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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

View Article: PubMed Central - PubMed

ABSTRACT

Background: 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.

Methods: 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).

Results: 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.

Conclusions: 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.

No MeSH data available.


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Immunohistochemical staining of AdipoR1 and AdipoR2 according to disc degeneration using a rat tail temporary static compression model. (Top) Photomicrographs demonstrating immunohistochemical localization of AdipoR1 and AdipoR2: bars = 100 μm in whole disc and NP and AF photographs. (Bottom) Percentage (%) of positive immunostained cells. Data were obtained from N = 9 and expression is shown as mean + SD
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Fig3: Immunohistochemical staining of AdipoR1 and AdipoR2 according to disc degeneration using a rat tail temporary static compression model. (Top) Photomicrographs demonstrating immunohistochemical localization of AdipoR1 and AdipoR2: bars = 100 μm in whole disc and NP and AF photographs. (Bottom) Percentage (%) of positive immunostained cells. Data were obtained from N = 9 and expression is shown as mean + SD

Mentions: All animals tolerated surgery well and gained body weight throughout the experiment. All springs maintained their compressive length and were fully recovered immediately after release, indicating sustained axial loading and no apparent buckling. Infection, skin necrosis, neurological problems, or instrument failure were not observed. As shown in Fig. 3, AdipoR1 and AdipoR2 were widely observed in the sham group in both the NP and AF. Expression levels of AdipoR1 and AdipoR2 in both the NP and AF were gradually decreased with increased disc degeneration. AdipoR1 (% cells) decreased in the NP from 81.8 ± 16.7% (sham group) to 48.8 ± 10.8% (D1 group) and 11.4 ± 7.0% (D7 group) (P < 0.05) and in the AF from 67.6 ± 16.6% (sham group) to 30.8 ± 9.0% (D1 group) and 11.8 ± 5.5% (D7 group) (P < 0.05). AdipoR2 (% cells) decreased in the NP from 70.8 ± 17.6% (sham group) to 25.8 ± 12.6% (D1 group) and 4.8 ± 3.4% (D7 group) and in the AF from 68.8 ± 8.3% (sham group) to 33.8 ± 10.4% (D1 group) and 7.8 ± 3.3% (D7 group) (P < 0.05). In summary, these results showed that expression of both adiponectin receptors decreased in the NP and AF in accordance to the severity of IVD degeneration.Fig. 3


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
Immunohistochemical staining of AdipoR1 and AdipoR2 according to disc degeneration using a rat tail temporary static compression model. (Top) Photomicrographs demonstrating immunohistochemical localization of AdipoR1 and AdipoR2: bars = 100 μm in whole disc and NP and AF photographs. (Bottom) Percentage (%) of positive immunostained cells. Data were obtained from N = 9 and expression is shown as mean + SD
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Related In: Results  -  Collection

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Fig3: Immunohistochemical staining of AdipoR1 and AdipoR2 according to disc degeneration using a rat tail temporary static compression model. (Top) Photomicrographs demonstrating immunohistochemical localization of AdipoR1 and AdipoR2: bars = 100 μm in whole disc and NP and AF photographs. (Bottom) Percentage (%) of positive immunostained cells. Data were obtained from N = 9 and expression is shown as mean + SD
Mentions: All animals tolerated surgery well and gained body weight throughout the experiment. All springs maintained their compressive length and were fully recovered immediately after release, indicating sustained axial loading and no apparent buckling. Infection, skin necrosis, neurological problems, or instrument failure were not observed. As shown in Fig. 3, AdipoR1 and AdipoR2 were widely observed in the sham group in both the NP and AF. Expression levels of AdipoR1 and AdipoR2 in both the NP and AF were gradually decreased with increased disc degeneration. AdipoR1 (% cells) decreased in the NP from 81.8 ± 16.7% (sham group) to 48.8 ± 10.8% (D1 group) and 11.4 ± 7.0% (D7 group) (P < 0.05) and in the AF from 67.6 ± 16.6% (sham group) to 30.8 ± 9.0% (D1 group) and 11.8 ± 5.5% (D7 group) (P < 0.05). AdipoR2 (% cells) decreased in the NP from 70.8 ± 17.6% (sham group) to 25.8 ± 12.6% (D1 group) and 4.8 ± 3.4% (D7 group) and in the AF from 68.8 ± 8.3% (sham group) to 33.8 ± 10.4% (D1 group) and 7.8 ± 3.3% (D7 group) (P < 0.05). In summary, these results showed that expression of both adiponectin receptors decreased in the NP and AF in accordance to the severity of IVD degeneration.Fig. 3

View Article: PubMed Central - PubMed

ABSTRACT

Background: 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.

Methods: Adipose and IVD tissues were obtained from human patients undergoing surgery (n&thinsp;=&thinsp;4) and from skeletally mature Sprague&ndash;Dawley rats (n&thinsp;=&thinsp;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&nbsp;&mu;g/ml) and/or interleukin-1 beta (IL-1&beta;) (0.2&nbsp;&mu;g/ml) for 24&nbsp;h. The four groups were as follows: control group (no treatment), IL-1&beta; group (IL-1&beta;-only treatment), IL-1&beta;+Ad (0.1) group (IL-1&beta; and adiponectin [0.1&nbsp;&mu;g/ml] treatment), and IL-1&beta;+Ad (1.0) group (IL-1&beta; and adiponectin [1.0&nbsp;&mu;g/ml]). Real-time reverse transcription-polymerase chain reaction was performed to evaluate messenger-RNA (mRNA) expression of tumor necrosis factor-alpha (TNF-&alpha;) and interleukin-6 (IL-6).

Results: 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-&alpha; and IL-6 were significantly upregulated by IL-1&beta; stimulation. TNF-&alpha; expression in the IL-1&beta;+Ad 1.0 group was significantly lower than that in the IL-1&beta; group in both NP and AF cells (P&thinsp;&lt;&thinsp;0.05). Finally, IL-6 expression was not affected by adiponectin treatment in IVD cells.

Conclusions: 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.

No MeSH data available.


Related in: MedlinePlus