Publication Details

Category Text Publication
Reference Category Journals
DOI 10.1002/pmic.200600848
Title (Primary) Comparison of lung proteome profiles in two rodent models of pulmonary arterial hypertension
Author Laudi, S.; Steudel, W.; Jonscher, K.; Schöning, W.; Schniedewind, B.; Kaisers, U.; Christians, U.; Trump, S.
Source Titel Proteomics
Year 2007
Department IMMU
Volume 7
Issue 14
Page From 2469
Page To 2478
Language englisch
Keywords Hypoxia; Monocrotaline; Protein expression analysis; Pulmonary arterial hypertension
Abstract We studied the lung proteome changes in two widely used models of pulmonary arterial hypertension (PAH): monocrotaline (MCT) injection and chronic hypoxia (CH); untreated rats were used as controls (n = 6/group). After 28 days, invasive right ventricular systolic pressure (RVSP) was measured. Lungs were immunostained for -smooth muscle actin (SMA). 2-DE (n = 4/group) followed by nano-LC-MS/MS was applied for protein identification. Western blotting was used additionally if possible. RVSP was significantly increased in MCT- and CH-rats (MCT 62.5 ± 4.4 mmHg, CH 62.2 ± 4.1 mmHg, control 25.0 ± 1.7 mmHg, p<0.001). This was associated with an increase of SMA positive vessels. In both groups, there was a significantly increased expression of proteins associated with the contractile apparatus (diphosphoHsp27 (p<0.001), Septin2 (p<0.001), F-actin capping protein (p<0.01), and tropomyosin (p<0.02)). In CH, proteins of the nitric oxide (Hsc70; p = 0.002), carbon monoxide (biliverdin reductase; p = 0.005), and vascular endothelial growth factor (VEGF) pathway (annexin 3; p<0.001) were significantly increased. In MCT, proteins involved in serotonin synthesis (14-3-3; p = 0.02), the enhanced unfolded protein response (ERp57; p = 0.02), and intracellular chloride channels (CLIC 1; p = 0.002) were significantly elevated. Therefore, MCT- and CH-induced vasoconstriction and remodeling seemed to be mediated via different signaling pathways. These differences should be considered in future studies using either PAH model.
Laudi, S., Steudel, W., Jonscher, K., Schöning, W., Schniedewind, B., Kaisers, U., Christians, U., Trump, S. (2007):
Comparison of lung proteome profiles in two rodent models of pulmonary arterial hypertension
Proteomics 7 (14), 2469 - 2478 10.1002/pmic.200600848