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Nitric oxide inhibits hypoxia‐induced impairment of human RBC deformability through reducing the cross‐linking of membrane protein band 3
Author(s) -
Zhao Yajin,
Wang Xiang,
Wang Ruofeng,
Chen Dong,
Noviana Milody,
Zhu Hongliang
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.27359
Subject(s) - hypoxia (environmental) , nitric oxide , sodium nitroprusside , chemistry , methemoglobin , nitric oxide synthase , band 3 , hemoglobin , red blood cell , medicine , biochemistry , endocrinology , pharmacology , membrane , oxygen , erythrocyte membrane , organic chemistry
Aim Nitric oxide (NO) prevents the decline of RBC deformability under high altitude and other ischemic and hypoxic conditions, but the clear mechanisms remain unknown. Here, we have carried out a systematic study to find the mechanisms of NO‐induced regulation of RBC deformability under hypoxia. Methods NO levels, RBCs membrane elongation index (EI), membrane protein band 3 methemoglobin (MetHb) were determined during hypoxia (0 to 120 minutes). To validate the role of NO in regulating RBC deformability, tests were also performed with a NO donor (sodium nitroprusside) or a NO synthase inhibitor ( l ‐nitro‐arginine methylester) under 60 minutes hypoxia. Results Hypoxia for 45 minutes increased NO levels from 25.65 ± 1.95 to 35.26 ± 2.01 μmol/L, and there was a plateau after 60 minutes hypoxia. The EI did not change before 45 minutes hypoxia, but decreased from 0.567 ± 0.019 to 0.409 ± 0.042 (30 Pa) after 60 minutes hypoxia. The cross‐linking of band 3 and phosphotyrosine increased after 45 minutes hypoxia. All can be alleviated by supplement NO and aggregated by inhibiting NOS. However, the MetHb was not present this trend. Conclusion NO may prevent decreased of RBCs deformability through reducing the cross‐linking of membrane band 3 under hypoxia; this helps microvascular perfusion of RBCs during ischemic and hypoxic disease states.