2. Academic Validation
  3. TAZ Activator Is Involved in IL-10-Mediated Muscle Responses in an Animal Model of Traumatic Brain Injury

TAZ Activator Is Involved in IL-10-Mediated Muscle Responses in an Animal Model of Traumatic Brain Injury

  • Inflammation. 2017 Feb;40(1):100-105. doi: 10.1007/s10753-016-0457-5.
Ruyi Zou 1,  Da Li 2,  Gang Wang 3,  Mo Zhang 4,  Yili Zhao 5,  Zeyu Yang 6
Affiliations

Affiliations

  • 1 Department of Neurosurgery, General Hospital of Benxi Iron and Steel CO. LTD, Benxi, 117000, China.
  • 2 Department of Obstetrics and Gynecology, Shengjing Hospital of China Medical University, Shenyang, 110004, China.
  • 3 Department of Emergency Medicine, Shengjing Hospital of China Medical University, Shenyang, 110004, China.
  • 4 Department of Urology, Shengjing Hospital of China Medical University, Shenyang, 110004, China.
  • 5 Department of Obstetrics and Gynecology, Eastern Virginia Medical School, Norfolk, 23507, VA, USA.
  • 6 Department of Ultrasound, Shengjing Hospital of China Medical University, No. 36 Sanhao Street, Heping District, Shenyang, 110004, China. yangzy1@sj-hospital.org.
PMID: 27718096 DOI: 10.1007/s10753-016-0457-5
Abstract

The transcriptional coactivator with PDZ-binding motif (TAZ) functions as a downstream regulatory target in the Hippo signaling pathway that plays various roles. We previously developed a cell-based assay and identified the TAZ activator IBS008738 as a potential therapeutic target for glucocorticoid-induced atrophy. To further explore the application of IBS008738 in various muscle-related diseases, we examined the function of IBS008738 in inflammatory cytokine-mediated mouse muscle responses after traumatic brain injury (TBI). Preliminary screening suggested that IBS008738 treatments increased the levels of IL-10 in C2C12 cells. In TBI and sham control mice, we compared the effect of IBS008738 treatments on TNF α, IL-6, and IL-10 mRNA levels, muscle morphologic changes, and macrophage phenotype changes. Our findings support that the TAZ activator IBS008738 decreases muscle wasting by upregulating IL-10 and inhibiting TNF α and IL-6, and this process is implemented by changing the macrophage phenotypes. These results indicate a new mechanism of the TAZ activator as a potential therapy for atrophy.

Keywords

interleukin-10; macrophage; muscle responses; traumatic brain injury.

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