NDLI: Functions of serotonin in hypoxic pulmonary vascular remodeling

Content Provider	Springer Nature Link
Author	Esteve, Juan M. Launay, Jean Marie Kellermann, Odile Maroteaux, Luc
Copyright Year	2007
Abstract	In lung vasculature, reversible constriction of smooth muscle cells exists in response to acute decrease in oxygen levels (hypoxia). Progressive and irreversible structural remodeling that reduces blood vessel lumen takes place in response to chronic hypoxia and results in pulmonary hypertension. Several studies have shown a role of serotonin in regulating acute and chronic hypoxic responses. In this review the contribution of serotonin, its receptors and transporter in lung hypoxic responses is discussed. Hypoxic conditions modify plasma levels of serotonin, serotonin transporter activity, and expression of 5-HT$_{1B}$ and 5-HT$_{2B}$ receptors. These appear to be required for pulmonary vascular cell proliferation, which depends on the ratio between reactive oxygen species and nitric oxide. A heterozygous mutation was identified in the 5-HT$_{2B}$ receptor gene of a patient who developed pulmonary hypertension after fenfluramines anorexigen treatment. This C-terminus truncated 5-HT$_{2B}$ mutant receptor presents lower nitric oxide coupling, and higher cell proliferation capacity than the wild-type receptor. Under low oxygen tension, cells increase the transcription of specific genes via stabilization of the transcription factor hypoxia-inducible factor (HIF)-1. Factors such as angiotensin II or thrombin that can also control HIF-1 pathway contribute to pulmonary vascular remodeling. The 5-HT$_{2B}$ receptor via phosphatidylinositol-3 kinase/Akt activates nuclear factor-κB, which is involved in the regulation of HIF-1 expression. A control of HIF-1 by 5-HT$_{2B}$ receptors explains why expression of pulmonary vascular remodeling factors, such as endothelin-1 or transforming growth factor-β, which is HIF-1-α regulated, is not modified in hypoxic 5-HT$_{2B}$ receptor mutant mice. Understanding the detailed mechanisms involved in lung hypoxic responses may provide general insight into pulmonary hypertension pathogenesis.
Starting Page	33
Ending Page	43
Page Count	11
File Format	PDF
ISSN	10859195
Journal	Cell Biochemistry and Biophysics
Volume Number	47
Issue Number	1
e-ISSN	15590283
Language	English
Publisher	Humana Press
Publisher Date	2007-01-01
Publisher Place	Totowa
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Biochemistry Pharmacology/Toxicology Biotechnology Cell Biology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Medicine Biochemistry Biophysics

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1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
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