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Nicotine-induced ER Stress and ASM Cell Proliferation is Mediated by α7nAChR and Chaperones-RIC-3 and TMEM35.
Borkar, Niyati A; Thompson, Michael A; Kelley, Brian; Shiferaw, Barnabas T; Hamrick, Samantha K; Venkatachalem, Sathish; Prakash, Y S; Pabelick, Christina M.
Afiliación
  • Borkar NA; Mayo Clinic, Department of Anesthesiology, Rochester, Minnesota, United States.
  • Thompson MA; Mayo Clinic, Department of Anesthesiology, Rochester, Minnesota, United States.
  • Kelley B; Mayo Clinic, Department of Anesthesiology, Rochester, Minnesota, United States.
  • Shiferaw BT; University of Wisconsin-Madison, School of Medicine and Public Health, Madison, Wisconsin, United States.
  • Hamrick SK; Mayo Clinic, Anesthesiology, Rochester, Minnesota, United States.
  • Venkatachalem S; North Dakota State University, Pharmaceutical Sciences, School of Pharmacy, College of Health Professions, Fargo, North Dakota, United States.
  • Prakash YS; Mayo Clinic, Department of Anesthesiology and Perioperative Medicine, Department of Physiology and Biomedical Engineering, Rochester, Minnesota, United States.
  • Pabelick CM; Mayo Clinic, Department of Anesthesiology, Rochester, Minnesota, United States.
Am J Respir Cell Mol Biol ; 2024 Sep 05.
Article en En | MEDLINE | ID: mdl-39236288
ABSTRACT
Nicotine exposure in the context of smoking or vaping worsens airway function. Although commonly thought to exert effects through the peripheral nervous system, we previously showed airway smooth muscle (ASM) expresses nicotinic acetylcholine receptors (nAChRs), particularly alpha7 subtype (α7nAChR) with functional effects on contractility and metabolism. However, the mechanisms of nAChR regulation and downstream effects in ASM are not fully understood. Using human ASM cells from non-asthmatics vs. mild-moderate asthmatics, we tested the hypothesis that nAChR-specific ER chaperones RIC-3 and TMEM35 promote cell surface localization of α7nAChR with downstream influence on its functionality effects exacerbated by inflammation. We found that mild-moderate asthma and exposure to pro-inflammatory cytokines relevant to asthma promote chaperone and α7nAChR expression in ASM. Downstream, ER stress was linked to nicotine/α7nAChR signaling, where RIC-3 and TMEM35 regulate nicotine-induced ER stress, Ca2+ regulation and ASM cell proliferation. Overall, our data highlights the importance α7nAChR chaperones in mediating and modulating nicotine effects in ASM towards airway contractility and remodeling.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Am J Respir Cell Mol Biol Asunto de la revista: BIOLOGIA MOLECULAR Año: 2024 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Am J Respir Cell Mol Biol Asunto de la revista: BIOLOGIA MOLECULAR Año: 2024 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos