RGD Reference Report - Up-regulated lipocalin-2 in pulmonary hypertension involving in pulmonary artery SMC resistance to apoptosis. - Rat Genome Database

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Up-regulated lipocalin-2 in pulmonary hypertension involving in pulmonary artery SMC resistance to apoptosis.

Authors: Wang, Guoliang  Liu, Xiaoyan  Meng, Liukun  Liu, Shenghua  Wang, Li  Li, Jun  Cui, Chuanjue  Meng, Jian  Hu, Shengshou  Wei, Yingjie 
Citation: Wang G, etal., Int J Biol Sci. 2014 Jul 17;10(7):798-806. doi: 10.7150/ijbs.9470. eCollection 2014.
RGD ID: 126781744
Pubmed: PMID:25076856   (View Abstract at PubMed)
PMCID: PMC4115200   (View Article at PubMed Central)
DOI: DOI:10.7150/ijbs.9470   (Journal Full-text)

A key feature of pulmonary hypertension (PH) is the remodeling of small pulmonary arteries due to abnormal pulmonary artery smooth muscle cell (PASMC) proliferation and resistance to apoptosis. However, the cellular mechanisms underlying how PASMCs in the pathological condition of pulmonary hypertension become resistant to apoptosis remain unknown. It was recently reported that lipocalin 2 (Lcn2) is up-regulated in a wide array of malignant conditions, which facilitates tumorigenesis partly by inhibiting cell apoptosis. In this study, we observed that the expression levels of Lcn2 were significantly elevated in a rat PH model induced with monocrotaline and in patients with congenital heart disease-associated PH (CHD-PH) when compared with respective control. Therefore, we hypothesize that Lcn2 could regulate human PASMC (HPASMC) apoptosis through a mechanism. By the detection of DNA fragmentation using the TUNEL assay, the detection of Annexin V/PI-positive cells using flow cytometry, and the detection of cleaved caspase-3 and caspase-3 activity, we observed that Lcn2 significantly inhibited HPASMC apoptosis induced by serum withdrawal and H2O2 treatment. We also observed that Lcn2 down-regulated the proapoptotic protein Bax, decreased the levels of cellular ROS, and up-regulated the expression of superoxide dismutases (SOD1 and SOD2). In conclusion, Lcn2 significantly inhibits HPASMC apoptosis induced by oxidative stress via decreased intracellular ROS and elevated SODs. Up-regulation of Lcn2 in a rat PH model and CHD-PH patients may be involved in the pathological process of PH.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
pulmonary hypertension  ISOLcn2 (Rattus norvegicus)126781744; 126781744mRNA and protein:increased expression:lungRGD 
pulmonary hypertension  IEP 126781744associated with congenital heart disease and protein:increased expression:plasmaRGD 
pulmonary hypertension  ISOLCN2 (Homo sapiens)126781744; 126781744associated with congenital heart disease and protein:increased expression:plasmaRGD 
pulmonary hypertension  IEP 126781744mRNA and protein:increased expression:lungRGD 

Objects Annotated

Genes (Rattus norvegicus)
Lcn2  (lipocalin 2)

Genes (Mus musculus)
Lcn2  (lipocalin 2)

Genes (Homo sapiens)
LCN2  (lipocalin 2)


Additional Information