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首页> 外文期刊>Molecular and Cellular Biology >GATA-6 and NF-κB Activate CPI-17 Gene Transcription and Regulate Ca2+ Sensitization of Smooth Muscle Contraction
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GATA-6 and NF-κB Activate CPI-17 Gene Transcription and Regulate Ca2+ Sensitization of Smooth Muscle Contraction

机译：GATA-6和NF-κB激活CPI-17基因转录并调节平滑肌收缩的Ca2 +敏感性。

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Protein kinase C (PKC)-potentiated inhibitory protein of 17 kDa (CPI-17) inhibits myosin light chain phosphatase, altering the levels of myosin light chain phosphorylation and Ca2+ sensitivity in smooth muscle. In this study, we characterized the CPI-17 promoter and identified binding sites for GATA-6 and nuclear factor kappa B (NF-κB). GATA-6 and NF-κB upregulated CPI-17 expression in cultured human and mouse bladder smooth muscle (BSM) cells in an additive manner. CPI-17 expression was decreased upon GATA-6 silencing in cultured BSM cells and in BSM from NF-κB knockout (KO) mice. Moreover, force maintenance by BSM strips from KO mice was decreased compared with the force maintenance of BSM strips from wild-type mice. GATA-6 and NF-κB overexpression was associated with CPI-17 overexpression in BSM from men with benign prostatic hyperplasia (BPH)-induced bladder hypertrophy and in a mouse model of bladder outlet obstruction. Thus, aberrant expression of NF-κB and GATA-6 deregulates CPI-17 expression and the contractile function of smooth muscle. Our data provide insight into how GATA-6 and NF-κB mediate CPI-17 transcription, PKC-mediated signaling, and BSM remodeling associated with lower urinary tract symptoms in patients with BPH.
机译：蛋白激酶C（PKC）增强的抑制蛋白17 kDa（CPI-17）抑制肌球蛋白轻链磷酸酶，改变平滑肌中肌球蛋白轻链磷酸化的水平和Ca 2 + 的敏感性。在这项研究中，我们表征了CPI-17启动子并鉴定了GATA-6和核因子κB（NF-κB）的结合位点。 GATA-6和NF-κB以加和方式上调了培养的人和小鼠膀胱平滑肌（BSM）细胞中的CPI-17表达。在培养的BSM细胞和NF-κB敲除（KO）小鼠的BSM中，GATA-6沉默后CPI-17表达降低。而且，与野生型小鼠的BSM条的力维持相比，KO小鼠的BSM条的力维持降低。 GATA-6和NF-κB的过度表达与BSM引起的前列腺增生（BPH）引起的膀胱肥大的男性以及小鼠膀胱出口梗阻模型中CPI-17的过度表达有关。因此，NF-κB和GATA-6的异常表达会降低CPI-17的表达和平滑肌的收缩功能。我们的数据提供了有关BATA患者下尿路症状的GATA-6和NF-κB如何介导CPI-17转录，PKC介导的信号传导和BSM重塑的见解。

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