Paradoxical expressions of natriuretic peptide receptor-C and neutral endopeptidase account for C-type natriuretic peptide decline during the progression of experimental obstructive nephropathy
Paradoxical expressions of natriuretic peptide receptor-C and neutral endopeptidase account for C-type natriuretic peptide decline during the progression of experimental obstructive nephropathy
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实验性梗阻性肾病进展过程中利钠肽受体-C 和中性肽链内切酶的矛盾表达导致 C 型利钠肽下降
DOI:
10.1177/1470320313507121
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发表时间:
2014-12
影响因子:
2.9
通讯作者:
胡鹏
中科院分区:
文献类型:
--
作者:
胡鹏
Introduction: C-type natriuretic peptide (CNP) selectively binds to the guanylyl cyclase coupled natriuretic peptide receptor (NPR)-B and exerts more potent antihypertrophic and antifibrotic properties. Elimination of CNP occurs mainly by neutral endopeptidase (NEP) and NPR-C. Methods: We established a rat model of unilateral ureteral obstruction (UUO) to examine the continuous change of the CNP expression and to assess the correlations of NPR-B, NPR-C, NEP with CNP in the obstructed kidneys. Results: The expressions of CNP mRNA and protein in the obstructed kidneys tended to be higher immediately after ligation and declined at later time points compared to sham-operated rats, measured by real-time polymerase chain reaction (PCR) and western blot analysis. Subsequent correlation analysis indicated that CNP mRNA was positively correlated with NPR-B mRNA (r=+0.673, p<0.05). In addition, the increased expression of NPR-C (r=−0.943 and −0.837 for mRNA and protein respectively, p<0.05) and NEP (r=−0.687 and −0.823 for mRNA and protein respectively, p<0.05) were accompanied by a significant decline in CNP. Conclusions: A high level of CNP may contribute to the elevated expression of NPR-B in the early phase of UUO. More interestingly, paradoxical expressions of NPR-C and NEP may account for the decline of CNP in the obstructed kidneys.
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影响因子:
2.9
作者:
Robinder S. Garcha;A. Hughes
通讯作者:
Robinder S. Garcha;A. Hughes
DOI:
10.1677/joe.0.1580035
发表时间:
1998-07
期刊:
The Journal of endocrinology
影响因子:
--
作者:
S. Shin;J. Wen;Y. J. Lee;I. Chen;J. Tsai
通讯作者:
S. Shin;J. Wen;Y. J. Lee;I. Chen;J. Tsai
DOI:
10.1016/s0735-1097(02)02127-7
发表时间:
2002-09-18
影响因子:
24
作者:
Chen, HH;Lainchbury, JG;Burnett, JC
通讯作者:
Burnett, JC
DOI:
--
发表时间:
2006
期刊:
The Korean Journal of Physiology and Pharmacology
影响因子:
--
作者:
E. Bae;S. Kim
通讯作者:
E. Bae;S. Kim
影响因子:
3
作者:
Hu, Peng;Wang, Jing;Qin, Yuan Han
通讯作者:
Qin, Yuan Han