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Quantification of the Immunosuppressant Tacrolimus on Dried Blood Spots Using LC-MS/MS
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Transforming growth factor-beta1, vascular endothelial growth factor, and bone morphogenic protein-7 expression in

B Oğütmen1, S Tuğlular, F Cakalağaoğlu

  • 1Department of Pathology, Division of Nephrology, Marmara University Medical School, Istanbul, Turkey. betulogutmen@yahoo.com

Transplantation Proceedings
|March 22, 2006
PubMed

Insights

Chronic tacrolimus (TAC) toxicity in rats increased kidney damage markers and altered key protein expressions. TAC-induced nephrotoxicity is linked to higher transforming growth factor-beta1 and vascular endothelial growth factor, with lower bone morphogenic protein-7.

Area of Science:

  • Nephrology
  • Toxicology
  • Molecular Biology

Background:

  • Tacrolimus (TAC) is an immunosuppressant with known nephrotoxicity.
  • Understanding the molecular mechanisms of TAC-induced kidney damage is crucial for patient management.

Purpose of the Study:

  • To investigate the expression of transforming growth factor-beta1 (TGF-beta1), vascular endothelial growth factor (VEGF), and bone morphogenic protein-7 (BMP-7) in a rat model of chronic TAC toxicity.
  • To correlate these molecular changes with histological findings and renal function parameters.

Main Methods:

  • Wistar rats were administered TAC (1 mg/kg/day) for 8 weeks or received no treatment (controls).
  • Renal function was assessed via blood urea nitrogen (BUN), serum creatinine, and creatinine clearance.
  • Renal tissues were analyzed for histological changes (afferent arteriolopathy, interstitial fibrosis) and protein expression (TGF-beta1, VEGF, BMP-7) using immunohistochemistry.

Main Results:

  • TAC-treated rats showed significantly increased BUN, afferent arteriolopathy, and interstitial fibrosis compared to controls.
  • Expression of TGF-beta1 and VEGF was significantly elevated in TAC-treated rats.
  • Expression of BMP-7 was significantly decreased in TAC-treated rats.

Conclusions:

  • Chronic tacrolimus toxicity in rats is associated with significant renal damage and functional impairment.
  • The observed nephrotoxicity correlates with increased TGF-beta1 and VEGF expression and decreased BMP-7 expression.
  • These findings elucidate potential molecular pathways involved in TAC-induced kidney injury.

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