Imperial College London


Faculty of MedicineNational Heart & Lung Institute

Senior Research Fellow







B140BGuy Scadding BuildingRoyal Brompton Campus






BibTex format

author = {Ramakrishnan, L and Mumby, S and Meng, C and Wort, SJ and Quinlan, GJ},
title = {IL-6 mediated proliferative responses in human pulmonary vascular cells are differentially modulated by Iron/Heme/Hemoglobin},
year = {2013}

RIS format (EndNote, RefMan)

AB - Pulmonary Arterial Hypertension (PAH) is characterised by progressive pulmonary vascular remodelling culminating in heart failure. Disrupted iron metabolism and anaemia have been linked to development of PAH suggesting iron supplementation may be bene cial. However iron compounds are known proliferative agents. IL-6 which is both proin ammatory and central to iron homeostasis is elevated in PAH. With emerging evidence of minor hemolysis in PAH patients, the availability of heme and/or haemoglobin (Hb) to PVCs may further impact on cellular responses. We aim to address the above issues in this study.Human pulmonary arterial smooth muscle cells (PASMCs) & endothelial cells (PAECs) were exposed to iron (FAC)/Heme/Hb prior to treatment with IL6. Cell proliferation was quantied by Cyquant. RTPCR for expression of Hepcidin (regulatory hormone), Ferroportin (exporter), HO1, CD163(Hb scavenger) was also performed.IL-6 alone caused proliferation reversed by iron in PASMCs but not in PAECs. Heme restricted while Hb supported proliferation in both cell types. Basal CD163 mRNA was undetectable in PAECs but induced by IL-6. Hepcidin, Ferroportin and HO1 were also contrastingly regulated by IL6.[table1]Thus PVCs respond distinctly to the IL-6 stimulus which is further modulated by the availability of Iron/Heme/Hb. Besides IL-6 differentially regulated mRNA expression of genes involved in iron homeostasis. Further investigation of iron handling in PVCs seems warranted.
AU - Ramakrishnan,L
AU - Mumby,S
AU - Meng,C
AU - Wort,SJ
AU - Quinlan,GJ
PY - 2013///
TI - IL-6 mediated proliferative responses in human pulmonary vascular cells are differentially modulated by Iron/Heme/Hemoglobin
ER -