Sustained hypoxia-induced proliferation of carotid body type I cells in rats.

Sustained hypoxia-induced proliferation of carotid body type I cells in rats.
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DOI:
10.1152/japplphysiol.00393.2007
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发表时间:
2008-03
影响因子:
3.3
通讯作者:
Zun-Yi Wang;E. B. Olson;D. Bjorling;Gordon S. Mitchell;G. Bisgard
Zun-Yi Wang;E. B. Olson;D. Bjorling;Gordon S. Mitchell;G. Bisgard
中科院分区:
医学2区
文献类型:
--
作者:
Zun-Yi Wang;E. B. Olson;D. Bjorling;Gordon S. Mitchell;G. Bisgard

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持续缺氧(SH)可引起颈动脉体(CB)的形态学和细胞学改变。然而,关于SH是否引起CB I型细胞增殖的结果是相互矛盾的。通过使用溴脱氧尿苷,尿苷类似物,是稳定地纳入细胞进行DNA合成,我们发现,SH导致的CB中的I型细胞增殖,增殖主要发生在前1-3天的缺氧暴露。此外,新细胞在恢复到常氧状态后存活至少1个月。此外,SH不会导致任何细胞死亡CB检查的末端脱氧核苷酸转移酶介导的dUTP-X缺口末端标记试验。两者合计,我们的研究结果表明,SH刺激CB I型细胞增殖,这可能会产生持久的CB形态和功能的变化。
Sustained hypoxia (SH) has been shown to cause profound morphological and cellular changes in carotid body (CB). However, results regarding whether SH causes CB type I cell proliferation are conflicting. By using bromodeoxyuridine, a uridine analog that is stably incorporated into cells undergoing DNA synthesis, we have found that SH causes the type I cell proliferation in the CB; the proliferation occurs mainly during the first 1-3 days of hypoxic exposure. Moreover, the new cells survive for at least 1 mo after the return to normoxia. Also, SH does not cause any cell death in CB as examined by the terminal deoxynucleotidyl transferase-mediated dUTP-X nick-end labeling assay. Taken together, our results suggest that SH stimulates CB type I cell proliferation, which may produce long-lasting changes in CB morphology and function.