Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0403608 (ureter)
 9,655 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Distinct patterns of cell proliferation and apoptosis have been recognized for tubular, interstitial, and glomerular cells in chronic obstructive uropathy (OU). In many experimental models of OU, tubular cell apoptosis develops quickly after ureter ligation, peaks between 7 and 24 days postobtruction (about 30-fold of control), and tapers thereafter. Apoptosis initially involves the dilated collecting ducts, but subsequently spreads to other tubules. Tubular cell apoptosis probably accounts for renal tissue loss in OU because a direct correlation between its degree and the decline in dry kidney weight is well-documented. Pronounced tubular cell proliferation occurs shortly after ureter ligation, peaks at about day 6 (60-fold above control), and quickly subsides to baseline. Because the peak of tubular cell proliferation immediately precedes the onset of tubular cell apoptosis, a pathogenetic link may exist between these two processes. Interstitial cell apoptosis occurs with an increasing frequency throughout the course of OU (up to 35-fold above control). Interstitial cell proliferation appears in a bimodal pattern with the early peak coinciding with that of tubular cell proliferation and consisting mostly of fibroblasts, whereas the later peak consists mostly of inflammatory cells. Glomerular cell apoptosis and proliferation are not different from control, which explains, in part, the structural integrity of the glomeruli throughout the disease course. Although the general pathways of cell apoptosis and proliferation are well known, the molecular control of these processes in OU is poorly understood. In addition, whether apoptosis or proliferation of tubular and interstitial cells is differentially regulated remains to be studied. However, several molecules known to be activated or overexpressed in kidney with OU may modulate cell apoptosis and proliferation. The relevant functions of these molecules include induction of apoptosis (angiotensin II, reactive oxygen species, jun-N-terminal kinase, p53), inhibition of the cell cycle (transforming growth factor-beta, p21), inhibition of apoptosis (clusterin, epidermal growth factor, insulin-like growth factor, bcl-2, osteopontin), or promotion of interstitial fibroblast proliferation (platelet-derived growth factor).
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PMID:Cell apoptosis and proliferation in obstructive uropathy. 981 55

Urine has the potential to become a better source of biomarkers. Urinary proteins are affected by many factors; therefore, differentiating between the variables associated with any particular pathophysiological condition in clinical samples is challenging. To circumvent these problems, simpler systems, such as animal models, should be used to establish a direct relationship between disease progression and urine changes. In this study, a unilateral ureteral obstruction (UUO) model was used to observe tubular injury and the eventual development of renal fibrosis, as well as to identify differential urinary proteins in this process. Urine samples were collected from the residuary ureter linked to the kidney at 1 and 3 weeks after UUO. Five hundred proteins were identified and quantified by LC-MS/MS, out of which 7 and 19 significantly changed in the UUO 1- and 3-week groups, respectively, compared with the sham-operation group. Validation by western blot showed increased levels of Alpha-actinin-1 and Moesin in the UUO 1-week group, indicating that they may serve as candidate biomarkers of renal tubular injury, and significantly increased levels of Vimentin, Annexin A1 and Clusterin in the UUO 3-week group, indicating that they may serve as candidate biomarkers of interstitial fibrosis.
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PMID:Urinary candidate biomarker discovery in a rat unilateral ureteral obstruction model. 2579 74