Pericytes in Brain Injury and Repair After Ischemic Stroke

Cai, Wei; Liu, Huan; Zhao, Jingyan; Chen, Lily Y.; Chen, Jun; Lu, Zhengqi; Hu, Xiaoming

doi:10.1007/s12975-016-0504-4

Cited by 142 publications

(117 citation statements)

References 113 publications

(162 reference statements)

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“…37 Similarly, brain-derived pericytes are primed to participate in neural repair. 38,39 Skeletal muscle derived pericytes participate in myogenesis and incorporate into injured muscle, whereas other tissuespecific pericytes do not. 40 Our results show that the frequency of PDGFRα + adventitial cells differs somewhat widely across organs.…”

Section: Discussionmentioning

confidence: 99%

PDGFRα marks distinct perivascular populations with different osteogenic potential within adipose tissue

Wang

Meyers

et al. 2019

Stem Cells

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The perivascular niche within adipose tissue is known to house multipotent cells, including osteoblast precursors. However, the identity of perivascular subpopulations that may mineralize or ossify most readily is not known. Here, we utilize inducible PDGFRα (platelet-derived growth factor alpha) reporter animals to identify subpopulations of perivascular progenitor cells. Results showed that PDGFRα-expressing cells are present in four histologic niches within inguinal fat, including two perivascular locations. PDGFRα + cells are most frequent within the tunica adventitia of arteries and veins, where PDGFRα + cells populate the inner aspects of the adventitial layer.Although both PDGFRα + and PDGFRα − fractions are multipotent progenitor cells, adipose tissue-derived PDGFRα + stromal cells proliferate faster and mineralize to a greater degree than their PDGFRα − counterparts. Likewise, PDGFRα + ectopic implants reconstitute the perivascular niche and ossify to a greater degree than PDGFRα − cell fractions. Adventicytes can be further grouped into three distinct groups based on expression of PDGFRα and/or CD34. When further partitioned, adventicytes co-expressing PDGFRα and CD34 represented a cell fraction with the highest mineralization potential. Long-term tracing studies showed that PDGFRαexpressing adventicytes give rise to adipocytes, but not to other cells within the vessel wall under homeostatic conditions. However, upon bone morphogenetic protein 2 (BMP2)-induced ossicle formation, descendants of PDGFRα + cells gave rise to osteoblasts, adipocytes, and "pericyte-like" cells within the ossicle. In sum, PDGFRα marks distinct perivascular osteoprogenitor cell subpopulations within adipose tissue.

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Section: Discussionmentioning

confidence: 99%

PDGFRα marks distinct perivascular populations with different osteogenic potential within adipose tissue

Wang

Meyers

et al. 2019

Stem Cells

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“…187 In acute focal cerebral ischemia, the "no-reflow phenomenon" and secondary hypoperfusion occur due to structural changes of the ischemic capillary bed because of astrocytic endfeet and endothelial swelling and constrictions of the capillary pericytes. 188,189 Several pathways, especially ROS-mediated translocation of myosin, thromboxane A2 release, and cytosolic calcium increase, cause pericytes constriction and death after ischemic stroke. 190 However, ischemic hypoxia results in activation of A2a receptors, and the NO/guanylate cyclase pathway leads to the dilation of pericytes.…”

Section: Role Of Neurovascular Unit In Ischemia and Glioma Astrocytesmentioning

confidence: 99%

The interrelationship between cerebral ischemic stroke and glioma: a comprehensive study of recent reports

Ghosh

Chakraborty

Sarkar

et al. 2019

Sig Transduct Target Ther

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Glioma and cerebral ischemic stroke are two major events that lead to patient death worldwide. Although these conditions have different physiological incidences,~10% of ischemic stroke patients develop cerebral cancer, especially glioma, in the postischemic stages. Additionally, the high proliferation, venous thrombosis and hypercoagulability of the glioma mass increase the significant risk of thromboembolism, including ischemic stroke. Surprisingly, these events share several common pathways, viz. hypoxia, cerebral inflammation, angiogenesis, etc., but the proper mechanism behind this co-occurrence has yet to be discovered. The hypercoagulability and presence of the D-dimer level in stroke are different in cancer patients than in the noncancerous population. Other factors such as atherosclerosis and coagulopathy involved in the pathogenesis of stroke are partially responsible for cancer, and the reverse is also partially true. Based on clinical and neurosurgical experience, the neuronal structures and functions in the brain and spine are observed to change after a progressive attack of ischemia that leads to hypoxia and atrophy. The major population of cancer cells cannot survive in an adverse ischemic environment that excludes cancer stem cells (CSCs). Cancer cells in stroke patients have already metastasized, but early-stage cancer patients also suffer stroke for multiple reasons. Therefore, stroke is an early manifestation of cancer. Stroke and cancer share many factors that result in an increased risk of stroke in cancer patients, and vice-versa. The intricate mechanisms for stroke with and without cancer are different. This review summarizes the current clinical reports, pathophysiology, probable causes of co-occurrence, prognoses, and treatment possibilities.

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“…1) can occur as a result of the initial injury or arise secondarily to the extensive neuroinflammation, astrocytic dysfunction, and metabolic disturbances. These damages result in vascular leakage, brain edema, cerebral hemorrhage, and hypoxia [27,29,[33][34][35]. Neuronal apoptosis also significantly contributes to secondary injury [36,37].…”

Section: Introductionmentioning

confidence: 99%

Dual roles of astrocytes in plasticity and reconstruction after traumatic brain injury

et al. 2020

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Traumatic brain injury (TBI) is one of the leading causes of fatality and disability worldwide. Despite its high prevalence, effective treatment strategies for TBI are limited. Traumatic brain injury induces structural and functional alterations of astrocytes, the most abundant cell type in the brain. As a way of coping with the trauma, astrocytes respond in diverse mechanisms that result in reactive astrogliosis. Astrocytes are involved in the physiopathologic mechanisms of TBI in an extensive and sophisticated manner. Notably, astrocytes have dual roles in TBI, and some astrocyte-derived factors have double and opposite properties. Thus, the suppression or promotion of reactive astrogliosis does not have a substantial curative effect. In contrast, selective stimulation of the beneficial astrocytederived molecules and simultaneous attenuation of the deleterious factors based on the spatiotemporalenvironment can provide a promising astrocyte-targeting therapeutic strategy. In the current review, we describe for the first time the specific dual roles of astrocytes in neuronal plasticity and reconstruction, including neurogenesis, synaptogenesis, angiogenesis, repair of the blood-brain barrier, and glial scar formation after TBI. We have also classified astrocyte-derived factors depending on their neuroprotective and neurotoxic roles to design more appropriate targeted therapies.

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Pericytes in Brain Injury and Repair After Ischemic Stroke

Cited by 142 publications

References 113 publications

PDGFRα marks distinct perivascular populations with different osteogenic potential within adipose tissue

PDGFRα marks distinct perivascular populations with different osteogenic potential within adipose tissue

The interrelationship between cerebral ischemic stroke and glioma: a comprehensive study of recent reports

Dual roles of astrocytes in plasticity and reconstruction after traumatic brain injury

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