Expression of adiponectin receptors in the brain of adult zebrafish and mouse: Links with neurogenic niches and brain repair. Issue 14 (29th March 2019)

• Record Type: Journal Article
• Authors: Rastegar, Sepand; Parimisetty, Avinash; Cassam Sulliman, Nora; Narra, Sai Sandhya; Weber, Sabrina; Rastegar, Maryam; Viranaicken, Wildriss; Couret, David; Planesse, Cynthia; Strähle, Uwe; Meilhac, Olivier; Lefebvre d'Hellencourt, Christian; Diotel, Nicolas
• Is Part Of: Journal of comparative neurology. Volume 527:Issue 14(2019)
• Page Start: 2317
• Page End: 2333
• Publication Date: 2019-03-29
• Subjects: adipor -- brain ischemia -- brain repair -- neural stem cells -- RRID:AB_10013383 -- RRID:AB_10049650 -- RRID:AB_141372 -- RRID:AB_2160651 -- RRID:AB_221448 -- RRID:AB_2314535 -- RRID:AB_2534069 -- RRID:AB_514497 -- RRID:AB_514499 -- RRID:SCR_003070 -- stab wound; Comparative neurobiology -- Periodicals; Neurology -- Periodicals; 616
• DOI: 10.1002/cne.24669
• Languages: English
• ISSNs: 0021-9967

Abstract

Abstract: Adiponectin and its receptors ( adipor) have been initially characterized for their role in lipid and glucose metabolism. More recently, adiponectin signaling was shown to display anti‐inflammatory effects and to participate in brain homeostasis and neuroprotection. In this study, we investigated adipor gene expression and its regulation under inflammatory conditions in two complementary models: mouse and zebrafish. We demonstrate that adipor1a, adipor1b, and adipor2 are widely distributed throughout the brain of adult fish, in neurons and also in radial glia, behaving as neural stem cells. We also show that telencephalic injury results in a decrease in adipor gene expression, inhibited by an anti‐inflammatory treatment (Dexamethasone). Interestingly, adiponectin injection after brain injury led to a consistent decrease (a) in the recruitment of microglial cells at the lesioned site and (b) in the proliferation of neural progenitors, arguing for a neuroprotective role of adiponectin. In a comparative approach, we investigate Adipor1 and Adipor2 gene distribution in the brain of mice and demonstrated their expression in regions shared with fish including neurogenic regions. We also document Adipor gene expression in mice after middle cerebral artery occlusion and lipopolysaccharide injection. In contrast to zebrafish, these inflammatory stimuli do no impact cerebral adiponectin receptor gene expression in mouse. This work provides new insights regarding adipor expression in the brain of fish, and demonstrates evolutionary conserved distribution of adipor with mouse. This is the first report of adipor expression in adult neural stem cells of fish, suggesting a potential role of adiponectin signaling during vertebrate neurogenesis. It also suggests a potential contribution of inflammation in the regulation of adipor in fish. Abstract : By transcriptomic study analyses and in situ hybridization coupled with immunohistochemistry, we showed that adiponectin receptor genes are expressed in neurons and neurogenic niches of mouse and zebrafish. After brain injury, adipor gene expression decreased through an inflammatory‐induced mechanism in fish while adipor expression remains stable in mouse.