and promising approach to the development of novel therapies for PAH. Pulmonary endothelial serotonin synthesis via tryptophan hydroxlase 1 (TPH1) is increased in patients with PAH and serotonin can act in a paracrine fashion on underlying pulmonary arterial smooth muscle cells (PASMCs), In humans, serotonin can enter PASMCs via the serotonin transporter (SERT) or activate the 5-HT1B receptor; 5-HT1B activation and SERT activity cooperate to induce PASMC contraction and proliferation via activation of downstream proliferative and contractile signaling pathways. Here we will review the current status of the serotonin hypothesis and discuss potential and novel therapeutic targets.
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PMID:The serotonin hypothesis in pulmonary hypertension revisited: targets for novel therapies (2017 Grover Conference Series). 2946 41

The main initiator of the development of PAH is the development of endothelial dysfunction of the pulmonary vessels. The cause of this dysfunction is associated with functional disorders of the serotonin system. This research is devoted to study the role of the serotonin system in the development mechanism of PAH in children with CHD. We examined 30 young children (from 1 month to 2 years) with congenital heart defects (CHD), which were divided into 3 groups: group I - 12 children with CHD complicated by pulmonary arterial hypertension (PAH); Group II - 9 children with CHD, not complicated by PAH; Group III - 9 relatively healthy children (control). The serotonin content of platelets, serum and serotonin transporter (SERT) in platelets was determined. To determine serotonin and its carrier, a quantitative enzyme-linked immunosorbent assay (Elisa kit) was used. The study was performed using the Serotonin ELISA diagnostic kit, IBL Hamburg at the automatic ELISA of the Evolis robotic station (BioRad). The results of our studies showed a pronounced (p <0.001) increase in SERT concentration in platelets in the group of children with CHD complicated by PAH compared with the group of children with CHD and the control group. The amount of serotonin in serum tended to increase in this group compared with the control groups and CHD, and the amount of serotonin in platelets tended to decrease. It is likely that an increase in the serotonin transporter in platelets against the background of an increase in serotonin in the blood plasma and a decrease in serotonin in the platelets indicates the inadequacy of SERT activity as a serotonin carrier. However, by activating the proliferation of smooth muscle cells in the pulmonary artery, SERT leads to the development of PAH in children with congenital heart defects. It is necessary to continue research in this direction, which will reveal the molecular mechanisms by which SERT regulates PASMC proliferation and clarify the role of serotonin and its transporter in the development of PAH in children with CHD.
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PMID:[THE SYSTEM OF SEROTONIN AND ITS METABOLISM IN PLATELETS IN CHILDREN WITH CONGENITAL HEART DEFECTS OF AN EARLY AGE]. 3214 46


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