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Immunoexpression pattern of autophagy mediators in alveolar bone osteoclasts following estrogen withdrawal in female rats
Journal of Molecular Histology ( IF 2.9 ) Pub Date : 2021-01-06 , DOI: 10.1007/s10735-020-09953-x
Rinaldo Florencio-Silva 1 , Gisela Rodrigues da Silva Sasso 2 , Estela Sasso-Cerri 3 , Manuel de Jesus Simões 1 , Paulo Sérgio Cerri 3
Affiliation  

It is known that estrogen deficiency increases osteoclast formation and activity. Autophagy, a cell survival pathway, has been shown to be crucial for osteoclast function. However, little is known about the effects of estrogen depletion on osteoclast autophagy. Here, we evaluated the effects of estrogen deficiency in the immunoexpression of autophagy mediators in alveolar bone osteoclasts of ovariectomized rats. Twelve adult female rats were ovariectomized (OVX-group) or SHAM-operated (SHAM-group). After three weeks, the rats were euthanized and maxillary fragments containing alveolar bone of the first molars were processed for light microscopy or transmission electron microscopy (TEM). Paraffin-sections were subjected to the TRAP method (osteoclast marker) or to the immunohistochemical detections of beclin-1, LC3α, and p62 (autophagy mediators); araldite-sections were processed for TEM. The number of TRAP-positive osteoclasts and the number of immunolabeled-multinucleated cells (MNCs) along the alveolar bone surface of the first molar were computed. The number of TRAP-positive osteoclasts and the number of beclin-1-, LC3α- and p62-immunolabelled osteoclasts were significantly higher in OVX-group than the SHAM-group. MNCs were frequently located juxtaposed to Howship lacunae along the alveolar bone surface, indicating that these cells are osteoclasts. TEM revealed osteoclasts exhibiting autophagosomes. Our data indicate that autophagy plays an important role during estrogen deficiency-induced osteoclastogenesis. Thus, our results contribute to a better understanding on the role of autophagy on osteoclasts under estrogenic deficiency, and reinforce the idea that modulation of autophagy may be a useful tool to inhibit excessive oral bone resorption in post-menopausal women.



中文翻译:

雌性大鼠雌激素戒断后牙槽骨破骨细胞自噬介质的免疫表达模式

众所周知,雌激素缺乏会增加破骨细胞的形成和活性。自噬是一种细胞生存途径,已被证明对破骨细胞功能至关重要。然而,关于雌激素消耗对破骨细胞自噬的影响知之甚少。在这里,我们评估了雌激素缺乏对卵巢切除大鼠牙槽骨破骨细胞中自噬介质免疫表达的影响。12 只成年雌性大鼠被切除卵巢(OVX 组)或进行 SHAM 手术(SHAM 组)。三周后,对大鼠实施安乐死,并对含有第一磨牙牙槽骨的上颌骨碎片进行光学显微镜或透射电子显微镜(TEM)处理。石蜡切片进行 TRAP 方法(破骨细胞标记)或进行 beclin-1、LC3α、和 p62(自噬介质);Araldite 切片经过 TEM 处理。计算第一磨牙牙槽骨表面 TRAP 阳性破骨细胞的数量和免疫标记多核细胞 (MNC) 的数量。OVX组TRAP阳性破骨细胞数量以及beclin-1、LC3α和p62免疫标记破骨细胞数量显着高于SHAM组。MNC 经常沿着牙槽骨表面与 Howship 腔隙并列,表明这些细胞是破骨细胞。TEM 显示破骨细胞表现出自噬体。我们的数据表明自噬在雌激素缺乏诱导的破骨细胞生成过程中发挥重要作用。因此,我们的结果有助于更好地了解雌激素缺乏下自噬对破骨细胞的作用,

更新日期:2021-01-07
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