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首页> 外文期刊>American Journal of Physiology >Estrogen regulates pulmonary alveolar formation, loss, and regeneration in mice.
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Estrogen regulates pulmonary alveolar formation, loss, and regeneration in mice.

机译：雌激素调节小鼠肺泡的形成，丢失和再生。

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摘要

Lung tissue elastic recoil and the dimension and number of pulmonary gas-exchange units (alveoli) are major determinants of gas-exchange function. Loss of gas-exchange function accelerates after menopause in the healthy aged and is progressively lost in individuals with chronic obstructive pulmonary disease (COPD). The latter, a disease of midlife and later, though more common in men than in women, is a disease to which women smokers and never smokers may be more susceptible than men; it is characterized by diminished lung tissue elastic recoil and presently irremediable alveolar loss. Ovariectomy in sexually immature rats diminishes the formation of alveoli, and estrogen prevents the diminution. In the present work, we found that estrogen receptor-alpha and estrogen receptor-beta, the only recognized mammalian estrogen receptors, are required for the formation of a full complement of alveoli in female mice. However, only the absence of estrogen receptor-beta diminishes lung elastic tissue recoil. Furthermore, ovariectomy in adult mice results, within 3 wk, in loss of alveoli and of alveolar surface area without a change of lung volume. Estrogen replacement, after alveolar loss, induces alveolar regeneration, reversing the architectural effects of ovariectomy. These studies 1) reveal estrogen receptors regulate alveolar size and number in a nonredundant manner, 2) show estrogen is required for maintenance of already formed alveoli and induces alveolar regeneration after their loss in adult ovariectomized mice, and 3) offer the possibility estrogen can slow alveolar loss and induce alveolar regeneration in women with COPD.
机译：肺组织弹性后坐力和肺气体交换单位（肺泡）的尺寸和数量是气体交换功能的主要决定因素。在健康的老年人中，更年期后气体交换功能的丧失加速，而在慢性阻塞性肺疾病（COPD）患者中，这种功能的丧失逐渐加剧。后者是一种中年以后的疾病，尽管这种疾病在男人中比在女人中更为普遍，但它是一种女性吸烟者，从不吸烟者比男性更易感染这种疾病。它的特点是减少了肺组织弹性后坐力，目前无法修复的肺泡丢失。性不成熟大鼠的卵巢切除术减少了肺泡的形成，而雌激素则阻止了这种减少。在目前的工作中，我们发现雌激素受体-α和雌激素受体-β，唯一公认的哺乳动物雌激素受体，是在雌性小鼠中形成完整的肺泡所需的。然而，仅雌激素受体-β的缺乏会减少肺弹性组织后坐力。此外，成年小鼠的卵巢切除术在3周内导致肺泡和肺泡表面积的损失，而肺活量没有变化。肺泡丢失后，雌激素替代会引起肺泡再生，从而逆转卵巢切除术的建筑效果。这些研究1）显示雌激素受体以非冗余方式调节肺泡的大小和数量，2）显示雌激素是维持已形成的肺泡所必需的，并且在成年卵巢切除小鼠中丢失后诱导肺泡再生，以及3）提供了雌激素可以减慢其速度的可能性患有COPD的女性的肺泡丢失并诱导肺泡再生。

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