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

Title
Adenosine receptors are up-regulated in unilateral ureteral obstructed rat kidneys
Authors
Lee J.Hwang L.Ha H.
Ewha Authors
하헌주
SCOPUS Author ID
하헌주scopus
Issue Date
2012
Journal Title
Transplantation Proceedings
ISSN
0041-1345JCR Link
Citation
vol. 44, no. 4, pp. 1166 - 1168
Indexed
SCI; SCIE; SCOPUS WOS scopus
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 1AR, A 2AAR, A 2BAR, and A 3AR. 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 1AR mRNA expression in the obstructed kidney cortex was 3.2-fold higher than an the sham kidney cortex. Relative to the sham kidney A 2AAR and A 2BAR mRNA expressions were also 2.6- and 2.0-fold increased, respectively. A 3AR mRNA expression in the obstructed kidney cortex was also up-regulated by 3.3-fold. These data demonstrated that all 4 subtypes of AR were increased in the obstructed kidney, which was accompanied by tubulointerstitial fibrosis. Further studies are needed to determine which subtypes of AR play a protective or pathogenic role in tubulointerstitial fibrosis. © 2012 Elsevier Inc.
DOI
10.1016/j.transproceed.2012.01.079
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약학대학 > 약학과 > Journal papers
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