No abstract available.
Astrocytes*

No Abstract Available.
Astrocytes* ; Humans*

No abstract available.
Astrocytes* ; Humans*

Astrocytes ; Learning ; Memory

No abstract available.
Animals ; Astrocytes* ; Nitric Oxide* ; Rats*

Neuroinflammation in central nervous system, featured by glial cells activation, can always be found during the development of neurodegenerative diseases. Astrocytes, the most abundant glial cells in the brain, can release both pro-inflammatory and anti-inflammatory factors, thus playing a crucial role in the neuroinflammation. A variety of pattern-recognition receptors on astrocytes are involve d in the inflammatory response, particularly the scavenger receptor. Scavenger receptor is a cell surface glycoprotein and can identify diverse ligands. With a variety of biological functions, it may activate many signal pathways related to neuroinflammation, regulate the host defense and the development of neuroinflammation, and eventually regulate the process of neuroinflammation. Thus, it play a key role in the development of neurodegenerative diseases and many other conditions. This review summarizes the scavenger receptor expressed on astrocytes and how it regulates signal transduction pathways associated with neuroinflammation and thus participates in regulating neuroinflammation.
Astrocytes ; Humans ; Neuritis ; Receptors, Scavenger

No abstract available.
Astrocytes* ; Gene Expression* ; Humans* ; Polymerase Chain Reaction*

Astrocytes are non-excitable cells in the brain and their activity largely depends on the intracellular calcium (Ca²⁺) level. Therefore, maintaining the intracellular Ca²⁺ homeostasis is critical for proper functioning of astrocytes. One of the key regulatory mechanisms of Ca²⁺ homeostasis in astrocytes is the store-operated Ca²⁺ entry (SOCE). This process is mediated by a combination of the Ca²⁺-store-depletion-sensor, Stim, and the store-operated Ca²⁺-channels, Orai and TrpC families. Despite the existence of all those families in astrocytes, previous studies have provided conflicting results on the molecular identification of astrocytic SOCE. Here, using the shRNA-based gene-silencing approach and Ca²⁺-imaging from cultured mouse astrocytes, we report that Stim1 in combination with Orai1 and Orai3 contribute to the major portion of astrocytic SOCE. Gene-silencing of Stim1 showed a 79.2% reduction of SOCE, indicating that Stim1 is the major Ca²⁺-store-depletion-sensor. Further gene-silencing showed that Orai1, Orai2, Orai3, and TrpC1 contribute to SOCE by 35.7%, 20.3%, 26.8% and 12.2%, respectively. Simultaneous gene-silencing of all three Orai subtypes exhibited a 67.6% reduction of SOCE. Based on the detailed population analysis, we predict that Orai1 and Orai3 are expressed in astrocytes with a large SOCE, whereas TrpC1 is exclusively expressed in astrocytes with a small SOCE. This analytical approach allows us to identify the store operated channel (SOC) subtype in each cell by the degree of SOCE. Our results propose that Stim1 in combination with Orai1 and Orai3 are the major molecular components of astrocytic SOCE under various physiological and pathological conditions.
Animals ; Astrocytes* ; Brain ; Calcium* ; Homeostasis ; Humans ; Mice

Astrocytes ; metabolism ; pathology ; Epilepsy ; pathology ; Humans

Astrocytes are an abundant subgroup of cells in the central nervous system (CNS) that play a critical role in controlling neuronal circuits involved in emotion, learning, and memory. In clinical cases, multiple chronic brain diseases may cause psychosocial and cognitive impairment, such as depression and Alzheimer's disease (AD). For years, complex pathological conditions driven by depression and AD have been widely perceived to contribute to a high risk of disability, resulting in gradual loss of self-care ability, lower life qualities, and vast burden on human society. Interestingly, correlational research on depression and AD has shown that depression might be a prodrome of progressive degenerative neurological disease. As a kind of multifunctional glial cell in the CNS, astrocytes maintain physiological function via supporting neuronal cells, modulating pathologic niche, and regulating energy metabolism. Mounting evidence has shown that astrocytic dysfunction is involved in the progression of depression and AD. We herein review the current findings on the roles and mechanisms of astrocytes in the development of depression and AD, with an implication of potential therapeutic avenue for these diseases by targeting astrocytes.
Alzheimer Disease ; Astrocytes ; Depression ; Humans ; Neurons