ABSTRACT
Cyclin-dependent kinase 5 (CDK5) is a member of cyclin-dependent kinase family, which does not directly regulate cell cycle. Through phosphorylation of target protein, CDK5 plays an irreplaceable role in the development, reparation and degeneration of neurons. Brain injury refers to the organic injury of brain tissue caused by external force hit on the head. Owing to the stress and repair system activated by our body itself after injury, various proteins and enzymes of the brain tissues are changed quantitatively, which can be used as indicators for estimating the time of injury. This review summarizes the progress on the distribution, the activity mechanism and the physiological effects of CDK5 after brain injury and its corresponding potential served as a marker for brain injury determination.
Subject(s)
Brain/physiopathology , Brain Injuries/physiopathology , Cyclin-Dependent Kinase 5/metabolism , Nerve Tissue Proteins/metabolism , Neurons , Neuroprotective Agents/pharmacology , Phosphorylation/drug effects , Time FactorsABSTRACT
Hypoxic-ischemic brain damage (HIBD) is referred to a common type of cerebral damage, which is caused by injury, leading to shallow bleeding in the cortex with intact cerebral pia mater. In recent years, studies show that a various kinds of immune cells and immune cellular factors are involved in the occurrence of HIBD. CC chemokine receptor 2 (CCR2) is a representative of CC chemokine receptor, and is widely distributed in cerebral neuron, astrocyte, and microglial cells, and is the main chemo-tactic factor receptor in brain tissue. CC chemokine ligand 2 (CCL2) is a kind of basophilic protein and the ligand of CCR2, and plays an important role in inflammation. In order to provide evidence for correlational studies in HIBD, this review will introduce the biological characteristics of CCR2 and CCL2, and illustrate the relationship between the immunoreactivity and HIBD.