Angiotensin II Type 1 receptor (AT1) signaling in astrocytes regulates synaptic degeneration-induced leukocyte entry to the central nervous system

Angiotensin II type 1 receptor expression in astrocytes is upregulated leading to increased mortality in mice with myocardial infarction-induced heart failure

“…Consistent with our findings, a previous report indicated difficulties in identifying AT 1 R in cultured astrocytes using a variety of approaches, including immunohistochemistry, RT-qPCR, inositol phosphatase-signaling assay, and angiotensin receptor-binding assay (35). Other studies localizing AT 1 R expression in astrocytes have relied on immunohistochemical methods (4,11,26). We also examined AT 1 R expression in the brain stem by Western blotting and RT-qPCR.…”

“…Although AT 1 R are weakly expressed in astrocytes under basal conditions (28, 35), they have important roles in abnormal conditions, such as experimental autoimmune encephalomyelitis, and in the regulation of leukocyte infiltration into the central nervous system in response to a neurodegenerative stimulus as well as hypoxia (7,11,26). AT 1 R in glia cells in the RVLM are thought to be involved in the regulation of blood pressure associated with sympathetic activation (2).…”

Improvement in spatial memory dysfunction by telmisartan through reduction of brain angiotensin II and oxidative stress in experimental uremic mice

“…This result is consistent with findings of the RAWM test, and indicated that brain RAS is a crucial factor of cognitive impairment in CKD. The precise mechanism by which telmisartan prevented the increase of brain AII remains unclear, but we speculate that blockade of AII receptor by telmisartan contributed somehow not only to neurons but also to other brain parenchymal cells to cause a decrease in expression of RAS components in this uremic mouse model (Grobe et al, 2008;Füchtbauer et al, 2011;Zhou et al, 2006). There are numerous studies examining the role of brain RAS in cognitive dysfunction in experimental models of hypertension and cerebral ischemia (Pelisch et al, 2011;Inaba et al, 2009;Mogi et al, 2006;Tota et al, 2012), and the results suggest that inhibitors of RAS can preserve cognitive function without blood-lowering effects.…”

Angiotensin II and its receptor in activated microglia enhanced neuronal loss and cognitive impairment following pilocarpine-induced status epilepticus

“…Under physiological conditions, AT1 regulates blood pressure in the central nervous system (CNS) and AT1 and AII are mainly localized in neurons and astrocytes (McKinley et al, 2003;Füchtbauer et al, 2011). However, under neuropathological conditions (such as stroke, multiple sclerosis, and Parkinson's disease), AII and AT1 are increased in activated microglia and play a role in amplifying the inflammatory response, subsequently promoting neurodegeneration (Wright and Harding, 2013;Rodriguez-Pallares et al, 2008).…”