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Hypothalamic lipid-laden astrocytes induce microglia migration and activation
Kwon, Yoon-Hee,Kim, Jiye,Kim, Chu-Sook,Tu, Thai Hien,Kim, Min-Seon,Suk, Kyoungho,Kim, Dong Hee,Lee, Byung Ju,Choi, Hye-Seon,Park, Taesun,Choi, Myung-Sook,Goto, Tsuyoshi,Kawada, Teruo,Ha, Tae Youl,Yu, Wiley (John WileySons) 2017 FEBS letters Vol.591 No.12
<P>Obesity-induced hypothalamic inflammation is closely associated with various metabolic complications and neurodegenerative disorders. Astrocytes, the most abundant glial cells in the central nervous system, play a crucial role in pathological hypothalamic inflammatory processes. Here, we demonstrate that hypothalamic astrocytes accumulate lipid droplets under saturated fatty acid-rich conditions, such as obese environment, and that the lipid-laden astrocytes increase astrogliosis markers and inflammatory cytokines (TNF alpha, IL-1 beta, IL-6, MCP-1) at the transcript and/or protein level. Medium conditioned by the lipid-laden astrocytes stimulate microglial chemotactic activity and upregulate transcripts of the microglia activation marker Iba-1 and inflammatory cytokines. These findings indicate that the lipid-laden astrocytes formed in free fatty acid-rich obese condition may participate in obesity-induced hypothalamic inflammation through promoting microglia migration and activation.</P>
The Effects of Mechanical Strain on Bone Cell Proliferation and Recruitment Induced by Osteocytes
Seong-Hee Ko,Jiy Hye Lee,So Hee Kim KOREAN ACADAMY OF ORAL BIOLOGY 2008 International Journal of Oral Biology Vol.33 No.4
Several lines of evidence suggest that osteocytes play a critical role in bone remodeling. Both healthy and apoptotic osteocytes can send signals to other bone surface cells such as osteoblasts, osteoclasts, osteoclast precursors, and bone lining cells through canalicular networks. Osteocytes responding to mechanical strain may also send signals to other cells. To determine the role for osteocytes and mechanical strain in bone remodeling, we examined the effects of fluid flow shear stress on osteoclast precursor cell and osteoblast proliferation and recruitment induced by osteocytes. In addition, the effects of fluid flow shear stress on osteocyte M-CSF, RANKL, and OPG mRNA expression were also examined. MLO-Y4 cells were used as an in vitro model for osteocytes, RAW 264.7 cells and MOCP-5 cells as osteoclast precursors, and 2T3 cells as osteoblasts. MLO-Y4 cells conditioned medium (Y4-CM) was collected after 24h culture. For fluid flow experiments, MLO-Y4 cells were exposed to 2 h of pulsatile fluid flow (PFF) at 2, 4, 8, 16 ± 0.6 dynes/cm 2 using the Flexcell Streamer TM system. For proliferation assays, MOCP-5, RAW 264.7, and 2T3 cells were cultured with control media or 10 - 100 % Y4 CM. Cells were cultured for 3 d, and then cells were counted. RAW 264.7 and 2T3 cell migration was assayed using transwells with control media or 10 - 100 % Y4-CM. MCSF, RANKL and OPG in MLO-Y4 mRNA expression was determined by semiquantitative RT-PCR. Y4-CM increased osteoclast precursor proliferation and migration, but decreased 2T3 cell proliferation and migration. CM from MLO-Y4 cells exposed to PFF caused decreased RAW 267.4 cell proliferation and migration and 2T3 migration compared to control Y4-CM. However, Y4-CM from cells exposed to PFF had no effect on 2T3 osteoblastic cell proliferation. PFF decreased RNAKL mRNA and increased OPG mRNA in MLO-Y4 cells compared to control (without PFF). PFF had no effect on M-CSF mRNA expression in MLO-Y4 cells. These results suggest that osteocytes can regulate bone remodeling by communication with osteoclast precursors and osteoblasts and that osteocytes can communicate mechanical signals to other cells.