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缺氧条件下HIF-2α-整合素连接激酶参与多发性骨髓瘤中间充质基质细胞的血管生成

HIF-2α-ILK Is Involved in Mesenchymal Stromal Cell Angiogenesis in Multiple Myeloma Under Hypoxic Conditions.

作者信息

Zhang Xiaoying, Xu Yinhui, Liu Hongbo, Zhao Pan, Chen Yafang, Yue Zhijie, Zhang Zhiqing, Wang Xiaofang

机构信息

1 Department of Hematology, Key Laboratory of Cancer Prevention and Therapy, Cancer Hospital of Tianjin, Tianjin Medical University, Tianjin, China.

The authors contributed equally to this work.

出版信息

Technol Cancer Res Treat. 2018 Jan 1;17:1533033818764473. doi: 10.1177/1533033818764473.

Abstract

Mesenchymal stromal cells are proven to be likely induce the angiogenic response in multiple myeloma and thus represent an enticing target for antiangiogenesis therapies for multiple myeloma. Substantial evidence indicates that angiogenesis in multiple myeloma is complex and involves direct production of angiogenic cytokines by abnormal plasma cells and these B-cell neoplasia generated pathophysiology change within the microenvironment. In this study, we demonstrated that mesenchymal stromal cells cultured with U266/Lp-1 under hypoxic conditions resulted in an increased α-smooth muscle actin expression and high productive levels of both hypoxia-inducible factor-2α and integrin-linked kinase proteins. Moreover, inhibition of hypoxia-inducible factor-2α by Small interfering RNA (siRNA) in mesenchymal stromal cells decreased the protein levels of both α-smooth muscle actin and integrin-linked kinase after mesenchymal stromal cells cultured with U266 under hypoxic conditions. We further demonstrated that transfection of integrin-linked kinase-siRNA reduced the protein level of α-smooth muscle actin and attenuated angiogenesis in vitro by decreasing the attachment of Q-dot labeled cells and secretion of angiogenic factors. In conclusion, our research showed that mesenchymal stromal cells cultured with myeloma cells under hypoxia participated in the angiogenesis of multiple myeloma, which is regulated by the hypoxia-inducible factor-2α-integrin-linked kinase pathway. Thus, targeting integrin-linked kinase may represent an effective strategy to block hypoxia-inducible factor-2α-induced angiogenesis in the treatment of multiple myeloma.

摘要

间充质基质细胞已被证明可能在多发性骨髓瘤中诱导血管生成反应,因此是多发性骨髓瘤抗血管生成治疗的一个诱人靶点。大量证据表明,多发性骨髓瘤中的血管生成很复杂,涉及异常浆细胞直接产生血管生成细胞因子,并且这些B细胞肿瘤在微环境中产生病理生理学变化。在本研究中,我们证明在缺氧条件下与U266/Lp-1共同培养的间充质基质细胞导致α平滑肌肌动蛋白表达增加以及缺氧诱导因子-2α和整合素连接激酶蛋白的高表达水平。此外,在缺氧条件下与U266共同培养的间充质基质细胞中,用小分子干扰RNA(siRNA)抑制缺氧诱导因子-2α会降低α平滑肌肌动蛋白和整合素连接激酶的蛋白水平。我们进一步证明,整合素连接激酶-siRNA转染降低了α平滑肌肌动蛋白的蛋白水平,并通过减少量子点标记细胞的附着和血管生成因子的分泌在体外减弱了血管生成。总之,我们的研究表明,在缺氧条件下与骨髓瘤细胞共同培养的间充质基质细胞参与了多发性骨髓瘤的血管生成,这受缺氧诱导因子-2α-整合素连接激酶途径调控。因此,靶向整合素连接激酶可能是在多发性骨髓瘤治疗中阻断缺氧诱导因子-2α诱导的血管生成的有效策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e35/5912287/cbd559e72a75/10.1177_1533033818764473-fig1.jpg

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