Expression of adiponectin receptors in human and rat intervertebral disc cells and changes in receptor expression during disc degeneration using a rat tail temporary static compression model.
Expression of adiponectin receptors in human and rat intervertebral disc cells and changes in receptor expression during disc degeneration using a rat tail temporary static compression model.
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DOI：
10.1186/s13018-016-0481-z
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发表时间：
2016-11-22
影响因子：
2.6
通讯作者：
Nishida K
中科院分区：
文献类型：
--
作者：
Terashima Y;Kakutani K;Yurube T;Takada T;Maeno K;Hirata H;Miyazaki S;Ito M;Kakiuchi Y;Takeoka Y;Kuroda R;Nishida K
脂肪组织是已知的分泌脂联素的大型内分泌器官，脂联素具有抗糖尿病、抗动脉粥样硬化和抗炎特性。脂联素广泛参与全身性疾病、糖尿病和心脏梗死。本研究旨在探讨脂联素在椎间盘退变中的作用。脂肪和IVD组织取自接受手术的人类患者（n = 4）和骨骼成熟的Sprague-Dawley大鼠（n = 21）。组织免疫组织化学染色检测脂联素和脂联素受体AdipoR1和AdipoR2。脂联素受体表达随IVD退行性变严重程度的变化，然后使用大鼠尾巴临时压缩模型进行研究。用AdipoR1或AdipoR2免疫组化染色大鼠IVD组织，计算免疫阳性细胞百分比。分别分离大鼠髓核（NP）和纤维环（AF）组织，用重组脂联素（Ad 0.1或1.0 μg/ml）和/或白介素-1β (IL-1β) （0.2 μg/ml）处理24 h，四组分别为：对照组（未处理）、IL-1β组（IL-1β仅处理）、IL-1β+Ad（0.1）组（IL-1β和脂联素[0.1 μg/ml]处理）和IL-1β+Ad（1.0）组（IL-1β和脂联素[1.0 μg/ml]）。实时逆转录聚合酶链反应检测肿瘤坏死因子-α (TNF-α)和白细胞介素-6 (IL-6) mRNA的表达。脂联素在人皮下和硬膜外脂肪组织中广泛表达。在大鼠IVD组织中，NP和AF均未观察到脂联素。而AdipoR1和AdipoR2在人和大鼠IVD组织中均广泛表达，且受体之间表达水平无显著差异。此外，随着IVD退化程度的增加，AdipoR1和AdipoR2的表达水平逐渐降低。有趣的是，IL-1β刺激可显著上调TNF-α和IL-6的mRNA表达水平。IL-1β+Ad 1.0组TNF-α在NP和AF细胞中的表达均显著低于IL-1β组（P < 0.05）。最后，脂联素处理不影响IVD细胞IL-6的表达。本研究首次研究了脂联素受体在人和大鼠IVD细胞中的表达。研究结果表明，全身或硬膜外脂肪组织产生的脂联素可能参与了IVD变性的病理机制。
Adipose tissue is a large endocrine organ known to secret adiponectin, which has anti-diabetic, anti-atherogenic, and anti-inflammatory properties. Adiponectin is widely involved in systemic disease, diabetes mellitus, and cardiac infraction. This study aimed to investigate the involvement of adiponectin in intervertebral disc (IVD) degeneration. Adipose and IVD tissues were obtained from human patients undergoing surgery (n = 4) and from skeletally mature Sprague–Dawley rats (n = 21). Tissues were stained immunohistochemically for adiponectin and adiponectin receptors AdipoR1 and AdipoR2. Changes in adiponectin receptor expression with IVD degeneration severity were then investigated using a rat tail temporary compression model. Rat IVD tissues were stained immunohistochemically with AdipoR1 or AdipoR2, and immunopositive cell percentages were calculated. Rat nucleus pulposus (NP) and annulus fibrosus (AF) tissues were isolated separately and treated with recombinant adiponectin (Ad 0.1 or 1.0 μg/ml) and/or interleukin-1 beta (IL-1β) (0.2 μg/ml) for 24 h. The four groups were as follows: control group (no treatment), IL-1β group (IL-1β-only treatment), IL-1β+Ad (0.1) group (IL-1β and adiponectin [0.1 μg/ml] treatment), and IL-1β+Ad (1.0) group (IL-1β and adiponectin [1.0 μg/ml]). Real-time reverse transcription-polymerase chain reaction was performed to evaluate messenger-RNA (mRNA) expression of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6). Adiponectin was widely expressed in human subcutaneous and epidural adipose tissue. In rat IVD tissue, adiponectin was not observed in NP and AF. However, both AdipoR1 and AdipoR2 were widely expressed in both human and rat IVD tissues, with no significant differences in expression levels between receptors. Furthermore, expression levels of AdipoR1 and AdipoR2 were gradually decreased with increased IVD degeneration severity. Interestingly, mRNA expression levels of TNF-α and IL-6 were significantly upregulated by IL-1β stimulation. TNF-α expression in the IL-1β+Ad 1.0 group was significantly lower than that in the IL-1β group in both NP and AF cells (P < 0.05). Finally, IL-6 expression was not affected by adiponectin treatment in IVD cells. This study investigated for the first time the expression of adiponectin receptors in human and rat IVD cells. The findings indicate that adiponectin produced by the systemic or epidural adipose tissue may be involved in the pathomechanism of IVD degeneration.
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影响因子：
2.8
作者：
Fields, Aaron J.;Berg-Johansen, Britta;Metz, Lionel N.;Miller, Stephanie;La, Brandan;Liebenberg, Ellen C.;Coughlin, Dezba G.;Graham, James L.;Stanhope, Kimber L.;Havel, Peter J.;Lotz, Jeffrey C.
通讯作者：
Lotz, Jeffrey C.
影响因子：
2.7
作者：
Khabour OF;Abu-Rumeh L;Al-Jarrah M;Jamous M;Alhashimi F
通讯作者：
Alhashimi F
影响因子：
4.9
作者：
Kang EH;Lee YJ;Kim TK;Chang CB;Chung JH;Shin K;Lee EY;Lee EB;Song YW
通讯作者：
Song YW
DOI：
10.1016/j.bbrc.2005.02.081
发表时间：
2005-04-15
影响因子：
3.1
作者：
Blüher, M;Fasshauer, M;Paschke, R
通讯作者：
Paschke, R
影响因子：
--
作者：
Takada, Toru;Nishida, Kotaro;Kurosaka, Masahiro
通讯作者：
Kurosaka, Masahiro