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首页> 外文期刊>Journal of Cellular Physiology >BNP-induced activation of cGMP in human cardiac fibroblasts: interactions with fibronectin and natriuretic peptide receptors.
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BNP-induced activation of cGMP in human cardiac fibroblasts: interactions with fibronectin and natriuretic peptide receptors.

机译：人类心脏BNP-induced cGMP的激活成纤维细胞:与纤连蛋白的相互作用利钠肽受体。

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摘要

Cardiac remodeling involves the accumulation of extracellular matrix (ECM) proteins including fibronectin (FN). FN contains RGD motifs that bind integrins at DDX sequences allowing signaling from the ECM to the nucleus. We noted that the natriuretic peptide receptor A (NPR-A) sequence contains both RGD and DDX sequences. The goal of the current investigation was to determine potential interactions between FN and NPR-A on BNP induction of cGMP in cultured human cardiac fibroblasts (CFs). Further, we sought to determine whether a Mayo designed NPR-A specific RGD peptide could modify this interaction. Here we reconfirm the presence of all three natriuretic peptide receptors (NPR) in CFs. CFs plated on FN demonstrated a pronounced increase in cGMP production to BNP compared to non-coated plates. This production was also enhanced by the NPR-A specific RGD peptide, which further augmented FN associated cGMP production. Addition of HS-142-1, a NPR-A/B antagonist, abrogated the responses of BNP to both FN and the NPR-A specific RGD peptide. Finally, we defined a possible role for the NPR-C through non-cGMP mechanisms in mediating the anti-proliferative actions of BNP in CFs where the NPR-C antagonist cANF 4-28 but not HS-142-1 blocked BNP-mediated inhibition of proliferation of CFs. We conclude that NPR-A interacts with components of the ECM such as FN to enhance BNP activation of cGMP and that a small NPR-A specific RGD peptide augments this action of BNP with possible therapeutic implications. Lastly, the NPR-C may also have a role in mediating anti-proliferative actions of BNP in CFs.
机译：心脏重构涉及的积累包括细胞外基质(ECM)的蛋白质纤连蛋白(FN)。在DDX绑定整合蛋白序列允许信号从ECM到细胞核。利钠肽受体(NPR-A)序列包含RGD和DDX序列。目前的调查的目标确定潜在的FN和之间的相互作用NPR-A cGMP的法国巴黎诱导培养人心脏成纤维细胞(CFs)。确定一个梅奥NPR-A具体设计RGD肽可以修改这种交互。我们确认这三个的存在利钠肽受体在慢性疲劳综合症(NPR)。镀在FN表现出明显的增加cGMP生产法国巴黎non-coated相比盘子。进一步的NPR-A特定RGD肽增强FN cGMP生产有关。hs - 142 - 1的NPR-A / B拮抗剂,废除了反应FN和NPR-A的法国巴黎特定的RGD肽。通过non-cGMP NPR-C的可能角色在调停anti-proliferative机制行动的法国CFs NPR-C拮抗剂cANF 4-28但不是BNP-mediated hs - 142 - 1阻塞慢性疲劳综合症的抑制增殖。NPR-A与ECM成分相互作用如加强法国激活cGMP, FN小NPR-A特定RGD肽增强这一行动的法国巴黎银行(BNP可能的治疗的影响。在调解anti-proliferative行动中的作用法国巴黎银行(BNP在慢性疲劳综合症。

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