Adenosine receptors are up-regulated in unilateral ureteral obstructed rat kidneys

Transplantation Proceedings
J LeeHunjoo Ha

Abstract

Despite recent improvements in immunosuppressive regimens, chronic renal allograft rejection remains a major problem. Tubulointerstitial fibrosis is one of the major histological features of chronic renal allograft rejection, but its exact pathogenic mechanisms are not fully understood. Adenosine present in the normal kidney is significantly elevated in response to cellular damage. The cellular effect of adenosine occurs through 4 known adenosine receptor (AR) subtypes; A(1)AR, A(2A)AR, A(2B)AR, and A(3)AR. All AR subtypes are expressed in the kidney, but the expression of each AR subtype has not been defined under fibrotic conditions. In the present study, we examined AR subtype expression in kidneys that underwent unilateral ureteral obstruction (UUO), a well-characterized model for tubulointerstitial fibrosis. At 5 days after the induction of UUO, we observed α-smooth muscle actin (α-SMA), fibronectin, and collagen I messenger RNA (mRNA) and protein expressions to be significantly up-regulated in the obstructed compared with the sham kidneys, confirming that fibrosis had occurred in the former organs. A(1)AR mRNA expression in the obstructed kidney cortex was 3.2-fold higher than an the sham kidney cortex. Relative to the sh...Continue Reading

References

Mar 7, 2006·Nature Reviews. Drug Discovery·Kenneth A Jacobson, Zhan-Guo Gao
Jul 4, 2006·Physiological Reviews·Volker VallonHartmut Osswald
Jul 18, 2008·Transplantation Reviews·Surmeet BediArjang Djamali
Apr 3, 2009·Kidney International·Robert L ChevalierBarbara A Thornhill
Jan 7, 2011·Journal of the American Society of Nephrology : JASN·Jessica D BauerleHolger K Eltzschig
Feb 12, 2011·The Korean Journal of Physiology & Pharmacology : Official Journal of the Korean Physiological Society and the Korean Society of Pharmacology·Jehyun ParkHunjoo Ha
Apr 23, 2011·Journal of the American Society of Nephrology : JASN·Yingbo DaiYang Xia

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