Regulatory roles of NAT10 in airway epithelial cell function and metabolism in pathological conditions

Zheng, Nannan; Liu, Xuanqi; Yang, Ying; Liu, Yifei; Yan, Furong; Zeng, Yiming; Cheng, Yunfeng; Wu, Duojiao; Chen, Chengshui; Wang, Xiangdong

doi:10.1007/s10565-022-09743-z

Cited by 2 publications

(3 citation statements)

References 45 publications

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“…Cigarettes were combusted using a modified 50 mL syringe apparatus, in the presence of 5 mL of RPMI‐1640 medium devoid of serum. The quality of CSE was assessed by quantifying the absorbance value at a wavelength of 320λ (1.158), as reported previously 2,3,19 …”

Section: Methodsmentioning

confidence: 99%

“…The quality of CSE was assessed by quantifying the absorbance value at a wavelength of 320λ (1.158), as reported previously. 2 , 3 , 19 …”

Section: Methodsmentioning

confidence: 99%

“…Smoking is one of the common and critical factors for the induction and development of COPD and activates the interactions amongst multiple lung cells 1,2 . The airway epithelial cells serve as the initial defense separating the tissue microenvironment from the external environment, the primary receptors to face and bind the pathogens, and as the secondary inducer to result in localised and systemic inflammation, pulmonary dysfunction, and tissue impairment in COPD, as a prominent characteristic of the disease 3–5 . In addition, lung epithelial cells play crucial roles in preserving lung function and alveolar structures and are the main source to generate potential targets for therapeutic interventions to reduce inflammation and remodelling in COPD.…”

Section: Introductionmentioning

confidence: 99%

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Roles of glutamic pyruvate transaminase 2 in reprogramming of airway epithelial lipidomic and metabolomic profiles after smoking

Yan,

Zhang,

Duan

et al. 2024

Clinical & Translational Med

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Metabolic abnormalities represent one of the pathological features of chronic obstructive pulmonary disease (COPD). Glutamic pyruvate transaminase 2 (GPT2) is involved in glutamate metabolism and lipid synthesis pathways, whilst the exact roles of GPT2 in the occurrence and development of COPD remains uncertain. This study aims at investigating how GPT2 and the associated genes modulate smoking‐induced airway epithelial metabolism and damage by reprogramming lipid synthesis. The circulating or human airway epithelial metabolomic and lipidomic profiles of COPD patients or cell‐lines explored with smoking were assessed to elucidate the pivotal roles of GPT2 in reprogramming processes. We found that GPT2 regulate the reprogramming of lipid metabolisms caused by smoking, especially phosphatidylcholine (PC) and triacylglycerol (TAG), along with changes in the expression of lipid metabolism‐associated genes. GPT2 modulated cell sensitivities and survival in response to smoking by enhancing mitochondrial functions and maintaining lipid and energy homeostasis. Our findings provide evidence for the involvement of GPT2 in the reprogramming of airway epithelial lipids following smoking, as well as the molecular mechanisms underlying GPT2‐mediated regulation, which may offer an alternative of therapeutic strategies for chronic lung diseases.

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Section: Methodsmentioning

confidence: 99%

“…The quality of CSE was assessed by quantifying the absorbance value at a wavelength of 320λ (1.158), as reported previously. 2 , 3 , 19 …”

Section: Methodsmentioning

confidence: 99%