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首页> 外文期刊>American Journal of Physiology >Constitutive activation of prosurvival signaling in alveolar mesenchymal cells isolated from patients with nonresolving acute respiratory distress syndrome.
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Constitutive activation of prosurvival signaling in alveolar mesenchymal cells isolated from patients with nonresolving acute respiratory distress syndrome.

机译：从非解决性急性呼吸窘迫综合征患者中分离出的肺泡间充质细胞中生存信号的本构激活。

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Acute respiratory distress syndrome (ARDS) is a clinical syndrome characterized by stereotypic host inflammatory and repair cellular responses; however, mechanisms regulating the resolution of ARDS are poorly understood. Here, we report the isolation and characterization of a novel population of mesenchymal cells from the alveolar space of ARDS patients via fiber-optic bronchoscopy with bronchoalveolar lavage (BAL). BAL was performed on 17 patients during the course of ARDS. Immunofluorescence staining and multiparameter flow cytometric analysis defined a population of alveolar mesenchymal cells (AMCs) that are CD45-/prolyl-4-hydroxylase+/alpha-smooth muscle actin+/-. AMCs proliferated in ex vivo cell culture for multiple passages; early passage (3-5) cells were subsequently analyzed in 13 patients. AMCs isolated from patients with persistent or nonresolving ARDS (ARDS-NR, n = 4) demonstrate enhanced constitutive activation of prosurvival signaling pathways involving PKB/Akt, FKHR, and BCL-2 family proteins compared with AMCs from patients with resolving ARDS (ARDS-R, n = 9). Exogenous transforming growth factor-beta1 markedly induces PKB/Akt activation in AMCs from ARDS-R. ARDS-NR cells are more resistant to serum deprivation-induced apoptosis compared with ARDS-R. This study identifies a novel population of mesenchymal cells that can be isolated from the alveolar spaces of ARDS patients. AMCs in patients with ARDS-NR acquire an activational profile characterized by enhanced prosurvival signaling and an antiapoptotic phenotype. These findings support the concept that apoptosis of mesenchymal cells may be an essential component of normal repair and resolution of ARDS and suggest that dysregulation of this process may contribute to persistent ARDS.
机译：急性呼吸窘迫综合征（ARDS）是一种临床综合征，其特征是定型的宿主发炎并修复细胞反应。然而，人们对调节ARDS分辨率的机制知之甚少。在这里，我们报告通过纤维支气管镜与支气管肺泡灌洗（BAL）从ARDS患者的肺泡腔中分离和表征新型间充质细胞。在ARDS过程中对17例患者进行了BAL。免疫荧光染色和多参数流式细胞术分析定义了肺泡间充质细胞（AMC）的群体，其为CD45- /脯氨酰-4-羟化酶+ /α-平滑肌肌动蛋白+/-。 AMC在离体细胞培养物中增殖多次传代;随后在13例患者中分析了早期传代（3-5）细胞。从患有持续性或非解决性ARDS（ARDS-NR，n = 4）的患者中分离出的AMCs证明，与来自解决性ARDS（ARDS-NR）患者的AMCs相比，涉及PKB / Akt，FKHR和BCL-2家族蛋白的生存信号通路的组成性激活增强。 R，n = 9）。外源转化生长因子β1显着诱导ARDS-R的AMC中的PKB / Akt激活。与ARDS-R相比，ARDS-NR细胞对血清剥夺诱导的凋亡具有更高的抵抗力。这项研究确定了可以从ARDS患者的肺泡腔中分离的新的间充质细胞群体。 ARDS-NR患者的AMC具有激活特征，其特征是生存信号增强和抗凋亡表型。这些发现支持了间充质细胞凋亡可能是ARDS正常修复和消退的重要组成部分的观点，并表明该过程的失调可能导致持久性ARDS。

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