转化生长因子β1在气道平滑肌扩张中的作用：是否需要成纤维细胞生长因子-2
2010/08/11
支气管/细支气管周围支气管平滑肌（ASM）组织扩张是哮喘患者气道重构的一个特征，而且在哮喘患者肺阻力增加和气道高反应性中起到了重要作用。研究发现多效性细胞因子TGF-β1参与了哮喘患者的气道重构，而且影响了许多类型细胞的生长。TGF-β1表达和信号传导的增加及ASM生长的增加也常伴随出现在哮喘动物模型中。诸多研究也证实了上述联系，而且旨在减少或抑制TGF-β1过表达/细胞传导的策略则有助于减少或预防ASM扩大。近期的研究显示，TGF-β1过表达/信号与ASM组织过度生长之间存在直接联系。为确证述联系，许多研究者通过体外培养ASM细胞，评价TGF-β1对细胞增生和/或肥大的影响。体内外试验结果存在不一致性，体外结果认为TGF-β1对ASM的影响与环境条件相关。体内试验认为TGF-β1是哮喘患者ASM扩大所必须的，而体外试验未得到证实。在本文的结尾，提出了一个有关成纤维细胞生长因子-2的假说，该假说有助于将体内外试验的不一致性进行统一。
（刘国梁 审校）
Clin Exp Allergy. 2010 May;40(5):710-724.
Transforming growth factor-beta1 in asthmatic airway smooth muscle enlargement: is fibroblast growth factor-2 required?
Bossé Y, Stankova J, Rola-Pleszczynski M.
The James Hogg iCAPTURE Centre for Cardiovascular and Pulmonary Research, Department of Medicine, Respiratory Division, University of British Columbia, Vancouver, BC, Canada. ybosse@mrl.ubc.ca
Abstract
Enlargement of airway smooth muscle (ASM) tissue around the bronchi/bronchioles is a histopathological signature of asthmatic airway remodelling and has been suggested to play a critical role in the increased lung resistance and airway hyperresponsiveness seen in asthmatic patients. The pleiotropic cytokine, TGF-beta1, is believed to contribute to several aspects of asthmatic airway remodelling and is known to influence the growth of many cell types. Increased TGF-beta1 expression/signalling and ASM growth have been shown to occur concurrently in animal models of asthma. Abundant studies further substantiate this association by showing that therapeutic strategies that reduce or prevent TGF-beta1 overexpression/signalling lead to a parallel decrease or prevention of ASM enlargement. Finally, recent findings have supported a direct link of causality between TGF-beta1 overexpression/signalling and the overgrowth of ASM tissue. To follow-up on these in vivo studies, many investigators have pursued detailed investigation of ASM in cell culture conditions, assessing the direct role of TGF-beta1 on cellular proliferation and/or hypertrophy. Inconsistencies among the in vitro studies suggest that the effect of TGF-beta1 on ASM cell proliferation/hypertrophy is contextual. A hypothesis focusing on fibroblast growth factor-2 is presented at the end of this review, which could potentially reconcile the apparent discrepancy between the conflicting in vitro findings with the consistent in vivo finding that TGF-beta1 is required for ASM enlargement in asthma.
Clin Exp Allergy. 2010 May;40(5):710-24.
（刘国梁 审校）
Clin Exp Allergy. 2010 May;40(5):710-724.
Transforming growth factor-beta1 in asthmatic airway smooth muscle enlargement: is fibroblast growth factor-2 required?
Bossé Y, Stankova J, Rola-Pleszczynski M.
The James Hogg iCAPTURE Centre for Cardiovascular and Pulmonary Research, Department of Medicine, Respiratory Division, University of British Columbia, Vancouver, BC, Canada. ybosse@mrl.ubc.ca
Abstract
Enlargement of airway smooth muscle (ASM) tissue around the bronchi/bronchioles is a histopathological signature of asthmatic airway remodelling and has been suggested to play a critical role in the increased lung resistance and airway hyperresponsiveness seen in asthmatic patients. The pleiotropic cytokine, TGF-beta1, is believed to contribute to several aspects of asthmatic airway remodelling and is known to influence the growth of many cell types. Increased TGF-beta1 expression/signalling and ASM growth have been shown to occur concurrently in animal models of asthma. Abundant studies further substantiate this association by showing that therapeutic strategies that reduce or prevent TGF-beta1 overexpression/signalling lead to a parallel decrease or prevention of ASM enlargement. Finally, recent findings have supported a direct link of causality between TGF-beta1 overexpression/signalling and the overgrowth of ASM tissue. To follow-up on these in vivo studies, many investigators have pursued detailed investigation of ASM in cell culture conditions, assessing the direct role of TGF-beta1 on cellular proliferation and/or hypertrophy. Inconsistencies among the in vitro studies suggest that the effect of TGF-beta1 on ASM cell proliferation/hypertrophy is contextual. A hypothesis focusing on fibroblast growth factor-2 is presented at the end of this review, which could potentially reconcile the apparent discrepancy between the conflicting in vitro findings with the consistent in vivo finding that TGF-beta1 is required for ASM enlargement in asthma.
Clin Exp Allergy. 2010 May;40(5):710-24.
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