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<p>Airway remodeling is one of the hallmarks of asthma in which the dysregulation of airway smooth muscle cells (ASMCs) plays a part. However, the role of LAPTM5 in asthma is largely yet to be elucidated. In this study, the expression of LAPTM5 in ASMCs from the asthmatics and non-asthmatics was inspected using a publicly available dataset. The expression of LAPTM5 was next examined in ASMCs challenged by platelet-derived growth factor (PDGF). The establishment of LAPTM5 knockdown ASMCs was conducted with small interference RNA, and the proliferation, migration, and extracellular matrix production of ASMCs in the presence of PDGF were further determined. The activation of MAPK signaling was detected with western blot in LAPTM5 knockdown or overexpression ASMCs. Two MAPKs inhibitors, SB203580 and U0126, were employed to investigate the effects of MAPKs blockade on the proliferation, migration, and extracellular matrix production on LAPTM5-overexpressed ASMCs. The results revealed that the overexpression of LAPTM5 in the ASMCs of the asthmatics, and the knockdown of LAPTM5 in ASMCs suppressed PDGF-induced proliferation, migration, and extracellular matrix production. Furthermore, phosphor-p38 and -ERK enhanced by PDGF were reduced by LAPTM5 ablation. Pharmacal inhibition of MAPKs effectively abrogated the dysregulation of ASMCs induced by LAPTM5 overexpression in the presence of PDGF. Collectively, the expression of LAPTM5 is closely associated with the dysregulation of ASMCs and the consequent airway remodeling, and we proposed that LAPTM5 is a potential therapeutic target in asthma.</p>

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LAPTM5 potentiates airway remodeling by regulating MAPKs-mediated airway smooth muscle cells’ dysfunction

  • 期刊论文

  • 发表日期：

    2026年2月16日

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  • Lijiao Jiang,
  • Yaping Ying,
  • Haihong Jin,
  • Tingmin Zhou

摘要

Airway remodeling is one of the hallmarks of asthma in which the dysregulation of airway smooth muscle cells (ASMCs) plays a part. However, the role of LAPTM5 in asthma is largely yet to be elucidated. In this study, the expression of LAPTM5 in ASMCs from the asthmatics and non-asthmatics was inspected using a publicly available dataset. The expression of LAPTM5 was next examined in ASMCs challenged by platelet-derived growth factor (PDGF). The establishment of LAPTM5 knockdown ASMCs was conducted with small interference RNA, and the proliferation, migration, and extracellular matrix production of ASMCs in the presence of PDGF were further determined. The activation of MAPK signaling was detected with western blot in LAPTM5 knockdown or overexpression ASMCs. Two MAPKs inhibitors, SB203580 and U0126, were employed to investigate the effects of MAPKs blockade on the proliferation, migration, and extracellular matrix production on LAPTM5-overexpressed ASMCs. The results revealed that the overexpression of LAPTM5 in the ASMCs of the asthmatics, and the knockdown of LAPTM5 in ASMCs suppressed PDGF-induced proliferation, migration, and extracellular matrix production. Furthermore, phosphor-p38 and -ERK enhanced by PDGF were reduced by LAPTM5 ablation. Pharmacal inhibition of MAPKs effectively abrogated the dysregulation of ASMCs induced by LAPTM5 overexpression in the presence of PDGF. Collectively, the expression of LAPTM5 is closely associated with the dysregulation of ASMCs and the consequent airway remodeling, and we proposed that LAPTM5 is a potential therapeutic target in asthma.