Here researchers determine a pivotal role of synaptic IGF-1R/Fyn signaling controlled by MOR downstream signaling cascades were crucial for the age-dependent neuroimmune modulation following traumatic stress: Hui Zhao, Xiaocong Zhao, Xiaoding Cao and Gencheng Wu. Age-Dependent Neuroimmune Modulation of IGF-1R in the Traumatic Mice. Immunity & Ageing 2012, 9:12 doi:10.1186/1742-4933-9-12.
Highlights: Fyn activity, as well as its molecular connection with IGF-1R was dependent on MOR, on account of that their coupling was obviously not able to be observed when lack of MOR, accordingly, there was not improvement from the immuno-suppression mediated by traumatic stress in MOR (−/−) mice. Likewise, there was not remarkable change in MOR expression, as well as the association of MOR with IGF-1R or Fyn in the synaptic zone. Then, it is plausible that a characteristic feature of IGF-1R was probably due to age-dependent Fyn activation that was triggered by MOR signaling cascades, this specialized process was mainly concentrated within synaptic zone and might contribute to the recovery from traumatic stress mediated immuno-suppression.
Images: MOR expression during traumatic stress. 2-month and 1-year mice were killed 1 and 3 days after traumatic stress (n = 5 for each group), synaptoneurosome from frontal cortex was prepared, Western blot analysis was used to detect MOR expression (A). Immunoprecipitation was used to analyze alterations of MOR and IGF-1R/Fyn interaction. The immunoprecipitation antibody was anti-Fyn (B) or anti-IGF-1R (D) and the immunoblotting antibody was anti-MOR. Panel C and E depict quantitative analysis of B and D respectively. Data are presented as percentage of control, values represent mean ± SD for 3 independent experiments. Con: control; T3: 3 days after trauma.Highlights: Fyn activity, as well as its molecular connection with IGF-1R was dependent on MOR, on account of that their coupling was obviously not able to be observed when lack of MOR, accordingly, there was not improvement from the immuno-suppression mediated by traumatic stress in MOR (−/−) mice. Likewise, there was not remarkable change in MOR expression, as well as the association of MOR with IGF-1R or Fyn in the synaptic zone. Then, it is plausible that a characteristic feature of IGF-1R was probably due to age-dependent Fyn activation that was triggered by MOR signaling cascades, this specialized process was mainly concentrated within synaptic zone and might contribute to the recovery from traumatic stress mediated immuno-suppression.
I will continue to post new applications for our MOR antibodies.
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