scholarly journals A Synoptic Overview of Neurovascular Interactions in the Foot

2020 ◽  
Vol 11 ◽  
Author(s):  
Gayathri Balasubramanian ◽  
Prashanth Vas ◽  
Nachiappan Chockalingam ◽  
Roozbeh Naemi
Keyword(s):  
Neurovascular Interactions

scholarly journals Generation of Vascularized Brain Organoids to Study Neurovascular Interactions

2022 ◽  
Author(s):  
Zhen-Ge Luo ◽  
Xin-Yao Sun ◽  
Xiang-Chun Ju ◽  
Yang Li ◽  
Peng-Ming Zeng ◽  
...  
Keyword(s):  
Brain Development ◽  
Neural Development ◽  
Immune Cells ◽  
Aging Process ◽  
Neural Progenitors ◽  
Brain Disorders ◽  
Specific Population ◽  
Neurovascular Interactions ◽  
The Brain

The recently developed brain organoids have been used to recapitulate the processes of brain development and related diseases. However, the lack of vasculatures, which regulate neurogenesis, brain disorders, and aging process, limits the utility of brain organoids. In this study, we induced vessel and brain organoids respectively, and then fused two types of organoids together to obtain vascularized brain organoids. The fused brain organoids were engrafted with robust vascular network-like structures, and exhibited increased number of neural progenitors, in line with the possibility that vessels regulate neural development. Fusion organoids also contained functional blood-brain-barrier (BBB)-like structures, as well as microglial cells, a specific population of immune cells in the brain. The incorporated microglia responded actively to immune stimuli to the fused brain organoids. Thus, the fusion organoids established in this study allow modeling interactions between the neuronal and non-neuronal components in vitro, in particular the vasculature and microglia niche.

scholarly journals Progressive myoclonic epilepsy-associated geneKctd7regulates retinal neurovascular patterning and function

2019 ◽  
Author(s):  
Jonathan Alevy ◽  
Courtney A. Burger ◽  
Nicholas E. Albrecht ◽  
Danye Jiang ◽  
Melanie A. Samuel
Keyword(s):  
Bipolar Cells ◽  
Retinal Function ◽  
Myoclonic Epilepsy ◽  
Human Diseases ◽  
Inner Retina ◽  
Vascular Patterning ◽  
Neurovascular Interactions ◽  
Progressive Myoclonic Epilepsy ◽  
And Function ◽  
Neuron Function

AbstractNeuron function relies on and instructs the development and precise organization of neurovascular units that in turn support circuit activity. However, our understanding of the molecular cues that regulate this relationship remains sparse. Using a high-throughput screening pipeline, we recently identified several new regulators of vascular patterning. Among these was the potassium channel tetramerization domain-containing protein 7 (KCTD7). Mutations inKCTD7are associated with progressive myoclonic epilepsy, but how KCTD7 regulates neural development and function remains poorly understood. To begin to identify such mechanisms, we focus on mouse retina, a tractable part of the central nervous system that contains precisely ordered neuron subtypes supported by a trilaminar intravascular network. We find that deletion ofKctd7results in defective patterning of the adult retina vascular network, resulting in increased branching, vessel length, and lacunarity. These alterations reflect early and specific defects in vessel development, as emergence of the superficial and deep vascular layers were delayed. These defects are likely due to a role for Kctd7 in inner retina neurons. Kctd7 it is absent from vessels but present in neurons in the inner retina, and its deletion resulted in a corresponding increase in the number of bipolar cells in development and increased vessel branching in adults. These alterations were accompanied by retinal function deficits. Together, these data suggest that neuronal Kctd7 drives growth and patterning of the vasculature and suggest that neurovascular interactions may participate in the pathogenesis of KCTD7-related human diseases.Alevy et al. HighlightsKctd7 is required for normal retinal vascular organization and retinal function in adults.Deletion ofKctd7disrupts the emergence of the superficial and deep vessel layers.Kctd7 may impact vascular patterning through influencing neurons as it is expressed in and regulates bipolar cells.Kctd7 driven neurovascular interactions may participate in the pathogenesis of KCTD7-related human diseases.Lay SummaryNeuron function requires an organized vasculature to maintain brain health and prevent disease, but many neurovasculature regulatory genes remain unknown. Alevy et al. identify the progressive myoclonic epilepsy-associated geneKctd7as a key regulator of vascular development and retinal function. They further show that Kctd7 regulation of vessel patterning likely occurs downstream of its role in regulating the development or activity of specific neuron types. These data suggest that KCTD7-regulated neurovascular interactions may participate in the pathogenesis of associated human diseases.

Role of bone marrow-derived macrophages (BMDMs) in neurovascular interactions during stroke

2019 ◽  
Vol 129 ◽  
pp. 104480 ◽  
Author(s):  
Akriti Srivastava ◽  
Pranay Srivastava ◽  
Rajkumar Verma
Keyword(s):  
Bone Marrow ◽  
Neurovascular Interactions

scholarly journals Neurovascular Interactions in the Retina: Physiological and Pathological Roles

2013 ◽  
Vol 123 (2) ◽  
pp. 79-84 ◽  
Author(s):  
Tsutomu Nakahara ◽  
Asami Mori ◽  
Yuki Kurauchi ◽  
Kenji Sakamoto ◽  
Kunio Ishii
Keyword(s):  
Neurovascular Interactions

scholarly journals CX3CR1-CCR2-dependent monocyte-microglial signaling modulates neurovascular leakage and acute injury in a mouse model of childhood stroke

2019 ◽  
Vol 39 (10) ◽  
pp. 1919-1935 ◽  
Author(s):  
Joel Faustino ◽  
Sophorn Chip ◽  
Nikita Derugin ◽  
Amandine Jullienne ◽  
Mary Hamer ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Vascular Inflammation ◽  
Neutrophil Infiltration ◽  
Acute Injury ◽  
Arterial Ischemic Stroke ◽  
Vascular Abnormalities ◽  
Functional Deficits ◽  
Albumin Leakage ◽  
Neurovascular Interactions ◽  
Perinatal Arterial Ischemic Stroke

Stroke is among the top 10 causes of death in children. The developmental stage of the brain is central to stroke pathophysiology. The incidence of childhood arterial ischemic stroke (CAIS) is lower than of perinatal arterial ischemic stroke but the rate of recurrence is strikingly high. Vascular inflammation is seen as major contributor to CAIS but the mechanisms that govern structural-functional basis of vascular abnormalities remain poorly understood. To identify the contribution of immune-neurovascular interactions to CAIS, we established stroke model in postnatal day 21 (P21) mice. We demonstrate acute functional deficits and histological injury and chronic MRI-identifiable injury, brain atrophy and marked derangements in the vascular network. In contrast to negligible albumin leakage and neutrophil infiltration following acute perinatal stroke, CAIS leads to significantly increased albumin leakage and neutrophil infiltration in injured regions of wild type mice and mice with functional CX3CR1-CCR2 receptors. In mice with dysfunctional CX3CR1-CCR2 signaling, extravascular albumin leakage is significantly attenuated, infiltration of injurious Ccr2+-monocytes essentially aborted, accumulation of Ly6G+ neutrophils reduced and acute injury attenuated. Unique identifiers of microglia and monocytes revealed phenotypic changes in each cell subtype of the monocyte lineage after CAIS. Taken together, CX3CR1-CCR2-dependent microglia-monocyte signaling contributes to cerebrovascular leakage, inflammation and CAIS injury.

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