Aksaray University, Faculty of Science and Letters, Molecular Biology Department, Aksaray, Turkey.
Cytokine. 2012 Jan;57(1):61-7. doi: 10.1016/j.cyto.2011.10.004. Epub 2011 Nov 13.
Leptin and adiponectin receptors mediate the role of leptin in stimulating the growth of leukemic cells and the protective function of adiponectin undertaken in several malignancies such as leukemia. In this study, we investigated the involvement of the expression of leptin and adiponectin receptors in chronic myeloid leukemia (CML) pathogenesis.
The expression of leptin receptor isoforms, OB-Rt, OB-Ra, and OB-Rb, and the expression of adiponectin receptors, AdipoR1 and AdipoR2, were measured as mRNA levels in two CML cell lines (K562 and Meg-01) and 20 CML patients and 24 healthy controls by using RT-PCR.
OB-Rt and OB-Ra isoforms expression of the leptin receptors were found to be significantly lower in Meg-01 cell lines than K562 cells. All leptin receptors were downregulated in CML patients and more particularly OB-Rb level was found to be undetectably low in normal PBMC as well as in CML patients. AdipoR1 expression level was higher in Meg-01 than in K562, whereas AdipoR2 level was found to be unchanged in both cell lines. Interestingly, while AdipoR1 expression increased in CML patients, AdipoR2 decreased. Moreover, imatinib therapy did not affect both leptin and adiponectin isoform expressions.
While the decrease in leptin receptor levels in CML patients was confirmed, the increase in AdipoR1 levels and relevant decrease in AdipoR2 levels depicted their possible involvement in CML pathogenesis. This suggests different functions of adiponectin receptors in CML development.
瘦素和脂联素受体介导瘦素在刺激白血病细胞生长中的作用，以及脂联素在几种恶性肿瘤（如白血病）中发挥的保护功能。在这项研究中，我们研究了瘦素和脂联素受体的表达在慢性髓性白血病（CML）发病机制中的作用。
通过 RT-PCR，我们测量了两种 CML 细胞系（K562 和 Meg-01）和 20 名 CML 患者和 24 名健康对照者中瘦素受体亚型 OB-Rt、OB-Ra 和 OB-Rb，以及脂联素受体 AdipoR1 和 AdipoR2 的表达水平。
发现 Meg-01 细胞系中瘦素受体 OB-Rt 和 OB-Ra 亚型的表达明显低于 K562 细胞系。所有的瘦素受体在 CML 患者中均下调，尤其是 OB-Rb 水平在正常 PBMC 以及 CML 患者中均无法检测到。AdipoR1 在 Meg-01 中的表达水平高于 K562，而 AdipoR2 在两种细胞系中的表达水平均不变。有趣的是，虽然 AdipoR1 在 CML 患者中的表达增加，但 AdipoR2 却降低了。此外，伊马替尼治疗并未影响瘦素和脂联素亚型的表达。
虽然 CML 患者瘦素受体水平下降得到了证实，但 AdipoR1 水平的升高和 AdipoR2 水平的相应下降表明它们可能参与了 CML 的发病机制。这表明脂联素受体在 CML 发展中有不同的功能。
