@article {43028,
	title = {Placental proteomics provides insights into pathophysiology of pre-eclampsia and predicts possible markers in plasma},
	journal = {Journal of Proteome Research},
	volume = {16},
	year = {2017},
	month = {FEB},
	pages = {1050-1060},
	abstract = {<p>Pre-eclampsia is a hypertensive disorder characterized by the new onset of hypertension \&gt;140/90 mmHg and proteinuria after the 20th week of gestation. The disorder is multi-factorial and originates with abnormal placentation. Comparison of the placental proteome of normotensive (n=25) and pre-eclamptic (n=25) patients by gel-free proteomic techniques, identified a total of 2145 proteins in the placenta of which 180 were differentially expressed (\&gt;1.3 fold, p\&lt;0.05). Gene ontology enrichment analysis of biological process suggested that the differentially expressed proteins belonged to various physiological processes such as angiogenesis, apoptosis, oxidative stress, hypoxia, placental development, which are implicated in the pathophysiology of pre-eclampsia. Some of the differentially expressed proteins were monitored in the plasma by multiple reaction monitoring (MRM) analysis, which showed an increase in Apolipoprotein AI and AII in gestational week 26-30th (2-fold, p\&lt;0.01) while haptoglobin and hemopexin decreased in gestational week 26-30th and 40th week/at delivery (1.8 fold, p\&lt;0.01) in pre-eclamptic patients. This study provides a proteomic insight into the pathophysiology of pre-eclampsia. Identified candidate proteins can be evaluated further for the development of potential biomarkers associated with pre-eclampsia pathogenesis.</p>},
	doi = {10.1021/acs.jproteome.6b00955},
	author = {Mary, Sheon and Kulkarni, Mahesh J. and Malakar, Dipankar and Joshi, Sadhana Ramchandra and Mehendale, Savita S. and Giri, Ashok P.}
}
@article {45719,
	title = {Polymerization-incompetent uromodulin in the pregnant stroke-prone spontaneously hypertensive rat},
	journal = {Hypertension},
	volume = {69},
	year = {2017},
	month = {MAY},
	pages = {910+},
	type = {Article},
	abstract = {<p>The kidney is centrally involved in blood pressure regulation and undergoes extensive changes during pregnancy. Hypertension during pregnancy may result in an altered urinary peptidome that could be used to indicate new targets of therapeutic or diagnostic interest. The stroke-prone spontaneously hypertensive rat (SHRSP) is a model of maternal chronic hypertension. Capillary electrophoresis-mass spectrometry was conducted to interrogate the urinary peptidome in SHRSP and the control Wistar-Kyoto strain at three time points: prepregnancy and gestational days 12 and 18. The comparison within and between the Wistar-Kyoto and SHRSP peptidome at all time points detected 123 differentially expressed peptides (fold change \&gt;1.5; P\&lt;0.05). Sequencing of these peptides identified fragments of collagen a-chains, albumin, prothrombin, actin, serpin A3K, proepidermal growth factor, and uromodulin. Uromodulin peptides showed a pregnancy-specific alteration in SHRSP with a 7.8-fold (P\&lt;0.01) and 8.8-fold (P\&lt;0.05) increase at gestational days 12 and 18, respectively, relative to the Wistar-Kyoto. Further investigation revealed that these peptides belonged to the polymerization-inhibitory region of uromodulin. Two forms of uromodulin (polymerization competent and polymerization incompetent) were found in urine from both Wistar-Kyoto and SHRSP, where the polymerizationincompetent form was increased in a pregnancy-specific manner in SHRSP. Nifedipine-treated pregnant SHRSP showed only polymerization-competent uromodulin, indicating that calcium may be mechanistically involved in uromodulin polymerization. This study highlights, for the first time, a potential role of uromodulin and its polymerization in hypertensive pregnancy.</p>},
	keywords = {Hypertension, Kidney, Nifedipine, pregnancy, uromodulin},
	issn = {0194-911X},
	doi = {10.1161/HYPERTENSIONAHA.116.08826},
	author = {Mary, Sheon and Small, Heather Yvonne and Siwy, Justyna and Mullen, William and Giri, Ashok and Delles, Christian}
}
