Hydronephrosis Promotes Expression of Hypoxia-Inducible Factor 1 alpha

Επιστημονική δημοσίευση - Άρθρο Περιοδικού uoadl:3141405 12 Αναγνώσεις

Μονάδα:
Ερευνητικό υλικό ΕΚΠΑ
Τίτλος:
Hydronephrosis Promotes Expression of Hypoxia-Inducible Factor 1 alpha
Γλώσσες Τεκμηρίου:
Αγγλικά
Περίληψη:
Background: Obstructive uropathy is argued to involve an ischemia-type
tissue injury. Further, hypoxia-inducible factor 1 alpha (HIF-1 alpha)
constitutes a nuclear transcription factor normally upregulated under
hypoxic conditions. We hypothesized that HIF-1 alpha is expressed in the
hydronephrotic renal pelvis, as a result of tissue hypoxia. Patients and
Methods: Renal pelvis tissue specimens were obtained from 2 patient
groups. Group 1 (controls, n = 10) consisted of patients who underwent
nephrectomy due to nonobstructive renal malignancy. Group 2 (n = 18)
consisted of patients who underwent open procedures due to intractable
hydronephrosis, not amenable to conservative measures. HIF-1 alpha
detection was conducted via immunohistochemical techniques, while
histological alterations in both groups were also recorded. Results:
Smooth muscle hypertrophy and urothelial hyperplasia were major findings
in group 2. HIF-1 alpha-positive cells (fibroblasts and occasionally
macrophages), mainly localized in the stroma, were also found to a
greater extent in group 2 (p = 0.0066). Conclusion: We conclude that
HIF-1 alpha is mainly expressed in stroma fibroblasts of the
hydronephrotic renal pelvis, implying the presence of significant tissue
hypoxia at the dilated upper urinary tract. Copyright (C) 2009 S. Karger
AG, Basel
Έτος δημοσίευσης:
2009
Συγγραφείς:
Stravodimos, Konstantinos G.
Koritsiadis, Georgios
Lazaris,
Andreas C.
Agrogiannis, Georgios
Koutalellis, Georgios and
Constantinides, Constantinos
Patsouris, Efstratios
Kapetanakis,
Theodoros
Zervas, Anastasios
Περιοδικό:
Urologia Internationalis
Εκδότης:
Karger
Τόμος:
82
Αριθμός / τεύχος:
1
Σελίδες:
38-42
Λέξεις-κλειδιά:
Hydronephrosis; Hypoxia-inducible factor 1 alpha; Muscle hypertrophy
Επίσημο URL (Εκδότης):
DOI:
10.1159/000176023
Το ψηφιακό υλικό του τεκμηρίου δεν είναι διαθέσιμο.