Cai Pengcheng, Kovacs Laszlo, Dong Sam, Wu Guangyu, Su Yunchao
Department of Pharmacology and Toxicology, Medical College of Georgia, Augusta University, Augusta, Georgia.
Department of Clinical Laboratory, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
Am J Physiol Lung Cell Mol Physiol. 2017 May 1;312(5):L638-L648. doi: 10.1152/ajplung.00260.2016. Epub 2017 Feb 24.
In the present study, we investigated the effect of bone morphogenetic protein 4 (BMP4) on PDGF-induced cell proliferation and collagen synthesis in pulmonary artery smooth muscle cells (PASMCs). Normal human PASMCs were incubated with and without PDGF-BB in the absence and presence of BMP4 for 0.5 to 24 h. The protein levels of collagen-I, p-Smad2/3, p-Smad1/5, and intracellular active TGF-β1, calpain activity, and cell proliferation were then measured. The results showed that BMP4 induced an increase in p-Smad1/5 but had no effect on the protein levels of collagen-I, p-Smad2/3, and intracellular active TGF-β1 and calpain activity in control PASMCs. Nevertheless, BMP4 attenuated increases in cell proliferation and protein levels of collagen-I, p-Smad2/3, and intracellular active TGF-β1 and calpain activity in PASMCs exposed to PDGF-BB. Moreover, BMP4 increased PKA activity and inhibition of PKA prevented the inhibitory effects of BMP4 on PDGF-BB-induced calpain activation in normal PASMCs. The PKA activator forskolin recapitulated the suppressive effect of BMP4 on PDGF-induced calpain activation. Furthermore, BMP4 prevented a PDGF-induced decrease in calpain-2 phosphorylation at serine-369 in normal PASMCs. Finally, BMP4 did not attenuate PDGF-induced increases in cell proliferation, collagen-I protein levels, and calpain activation and did not induce PKA activation and did not prevent a PDGF-induced decrease in calpain-2 phosphorylation at serine-369 in PASMCs from idiopathic pulmonary arterial hypertension (PAH) patients. These data demonstrate that BMP4 inhibits PDGF-induced cell proliferation and collagen synthesis via PKA-mediated inhibition of calpain-2 in normal PASMCs. The inhibitory effects of BMP4 on PDGF-induced cell proliferation, collagen synthesis, and calpain-2 activation are impaired in PASMCs from PAH patients, which may contribute to pulmonary vascular remodeling in PAH.
在本研究中,我们调查了骨形态发生蛋白4(BMP4)对血小板衍生生长因子(PDGF)诱导的肺动脉平滑肌细胞(PASMCs)增殖及胶原蛋白合成的影响。将正常人PASMCs在有或无BMP4存在的情况下,与PDGF-BB一起孵育0.5至24小时。然后检测I型胶原蛋白、磷酸化Smad2/3、磷酸化Smad1/5的蛋白水平、细胞内活性转化生长因子-β1(TGF-β1)、钙蛋白酶活性及细胞增殖情况。结果显示,BMP4可使磷酸化Smad1/5增加,但对对照PASMCs中I型胶原蛋白、磷酸化Smad2/3、细胞内活性TGF-β1的蛋白水平及钙蛋白酶活性无影响。然而,BMP4可减弱暴露于PDGF-BB的PASMCs的细胞增殖以及I型胶原蛋白、磷酸化Smad2/3、细胞内活性TGF-β1的蛋白水平及钙蛋白酶活性的增加。此外,BMP4可增加蛋白激酶A(PKA)活性,抑制PKA可消除BMP4对正常PASMCs中PDGF-BB诱导的钙蛋白酶激活的抑制作用。PKA激活剂福斯高林可重现BMP4对PDGF诱导的钙蛋白酶激活的抑制作用。此外,BMP4可防止正常PASMCs中PDGF诱导的钙蛋白酶-2在丝氨酸369位点的磷酸化降低。最后,在特发性肺动脉高压(PAH)患者的PASMCs中,BMP4不能减弱PDGF诱导的细胞增殖增加、I型胶原蛋白蛋白水平增加及钙蛋白酶激活,不能诱导PKA激活,也不能防止PDGF诱导的钙蛋白酶-2在丝氨酸369位点的磷酸化降低。这些数据表明,在正常PASMCs中,BMP4通过PKA介导的对钙蛋白酶-2的抑制作用来抑制PDGF诱导的细胞增殖及胶原蛋白合成。在PAH患者的PASMCs中,BMP4对PDGF诱导的细胞增殖、胶原蛋白合成及钙蛋白酶-2激活的抑制作用受损,这可能促成了PAH中的肺血管重塑。