Enhanced expression of the calcium-sensing receptor in reactive astrocytes following ischemic injury in vivo and in vitro.
We recently demonstrated that the G protein-coupled calcium-sensing receptor (CaSR) is associated with the pathogenesis of ischemic stroke and may be involved in vascular remodeling and astrogliosis. To further substantiate the involvement of CaSR in the astroglial reaction common to ischemic insults, we investigated the temporal and cell type-specific expression patterns of CaSR in the hippocampus after transient forebrain ischemia. CaSR was constitutively expressed in neurons of the pyramidal and granule cell layers, whereas increased CaSR immunoreactivity was observed in reactive astrocytes, but not in activated microglia or macrophages, in the CA1 region of the post-ischemic hippocampus. Astroglial induction of CaSR expression was evident on days 3-7 after reperfusion and appeared to increase progressively through day 28, at which time CaSR expression was prominent in astrocytes with a highly reactive hypertrophic phenotype and elevated levels of glial fibrillary acidic protein. This expression pattern was supported by results of immunoblot analyses. Furthermore, CaSR expression was upregulated in rat primary cortical astrocytes exposed to oxygen-glucose deprivation, which undergo reactive gliosis-like changes. Thus, our results demonstrate that selective and long-lasting astroglial induction of CaSR expression is a common characteristic of ischemic injury and suggest its involvement in the ischemia-induced astroglial reaction.
Department of Anatomy, Catholic Neuroscience Institute, College of Medicine, The Catholic University of Korea, 137-701, Seoul, Korea.
Ha-Jin
HJ
Pak
Department of Anatomy, Catholic Neuroscience Institute, College of Medicine, The Catholic University of Korea, 137-701, Seoul, Korea.
Tae-Ryong
TR
Riew
Department of Anatomy, Catholic Neuroscience Institute, College of Medicine, The Catholic University of Korea, 137-701, Seoul, Korea.
Yoo-Jin
YJ
Shin
Department of Anatomy, Catholic Neuroscience Institute, College of Medicine, The Catholic University of Korea, 137-701, Seoul, Korea.
Jeong-Heon
JH
Choi
Department of Anatomy, Catholic Neuroscience Institute, College of Medicine, The Catholic University of Korea, 137-701, Seoul, Korea.
Xuyan
X
Jin
Department of Anatomy, Catholic Neuroscience Institute, College of Medicine, The Catholic University of Korea, 137-701, Seoul, Korea. Electronic address: munylee@catholic.ac.kr.
Mun-Yong
MY
Lee
D000818:Animals; D001253:Astrocytes / Q000378:metabolism* / Q000473:pathology; D002545:Brain Ischemia / Q000150:complications / Q000378:metabolism* / Q000473:pathology; D056547:CA1 Region, Hippocampal / Q000293:injuries / Q000378:metabolism* / Q000473:pathology; D015687:Cell Hypoxia / Q000502:physiology; D002478:Cells, Cultured; D004195:Disease Models, Animal; D018450:Disease Progression; D005911:Gliosis / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D005947:Glucose / Q000172:deficiency; D008264:Macrophages / Q000378:metabolism / Q000473:pathology; D008297:Male; D017628:Microglia / Q000378:metabolism / Q000473:pathology; D017207:Rats, Sprague-Dawley; D044169:Receptors, Calcium-Sensing / Q000378:metabolism*; D015427:Reperfusion Injury / Q000150:complications / Q000378:metabolism* / Q000473:pathology
D044169:Receptors, Calcium-Sensing; C473605:extracellular calcium cation-sensing receptor, rat; D005947:Glucose
Hippocampus; Ischemia; Oxygen–glucose deprivation; Reactive astrocytes