Mechanism of bronchoprotective effects of a novel natriuretic hormone peptide☆

Hellermann, Gary; Kong, Xiaoyuan; Gunnarsdottir, Johanna; Juan, Homero San; Singam, Raji; Behera, Sumita; Zhang, Weidong; Lockey, Richard F.; Mohapatra, Shyam S.

doi:10.1016/j.jaci.2003.10.009

Cited by 17 publications

(14 citation statements)

References 45 publications

(43 reference statements)

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“…This peptide was overexpressed in A549 alveolar type II and normal human bronchial epithelial cells to get an insight into the mechanism, and results showed increases in the intracellular Ca ++ release and release of NO by activation of constitutive nitric oxide synthase (NOS). 72 This is similar to ANP's effects on murine macrophages, which also results in increased intracellular calcium and inhibition of the inducible isoform of NOS. 67 Extracellular Ca ++ has been reported to affect eosinophil migration, 67 to affect IL-9 expression and mucus production, 73 and to represses inducible NOS in macrophages through destabilization of its mRNA.…”

Section: Mechanisms Of Np-mediated Protection Anpmentioning

confidence: 69%

Natriuretic peptides and genesis of asthma: An emerging paradigm?☆

Mohapatra

Lockey

Vesely

et al. 2004

Journal of Allergy and Clinical Immunology

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Section: Mechanisms Of Np-mediated Protection Anpmentioning

confidence: 69%

Natriuretic peptides and genesis of asthma: An emerging paradigm?☆

Mohapatra

Lockey

Vesely

et al. 2004

Journal of Allergy and Clinical Immunology

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“…In fact, ANP administration determines anti-inflammatory effects in airway epithelial cells [48], playing important roles in modulating inflammatory response. In consideration of such ANP anti-inflammatory action, we speculate that the observed TNF- α -induced ANP down-regulation could concur in enhancing an inflammatory status.…”

Section: Discussionmentioning

confidence: 99%

TNF-αRegulates Natriuretic Peptides and Aquaporins in Human Bronchial Epithelial Cells BEAS-2B

Mezzasoma

Cagini

Antognelli

et al. 2013

Mediators of Inflammation

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Postoperative-fluid retention is a severe complication frequently reported in patients undergoing major surgical procedures. The complex network of molecules involved in such a severe surgery-induced condition remains poorly understood. Inflammation has been proposed among the various causes of fluid retention. Since TNF-α is one of the main proinflammatory cytokine initially released after major surgery, it is reasonable to assume its involvement in fluid overload. Here, we showed that TNF-α selectively regulates key molecules involved in fluids balance, such as natriuretic peptides (NPs) and aquaporins, in human bronchial epithelial cells BEAS-2B. In particular, we found that TNF-α induced a decrease of arial natriuretic peptide, natriuretic peptide receptor-1, aquaporin-1 and aquaporin-5 and an increase of brain natriuretic peptide with a different involvement of nuclear factor-κB and mitogen-activated protein kinases signaling pathway activation. Moreover, the observed changes in NPs expression, demonstrate inflammation as an additional cause of brain natriuretic peptide elevation, adding an important piece of information in the novel area of study regarding NPs and inflammation. Finally, we suggest that inflammation is one of the mechanisms of Aquaporin-1 and aquaporin-5 expression regulation. Therefore, in this exploratory study, we speculate that TNF-α might be involved in postoperative-fluid retention related to major surgery.

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“…Previously, we reported that an NH 2 -terminal ANP prohormone peptide comprising residues 73 to 102 (NP73-102) significantly inhibits activation of several proinflammatory transcription factors, including nuclear factor-nB (NF-nB), activator protein 1 and Erk-1,2, in human bronchial epithelial adenocarcinoma A549 cells (20,21). Because these transcription factors augment the local inflammatory milieu, it was reasoned that NPRA signaling plays a role in and promotes tumorigenesis.…”

Section: Introductionmentioning

confidence: 99%

Natriuretic Peptide Receptor A as a Novel Anticancer Target

Kong¹,

Wang

et al. 2008

Cancer Research

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The receptor for atrial natriuretic peptide (ANP), natriuretic peptide receptor A (NPRA), is expressed in cancer cells, and natriuretic peptides have been implicated in cancers. However, the direct role of NPRA signaling in tumorigenesis remains elusive. Here, we report that NPRA expression and signaling is important for tumor growth. NPRA-deficient mice showed significantly reduced antigen-induced pulmonary inflammation. NPRA deficiency also substantially protected C57BL/6 mice from lung, skin, and ovarian cancers. Furthermore, a nanoparticle-formulated interfering RNA for NPRA attenuated B16 melanoma tumors in mice. Ectopic expression of a plasmid encoding NP73-102, the NH 2 -terminal peptide of the ANP prohormone, which down-regulates NPRA expression, also suppressed lung metastasis of A549 cells in nude mice and tumorigenesis of Line 1 cells in immunocompetent BALB/c mice. The antitumor activity of NP73-102 was in part attributed to apoptosis of tumor cells. Western blot and immunohistochemistry staining indicated that the transcription factor, nuclear factor-KB, was inactivated, whereas the level of tumor suppressor retinoblastoma protein was upregulated in the lungs of NPRA-deficient mice. Furthermore, expression of vascular endothelial growth factor was downregulated in the lungs of NPRA-deficient mice compared with that in wild-type mice. These results suggest that NPRA is involved in tumor angiogenesis and represents a new target for cancer therapy. [Cancer Res 2008;68(1):249-56]

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Mechanism of bronchoprotective effects of a novel natriuretic hormone peptide☆

Cited by 17 publications

References 45 publications

Natriuretic peptides and genesis of asthma: An emerging paradigm?☆

Natriuretic peptides and genesis of asthma: An emerging paradigm?☆

TNF-αRegulates Natriuretic Peptides and Aquaporins in Human Bronchial Epithelial Cells BEAS-2B

Natriuretic Peptide Receptor A as a Novel Anticancer Target

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