Faculty Collaboration Database

Impaired taurine transport contributes to bronchopulmonary dysplasia: a systems biology analysis. Am J Respir Cell Mol Biol 2026 Aug 01;74(8):1058-1072

Date

02/25/2026

Pubmed ID

41738245

DOI

10.1093/ajrcmb/aanag033

Scopus ID

2-s2.0-105046236328 (requires institutional sign-in at Scopus site)   1 Citation

Abstract

Metabolic dysregulation is implicated in the development of bronchopulmonary dysplasia (BPD). Taurine is an essential amino acid and a critical molecule in oxidative phosphorylation that mechanistically modulates angiogenesis. Using a neonatal hyperoxia model supported by metabolomic and single-cell RNA-seq analyses, we showed that insufficient taurine contributes to alveolar simplification in BPD. To model BPD, Sprague-Dawley rat pups were exposed to >90% oxygen. Plasma and lungs were obtained for multiomics. Pups received tunicamycin or tauroursodeoxycholic acid to study mechanisms that modulate taurine metabolism. Taurine was administered as rescue therapy after identifying its depletion in the BPD lungs. Genes and proteins of oxidative phosphorylation were enriched in BPD lungs, whereas complex I (C-I) activity was paradoxically decreased. The reduction of taurine and taurine-dependent C-I core subunits, NADH Dehydrogenase Subunits 5 and 6 (ND5, ND6), in BPD lungs explains this C-I paradox. The accompanying increase of plasma taurine in BPD pups indicates a decreased taurine transport, which can be explained by the reduced glycosylation and increased degradation of the taurine transporter. The results of complementary treatments with tunicamycin and tauroursodeoxycholic acid, indicate that endoplasmic reticulum stress contributes to impaired taurine transport in BPD rat lungs. Taurine treatment increased the expression of ND5 and ND6, the percentage of proliferating general capillary endothelial cells, and alveolar complexity in BPD lungs. Our multiomic approach reveals that taurine enhances endothelial resilience by activating the unfolded protein response, and might clinically benefit premature lungs. This represents a distinct antioxidant mechanism not previously characterized in hyperoxic lung injury.

Author List

Jing X, Wang Y, Roethle M, Jia S, Teng M, Konduri GG, Hessner MJ, Pritchard KA Jr, Day BW, Jin Y, Ma X, Naylor S, Lin CW, Gu H, Du J, Teng RJ

Authors

Martin J. Hessner PhD Professor in the Pediatrics department at Medical College of Wisconsin
Girija Ganesh Konduri MD Chief, Professor in the Pediatrics department at Medical College of Wisconsin
Chien-Wei Lin PhD Associate Professor in the Data Science Institute department at Medical College of Wisconsin
Kirkwood A. Pritchard PhD Professor in the Surgery department at Medical College of Wisconsin
Ru-Jeng Teng MD Professor in the Pediatrics department at Medical College of Wisconsin

MESH terms used to index this publication - Major topics in bold

Animals
Animals, Newborn
Biological Transport
Bronchopulmonary Dysplasia
Disease Models, Animal
Endoplasmic Reticulum Stress
Humans
Hyperoxia
Lung
Membrane Glycoproteins
Membrane Transport Proteins
Oxidative Phosphorylation
Rats
Rats, Sprague-Dawley
Systems Biology
Taurine
Taurochenodeoxycholic Acid