CST1 promotes the proliferation and migration of PDGF‐BB‐treated airway smooth muscle cells via the PI3K/AKT signaling pathway

Abstract

Typically, airway remodeling caused by migration and proliferation of airway smooth muscle cells (ASMCs) plays a crucial role in the pathophysiological characteristics of asthma development. Cystatin 1 (CST1), a protein‐coding gene referred to as Cystatin SN, is highly expressed in asthma patients. However, the role of CST1 and related molecular mechanisms in the development of asthma remains to be explored. This study aims to investigate the role of CST1 in asthma progression and present related molecular mechanisms. To explore these aspects, human ASMCs with platelet‐derived growth factor BB (PDGF‐BB) are initially stimulated and applied as a cellular model of asthma. Further, CST1 is knocked down with small interfering ribose nucleic acid (siRNA) overexpressed with plasmids. Then, 5‐ethynyl‐2′‐deoxyuridine (EdU) and Cell Count Kit (CCK)‐8 assays are applied to assess the cell proliferation rates. Further, Transwell and Western blot analyses for migration of cells and expression of MMP1 and MMP9 proteins are assessed, respectively. Under PDGF‐BB stimulation, human ASMCs showed an increased CST1 expression, enhanced proliferation, and migration abilities, as well as up‐regulated PI3K/AKT signaling pathway. Further, knockdown or overexpression of CST1 presented the declined or enhanced proliferation, migration, and up‐regulation of the PI3K/AKT signaling pathway of human ASMCs. Inhibiting PI3K/AKT signaling pathway displayed the reduced migration and proliferation of human ASMCs. In summary, these findings indicated that CST1 played an essential role in the progression of asthma by activating the PI3K/AKT signaling pathway and promoting the migration and proliferation abilities of human ASMCs treated with PDGF‐BB.

Identification of the role of DAB2 and CXCL8 in uterine spiral artery remodeling in early-onset preeclampsia

“…However, pAKT expression differed between the CM-HTR-8/SVneo shDAB2 group and the CM-HTR-8/SVneo shNC with the CXCR1/2 group, indicating that other cytokines, except CXCL8, activate the PI3K pathway. A study on asthma revealed that activating the PI3K/AKT signaling pathway could promote the migration and proliferation of hVSMC [ 52 ]. Additionally, PDGF-ββ could activate phosphorylation of Akt and induce proliferation and migration of VSMCs [ 53 ].…”

Type 2 Cystatins and Their Roles in the Regulation of Human Immune Response and Cancer Progression

“…One study showed that CYS1 promotes the proliferation and migration of airway smooth muscle cells by activating the PI3K/AKT signaling pathway in an in vitro asthma model. This indicates that CYS1 participates in airway remodeling events and maybe a main contributor to asthma development [91].…”