Deformation-induced ATP release from red blood cells requires CFTR activity
Deformation-induced ATP release from red blood cells requires CFTR activity
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DOI：
10.1152/ajpheart.1998.275.5.h1726
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发表时间：
1998-11-01
影响因子：
4.8
通讯作者：
Lonigro, AJ
中科院分区：
文献类型：
--
作者：
Sprague, RS;Ellsworth, ML;Lonigro, AJ
最近，有报道称兔和人红细胞(RBC)在机械变形时会释放三磷酸腺苷。在这里，我们研究了囊性纤维化跨膜电导调节器(CFTR)的活性，它是ATP结合盒的成员，是变形诱导的红细胞释放ATP所必需的。用两种CFTR活性抑制剂格列本脲(10 MU M)或尼氟米酸(20 MU M)孵育兔红细胞，可抑制变形诱导的ATP释放。为了证明CFTR在变形诱导的人红细胞释放ATP中的作用，研究了正常人、囊性纤维化(CF)患者或与囊性纤维化无关的慢性阻塞性肺疾病(COPD)患者的细胞。健康人和COPD患者的红细胞在机械变形时释放三磷酸腺苷。相反，CF患者的红细胞变形不会导致ATP的释放。我们的结论是，变形诱导的兔和人红细胞释放ATP需要CFTR活性，这表明CFTR在调节血管阻力方面发挥了先前未知的作用。
Recently, it was reported that rabbit and human red blood cells (RBCs) release ATP in response to mechanical deformation. Here we investigate the hypothesis that the activity of the cystic fibrosis transmembrane conductance regulator (CFTR), a member of the ATP binding cassette, is required for deformation-induced ATP release from RBCs. Incubation of rabbit RBCs with either of two inhibitors of CFTR activity, glibenclamide (10 mu M) or niflumic acid (20 mu M), resulted in inhibition of deformation-induced ATP release. To demonstrate the contribution of CFTR to deformation-induced ATP release from human RBCs, cells from healthy humans, patients with cystic fibrosis (CF), or patients with chronic obstructive lung disease (COPD) unrelated to CF were studied. RBCs of healthy humans and COPD patients released ATP in response to mechanical deformation. In contrast, deformation of RBCs from patients with CF did not result in ATP release. We conclude that deformation-induced ATP release from rabbit and human RBCs requires CFTR activity, suggesting a previously unrecognized role for CFTR in the regulation of vascular resistance.