TAILIEUCHUNG - Báo cáo sinh học: " Plasmid-encoded NP73-102 modulates atrial natriuretic peptide receptor signaling and plays a critical role in inducing tolerogenic dendritic cells"

Tuyển tập các báo cáo nghiên cứu về sinh học được đăng trên tạp chí sinh học Journal of Biology đề tài: Plasmid-encoded NP73-102 modulates atrial natriuretic peptide receptor signaling and plays a critical role in inducing tolerogenic dendritic cells | Zhang et al. Genetic Vaccines and Therapy 2011 9 3 http content 9 1 3 GENETIC VACCINES AND THERAPY RESEARCH Open Access Plasmid-encoded NP73-102 modulates atrial natriuretic peptide receptor signaling and plays a critical role in inducing tolerogenic dendritic cells Weidong ZhangH Xueqin Cao2t Dongqing Chen1 Jia-wang Wang3 Hong Yang4 Wenshi Wang5 2 6 1 1 13 136 Subhra Mohapatra Gary Hellermann Xiaoyuan Kong Richard F Lockey Shyam S Mohapatra Abstract Background Atrial natriuretic peptide ANP is an important endogenous hormone that controls inflammation and immunity by acting on dendritic cells DCs however the mechanism remains unclear. Objective We analyzed the downstream signaling events resulting from the binding of ANP to its receptor NPRA and sought to determine what aspects of this signaling modulate DC function. Methods We utilized the inhibitory peptide NP73-102 to block NPRA signaling in human monocyte-derived DCs hmDCs and examined the effect on DC maturation and induced immune responses. The potential downstream molecules and interactions among these molecules involved in NPRA signaling were identified by immunoprecipitation and immunoblotting. Changes in T cell phenotype and function were determined by flow cytometry and BrdU proliferation ELISA. To determine if adoptively transferred DCs could alter the in vivo immune response bone marrow-derived DCs from wild-type C57BL 6 mice were incubated with ovalbumin OVA and injected . into C57BL 6 NPRA- - knockout mice sensitized and challenged with OVA. Lung sections were stained and examined for inflammation and cytokines were measured in bronchoalveolar lavage fluid collected from parallel groups of mice. Results Inhibition of NPRA signaling in DCs primes them to induce regulatory T cells. Adoptive transfer of wild type DCs into NPRA- - mice reverses the attenuation of lung inflammation seen in the NPRA-knockout model. NPRA is associated with TLR-2 SOCS3 and STAT3 and inhibiting NPRA .

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