PT  - JOURNAL ARTICLE
AU  - Huang Huang Luo
AU  - Cheng Wu
AU  - Peng Hu
AU  - Yang Fang Wu
AU  - Dong Dong Zhang
AU  - Si Yan Liu
AU  - Guang Mei Jiang
AU  - Yao Xu
AU  - Yue Wu
AU  - Jing Jing Wang
AU  - Fei Fei Liu
AU  - Wei Wei
AU  - Bo Hu
TI  - Receptor signaling and neutral endopeptidase are involved in the resistance of C-type natriuretic peptide to human mesangial proliferation and collagen-IV expression
AID  - 10.1136/jim-2017-000533
DP  - 2018 Jun 01
TA  - Journal of Investigative Medicine
PG  - 1--9
VI  - 66
IP  - 5
4099  - http://hw-f5-jim.highwire.org/content/66/5/1.1.short
4100  - http://hw-f5-jim.highwire.org/content/66/5/1.1.full
SO  - J Investig Med2018 Jun 01; 66
AB  - C-type natriuretic peptide (CNP) is regarded as a local, paracrine hormone to regulate vascular tone and cell proliferation. Although several in vivo studies have documented that CNP exerts the inhibitory effects on mesangial cells (MCs) proliferation and collagen production, a limited number of studies exist about the resistance of CNP to MCs proliferation in vitro. Besides, whether its receptor signaling and neutral endopeptidase (NEP) are involved remains unclear. In the present study, human MCs were incubated in serum-containing medium in the absence or presence of CNP (0, 10 and 100 pM) for 24, 48 and 72 hours, respectively. CNP administration significantly suppresses MCs proliferation and collagen-IV (Col-IV) expression in a time-dependent and dose-dependent manner. As a down-stream signal molecule of CNP activation, the expressions of natriuretic peptide receptor (NPR)-B, cyclic guanosine monophosphate-dependent protein kinases II and NPR-C were obviously augmented, whereas NEP expression was significantly decreased after CNP treatment. In conclusion, receptor signaling and NEP are involved in the resistance of CNP to human mesangial proliferation and Col-IV expression.