Tag: proliferation

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MiR-23b controls TGF-?1 induced airway smooth muscle cell proliferation via TGF?R2/p-Smad3 signals.

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MiR-23b controls TGF-?1 induced airway smooth muscle cell proliferation via TGF?R2/p-Smad3 signals.

Mol Immunol. 2015 Dec 31;70:84-93

Authors: Chen M, Huang L, Zhang W, Shi J, Lin X, Lv Z, Zhang W, Liang R, Jiang S

Abstract
BACKGROUND: Abnormal proliferation of ASM (airway smooth muscle) directly contributes to the airway remodeling during development of lung diseases such as asthma. Here we report that a specific microRNA (miR-23b) controls ASMCs proliferation through directly inhibiting TGF?R2/p-Smad3 pathway.
METHODS: The expression of miR-23b in ASMCs was detected by quantitative real-time polymerase chain reaction (RT-PCR). The effects of miR-23b on cell proliferation and apoptosis of ASMCs were assessed by transient transfection of miR-23b mimics and inhibitor. The target gene of miR-23b and the downstream pathway were further investigated.
RESULTS: Overexpression of miR-23b significantly inhibited TGF-?1-induced ASMCs proliferation and promoted apoptosis. RT-PCR and Western blotting analysis showed miR-23b negatively regulates the expression of TGF?R2 and p-Smad3 in ASMCs. Subsequent analyses demonstrated that TGF?R2 was a direct and functional target of miR-23b, which was validated by the dual luciferase reporter assay.
CONCLUSIONS: MiR-23b may function as an inhibitor of airway smooth muscle cells proliferation through inactivation of TGF?R2/p-Smad3 pathway.

PMID: 26748386 [PubMed – as supplied by publisher]

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Apigenin inhibits TGF-?1-induced proliferation and migration of airway smooth muscle cells.

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Apigenin inhibits TGF-?1-induced proliferation and migration of airway smooth muscle cells.

Int J Clin Exp Pathol. 2015;8(10):12557-63

Authors: Li LH, Lu B, Wu HK, Zhang H, Yao FF

Abstract
It is well known that the proliferation and migration of ASM cells (ASMCs) plays an important role in the pathogenesis of airway remodeling in asthma. Previous studies reported that apigenin can inhibit airway remodeling in a mouse asthma model. However, its effects on the proliferation and migration of ASMCs in asthma remain unknown. Therefore, the aim of our present study was to investigate the effects of apigenin on ASMC proliferation and migration, and explore the possible molecular mechanism. We found that apigenin inhibited transforming growth factor-?1 (TGF-?1)-induced ASMC proliferation. The cell cycle was blocked at G1/S-interphase by apigenin. It also suppressed TGF-?1-induced ASMCs migration. Furthermore, apigenin inhibited TGF-?1-induced Smad 2 and Smad 3 phosphorylation in ASMCs. Taken together, these results suggested that apigenin inhibited the proliferation and migration of TGF-?1-stimulated ASMCs by inhibiting Smad signaling pathway. These data might provide useful information for treating asthma and show that apigenin has potential for attenuating airway remodeling.

PMID: 26722444 [PubMed – in process]

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Concomitant inhibition of primary equine bronchial fibroblast proliferation and differentiation by selective ?2-adrenoceptor agonists and dexamethasone.

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Concomitant inhibition of primary equine bronchial fibroblast proliferation and differentiation by selective ?2-adrenoceptor agonists and dexamethasone.

Eur J Pharmacol. 2014 Aug 13;

