• The Korean Journal of Physiology and Pharmacology
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• 제10권5호
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• pp.223-229
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• 2006

The emerging concept of the 'neurovascular unit' may enable a powerful paradigm shift for neuroscience. Instead of a pure focus on the 'neurobiology' of disease, an opportunity now exists to return to a more integrative approach. The neurovascular unit emphasizes that signaling between vascular and neuronal compartments comprise the basis for both function and dysfunction in brain. Hence, brain disorders are not just due to death of neurons, but instead manifested as cell signaling perturbations at the neurovascular interface. In this mini-review, we will examine 3 examples of this hypothesis: neurovascular mechanisms involved in the thrombolytic therapy of stroke, the crosstalk between neurogenesis and angiogenesis, and the link between vascular dysfunction and amyloid pathology in Alzheimer's disease. An understanding of cell-cell and cell-matrix signaling at the neurovascular interface may yield new approaches for targeting CNS disorders.

• Biomolecules & Therapeutics
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• 제26권2호
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• pp.93-100
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• 2018

Carbon monoxide (CO) is a gaseous molecule produced from heme by heme oxygenase (HO). Endogenous CO production occurring at low concentrations is thought to have several useful biological roles. In mammals, especially humans, a proper neurovascular unit comprising endothelial cells, pericytes, astrocytes, microglia, and neurons is essential for the homeostasis and survival of the central nervous system (CNS). In addition, the regeneration of neurovascular systems from neural stem cells and endothelial precursor cells after CNS diseases is responsible for functional repair. This review focused on the possible role of CO/HO in the neurovascular unit in terms of neurogenesis, angiogenesis, and synaptic plasticity, ultimately leading to behavioral changes in CNS diseases. CO/HO may also enhance cellular networks among endothelial cells, pericytes, astrocytes, and neural stem cells. This review highlights the therapeutic effects of CO/HO on CNS diseases involved in neurogenesis, synaptic plasticity, and angiogenesis. Moreover, the cellular mechanisms and interactions by which CO/HO are exploited for disease prevention and their therapeutic applications in traumatic brain injury, Alzheimer's disease, and stroke are also discussed.

• BMB Reports
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• 제41권5호
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• pp.345-352
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• 2008

The cerebral microvessels possess barrier characteristics which are tightly sealed excluding many toxic substances and protecting neural tissues. The specialized blood-neural barriers as well as the cerebral microvascular barrier are recognized in the retina, inner ear, spinal cord, and cerebrospinal fluid. Microvascular endothelial cells in the brain closely interact with other components such as astrocytes, pericytes, perivascular microglia and neurons to form functional 'neurovascular unit'. Communication between endothelial cells and other surrounding cells enhances the barrier functions, consequently resulting in maintenance and elaboration of proper brain homeostasis. Furthermore, the disruption of the neurovascular unit is closely involved in cerebrovascular disorders. In this review, we focus on the location and function of these various blood-neural barriers, and the importance of the cell-to-cell communication for development and maintenance of the barrier integrity at the neurovascular unit. We also demonstrate the close relation between the alteration of the blood-neural barriers and cerebrovascular disorders.

• Journal of Ginseng Research
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• 제45권5호
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• pp.599-609
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• 2021

Ginseng has long been considered as an herbal medicine. Recent data suggest that ginseng has antiinflammatory properties and can improve learning- and memory-related function in the central nervous system (CNS) following the development of CNS neuroinflammatory diseases such as Alzheimer's disease, cerebral ischemia, and other neurological disorders. In this review, we discuss the role of ginseng in the neurovascular unit, which is composed of endothelial cells surrounded by astrocytes, pericytes, microglia, neural stem cells, oligodendrocytes, and neurons, especially their blood-brain barrier maintenance, anti-inflammatory effects and regenerative functions. In addition, cell-cell communication enhanced by ginseng may be attributed to regeneration via induction of neurogenesis and angiogenesis in CNS diseases. Thus, ginseng may have therapeutic potential to exert cognitive improvement in neuroinflammatory diseases such as stroke, traumatic brain injury, multiple sclerosis, Parkinson's disease, and Alzheimer's disease.

• 대한의생명과학회지
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• 제12권2호
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• pp.127-130
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• 2006

It is important to coordinated interaction among neurons, astrocytes and endothelial cells to maintain the function of brain. To study their regulatory mechanisms in vitro system, the co-culture system among the isolated cells from brain may be needed. However, the method for purifying brain microvascular endothelial cells (BMEC) far culture have not established yet. In this study, the proper culture methods of mice cells using two different strains, CD1 and C57BL6, to obtain the pure and plentiful endothelial cells were described. The flatted-round forms of CD1 endothelial cells grew on the collagen-IV coating plates, while the purified cells from C57 mice preferred type collagen-I dishes for their growth. Both cells displayed anti-PECAM-1 (CD31) and von Willebrand Factor immune-reactivity. These results indicated that different coating materials not only improve attachment of isolated cells but also promoting growth of cells, suggesting that this method of purifying murine Brain microvascular endothelial cells (BMEC) provides a suitable model to investigate blood-brain-barrier (BBB) properties within neurovascular unit in vitro.

