title: Differential ConA-enriched urinary proteome in rat experimental glomerular diseases.
abstract: Glomerular diseases are leading causes of end-stage renal diseases worldwide. They are considered to be consequences of injury primarily to the three types of glomerular cells. Differential diagnosis typically relies on invasive biopsy findings. We expected that injuries of different glomerular cells would cause different changes in urinary proteome. The goal of this study was to identify differential urinary proteins distinguishing between injuries of different glomerular cells before significant histopathologic changes. Adriamycin nephropathy and Thy1.1 glomerulonephritis were employed as models with different primary impaired cells. ConA-enriched urinary glycoproteome on day3 were profiled by gel-free shotgun tandem mass spectrometry, and compared with self-healthy controls to identify differential urinary proteins for each model. By comparing the changes of the differential proteins between these two models, we identified 39 proteins with different directions of changes, which may potentially be useful in differentiation; and 7 proteins with the same direction of changes, which may be potential indicators of early renal damage. These differential proteins were of several origins: plasma proteins, proteins with urine or kidney specificity, proteins without tissue-specificity (mainly inflammatory mediators) etc. Our results may help better understand the effects of injuries of different glomerular cells at the initial stage, and lead to the discovery of novel early diagnostic markers for human focal segmental glomerulosclerosis (FSGS) and mesangioproliferative glomerulonephritis (MsPGN) which have the same primary impaired cells with adriamycin nephropathy and Thy1.1 glomerulonephritis, respectively.
authors.affiliation: Department of Physiology and Pathophysiology, School of Basic Medicine Peking Union Medical College, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, 5 Dongdan Santiao, Beijing 100005, China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Wang
authors.forename: Yong
authors.initials: Y
authors.lastname: Chen
authors.forename: Yang
authors.initials: Y
authors.lastname: Zhang
authors.forename: Shuzhen
authors.initials: S
authors.lastname: Wu
authors.forename: Sucan
authors.initials: S
authors.lastname: Ma
authors.forename: Siqi
authors.initials: S
authors.lastname: Hu
authors.forename: Ling
authors.initials: L
authors.lastname: Zhang
authors.forename: Chen
authors.initials: C
authors.lastname: Shao
authors.forename: Mingxi
authors.initials: M
authors.lastname: Li
authors.forename: Youhe
authors.initials: Y
authors.lastname: Gao
mesh_terms: D000818:Animals; D015415:Biomarkers / Q000652:urine; D003208:Concanavalin A / Q000737:chemistry; D003937:Diagnosis, Differential; D004195:Disease Models, Animal; D004317:Doxorubicin / Q000633:toxicity; D005921:Glomerulonephritis / Q000139:chemically induced / Q000175:diagnosis* / Q000652:urine*; D006023:Glycoproteins / Q000737:chemistry / Q000652:urine*; D008297:Male; D020543:Proteome; D051381:Rats; D017207:Rats, Sprague-Dawley; D053719:Tandem Mass Spectrometry; D018800:Thy-1 Antigens / Q000276:immunology
chemical_list: D015415:Biomarkers; D006023:Glycoproteins; D020543:Proteome; D018800:Thy-1 Antigens; D003208:Concanavalin A; D004317:Doxorubicin