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Publication

Excess neuropeptides in lung signal through endothelial cells to impair gas exchange.

Developmental cell | 2022

Although increased neuropeptides are often detected in lungs that exhibit respiratory distress, whether they contribute to the condition is unknown. Here, we show in a mouse model of neuroendocrine cell hyperplasia of infancy, a pediatric disease with increased pulmonary neuroendocrine cells (PNECs), excess PNEC-derived neuropeptides are responsible for pulmonary manifestations including hypoxemia. In mouse postnatal lung, prolonged signaling from elevated neuropeptides such as calcitonin gene-related peptide (CGRP) activate receptors enriched on endothelial cells, leading to reduced cellular junction gene expression, increased endothelium permeability, excess lung fluid, and hypoxemia. Excess fluid and hypoxemia were effectively attenuated by either prevention of PNEC formation, inactivation of CGRP gene, endothelium-specific inactivation of CGRP receptor gene, or treatment with CGRP receptor antagonist. Neuropeptides were increased in human lung diseases with excess fluid such as acute respiratory distress syndrome. Our findings suggest that restricting neuropeptide function may limit fluid and improve gas exchange in these conditions.

Pubmed ID: 35303432 RIS Download

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Associated grants

Agency: NHLBI NIH HHS, United States
Id: U01 HL148861
Agency: NHLBI NIH HHS, United States
Id: R01 HL157985
Agency: NHLBI NIH HHS, United States
Id: T32 HL134632
Agency: NHLBI NIH HHS, United States
Id: R01 HL085188
Agency: NHLBI NIH HHS, United States
Id: R01 HL146141
Agency: NHLBI NIH HHS, United States
Id: K24 HL143281
Agency: NHLBI NIH HHS, United States
Id: K24 HL132105
Agency: NIA NIH HHS, United States
Id: R01 AG063925
Agency: NHLBI NIH HHS, United States
Id: R35 HL140039
Agency: NHLBI NIH HHS, United States
Id: R01 HL154926
Agency: NHLBI NIH HHS, United States
Id: R01 HL148436

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RRID:SCR_002750

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RRID:SCR_021946

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