• Biomolecules & Therapeutics
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• 제28권1호
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• pp.45-57
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• 2020

In the neurovascular unit, the neuronal and vascular systems communicate with each other. O₂ and nutrients, reaching endothelial cells (ECs) through the blood stream, spread into neighboring cells, such as neural stem cells, and neurons. The proper function of neural circuits in adults requires sufficient O₂ and glucose for their metabolic demands through angiogenesis. In a central nervous system (CNS) injury, such as glioma, Parkinson's disease, and Alzheimer's disease, damaged ECs can contribute to tissue hypoxia and to the consequent disruption of neuronal functions and accelerated neurodegeneration. This review discusses the current evidence regarding the contribution of oxygen deprivation to CNS injury, with an emphasis on hypoxia-inducible factor (HIF)-mediated pathways and Notch signaling. Additionally, it focuses on adult neurological functions and angiogenesis, as well as pathological conditions in the CNS. Furthermore, the functional interplay between HIFs and Notch is demonstrated in pathophysiological conditions.

• The Journal of Korean Physical Therapy
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• 제15권4호
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• pp.412-430
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• 2003

Functional stability is dependent on integrated local and global muscle function. Movement dysfunction can present as a local and global problem, though both frequently occur together. To good understand how movement induces pain syndrome, the optimal actions and interaction of the multiple anatomic and functional systems involved in motion must be considered. Minor alterations in the precision of movement cause microtrauma and, if allowed to continue, will cause macrotrauma and pain. These alteration of the movement result in the development of compensatory movement and movement impairment. Muscle that become tight tend to pull the body segment to which they are attached, creating postural deviation. The antagonistic muscles may become weak and allow postural deviations due to lack of balanced support. Both hypertonic and inhibited muscles will cause an alteration of the distribution of pressure over the joint(s) that they cross and, thus, may not only result from muscle dysfunction, but produce joint dysfunction as well. Alteration of the shoulder posture and movement dysfunction may sometimes result in compression of neurovascular structures in the shoulder and arm. There is a clear link between reduced proprioceptive input, altered motor unit recruitment and the neurovascular compression. This report start with understanding of the impaired alignment, movement patterns and neuromuscular compression of the shoulder girdle by movement impairment to approach method of the movement dysfunction.

• Toxicological Research
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• 제29권3호
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• pp.157-164
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• 2013

Although stroke is one of the leading causes of death and disability worldwide, preventive or therapeutic options are still limited. Therefore, a better understanding of the pathophysiological characteristics of this life-threatening disease is urgently needed. The incidence and prevalence of ischemic stroke are increased by exposure to certain types of xenobiotics, including heavy metals, suggesting the possible toxicological contribution of these compounds to the onset or aggravation of stroke. Among the potential targets, we have focused on alterations to cerebral endothelial cells (CECs), which play important roles in maintaining the functional integrity of brain tissue.

• Animal cells and systems
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• 제10권2호
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• pp.79-83
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• 2006

Tissue plasminogen activator (tPA) is used to lyse clots and reperfuse brain in ischemic stroke. However, sideeffects of intracerebral hemorrhage (ICH) and edema limit their clinical application. In part, these phenomena has been linked with elevations in matrix metalloproteinase-9 (MMP-9) in neurovascular unit. However little is known about their regulatory signaling pathways in brain cells. Here, I examine the role of MAP kinase pathways in tPA-induced MMP-9 regulation in rat cortical astrocytes. tPA $(1-10\;{\mu}g/ml)$ induced dose-dependent elevations in MMP-9 and MMP-2 in conditioned media. Although tPA increased phosphorylation in two MAP kinases (ERK, JNK), only inhibition of the JNK pathway by the JNK inhibitor SP600126 significantly reduced MMP-9 upregulation. Neither ERK inhibition with U0126 nor p38 inhibition with SB203580 had any significant effects. Taken together, these results suggest that c-jun N-terminal kinase (JNK) plays an essential role for tPA-induced MMP-9 upregulation.

• Journal of Yeungnam Medical Science
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• 제40권3호
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• pp.225-232
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• 2023

Cognitive dysfunction is relatively less considered a complication of hypertension. However, there is sufficient evidence to show that high blood pressure in middle age increases the risk of cognitive decline and dementia in old age. The greatest impact on cognitive function in those with hypertension is on executive or frontal lobe function, similar to the area most damaged in vascular dementia. Possible cognitive disorders associated with hypertension are vascular dementia, Alzheimer disease, and Lewy body dementia, listed in decreasing strength of association. The pathophysiology of cognitive dysfunction in individuals with hypertension includes brain atrophy, microinfarcts, microbleeds, neuronal loss, white matter lesions, network disruption, neurovascular unit damage, reduced cerebral blood flow, blood-brain barrier damage, enlarged perivascular damage, and proteinopathy. Antihypertensive drugs may reduce the risk of cognitive decline and dementia. Given the high prevalence of dementia and its impact on quality of life, treatment of hypertension to reduce cognitive decline may be a clinically relevant intervention.