Authors: Franke J, Abraham G

Abstract
Altered airway cell proliferation plays an important role in the pathogenesis of human bronchial asthma and chronic obstructive pulmonary disease (COPD) as well as the equine recurrent airway obstruction (RAO) with consistent changes, i.e. narrowing the airway wall, explained by proliferation and differentiation of fibroblasts. In permanent cell lines, it has been suggested that ?2-adrenoceptor agonists and glucocorticoids regulate cell proliferation via the ?2-adrenoceptor pathway; indeed, no study was carried out in fresh isolated primary equine bronchial fibroblasts (EBF). We characterized the ?-adrenoceptors in EBF, and compared effects of long-acting (clenbuterol) and short-acting (salbutamol, isoproterenol) ?2-agonists and dexamethasone on proliferation, differentiation and collagen synthesis. High density (Bmax; 5037±494 sites/cell) of ?2-adrenoceptor subtype was expressed in EBF. ?2-agonists inhibited concentration-dependently EBF proliferation with potency of clenbuterol>salbutamol l» isoproterenol which was inhibited by ICI 118.551 and propranolol but not by CGP 20712A. In contrast, dexamethasone alone inhibited less EBF proliferation, but the effect was high when dexamethasone was combined with ?2-agonists. Transforming growth factor-?1 (TGF-?1) increased transformation of fibroblasts into myofibroblasts, and which was inhibited by clenbuterol and dexamethasone alone and drug combination resulted in high inhibition rate. Collagen synthesis in EBF was rather hampered by dexamethasone than by ?-agonists. Collectively, the expression of ?2-adrenoceptor subtype in EBF and the anti-proliferative effect of clenbuterol suggest that ?2-adrenoceptors are growth inhibitory and anti-fibrotic in EBF. These ?2-agonist effects in EBF were synergistically enhanced by dexamethasone, providing the additive effects of glucocorticoids to counteract airway remodelling and morbidity of asthma and RAO.

PMID: 25128704 [PubMed – as supplied by publisher]

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[Effect of peroxisome proliferator-activated receptor-gamma on proliferation of airway smooth muscle cells in mice with asthma].

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[Effect of peroxisome proliferator-activated receptor-gamma on proliferation of airway smooth muscle cells in mice with asthma].

Zhongguo Dang Dai Er Ke Za Zhi. 2013 Jul;15(7):583-7

Authors: Gu MX, Liu XC, Jiang L

Abstract
OBJECTIVE: To investigate the effects of peroxisome proliferator-activated receptor-gamma (PPAR?) agonist rosiglitazone on the expression of cyclin D1 in lung tissue, and the proliferation of airway smooth muscle cells (ASMCs) in mice with bronchial asthma.
METHODS: Thirty clean BALB/c mice were randomly divided into control group (n=10), asthma group (n=10), and rosiglitazone treatment group (n=10). A mouse model of asthma was established by ovalbumin (OVA) sensitization and challenge. The treatment group received rosiglitazone (5 mg/kg) by gavage 1 hour before each challenge and the control group received saline instead of OVA sensitization and challenge. Leukocytes and eosinophils in bronchoalveolar lavage fluid (BALF) were counted under a microscope. Airway structural changes were observed by hematoxylin-eosin staining. Protein and mRNA expression levels of cyclin D1 were measured by immunohistochemical staining and RT-PCR. Perimeter of the basement membrane (Pbm), total bronchial wall area (WAt), airway smooth muscle area (WAm), and number of nuclei in ASMCs (N) were determined using image analysis software, and WAt/Pbm, WAm/Pbm, and N/Pbm were calculated.
RESULTS: Compared with the control group, the asthma group showed significant increases in the total number of leukocytes and percentage of eosinophils in BALF, as well as in the mRNA and protein expression of cyclin D1, but changes in these indices were significantly reduced in the rosiglitazone treatment group (P<0.05). In addition, compared with the control group, the asthma group had significantly increased WAt/Pbm, WAm/Pbm, and N/Pbm, but rosiglitazone significantly decreased these ratios (P<0.05).
CONCLISONS: Rosiglitazone may delay the process of airway remodeling by inhibiting the proliferation of ASMCs, so it can be used for preventing and treating chronic asthma.

PMID: 23866284 [PubMed – in process]

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Inflammation signals airway smooth muscle cell proliferation in asthma … – 7thSpace Interactive (press release)

Inflammation signals airway smooth muscle cell proliferation in asthma …
7thSpace Interactive (press release)
It is now well recognized that chronic inflammation, as well as airway hyper-responsiveness and remodeling of airway during inflammation, are crucial to asthma. ASM is caused by increased cell proliferation or by hypertrophy of ASM cells depending on …

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