Endothelial progenitor cells and revascularization following stroke

Feifei Ma, Anna Morancho, Joan Montaner, Anna Rosell

Abstract
Brain injury after ischemia induces the mobilization of endothelial progenitor cells (EPCs), a population of bone marrow-derived cells with angio-vasculogenic capabilities. These cells have been also tested in pre-clinical models and proposed for neurorepair therapy aiming to treat patients in the delayed phases of stroke disease. Promising results in the pre-clinical field encourage the translation into a clinical therapeutic approach. In this review, we will describe EPCs actions for enhanced revascularization and neurorepair, which on one hand are by their direct incorporation into new vascular networks/structures or by direct cell–cell interactions with other brain cells, but also to indirect cell–cell communication thorough EPCs secreted growth factors. All these actions contribute to potentiate neurovascular remodeling and neurorepair. The data presented in this review encourages for a deep understanding of the mechanisms of the cross-talks between EPCs and other brain and progenitor cells, which deserves additional investigations and efforts that may lead to new EPCs-based therapies for stroke patients.

Source: CLICK HERE

Keywords:
Stroke, Endothelial progenitor cell, Growth factor, Angiogenesis, Vasculogenesis, Neurorepair

Mechanisms of cell–cell interaction in oligodendrogenesis and remyelination after stroke

Kanako Itoh, Takakuni Maki, Josephine Lok, Ken Arai

Abstract

White matter damage is a clinically important aspect of several central nervous system diseases, including stroke. Cerebral white matter primarily consists of axonal bundles ensheathed with myelin secreted by mature oligodendrocytes, which play an important role in neurotransmission between different areas of gray matter. During the acute phase of stroke, damage to oligodendrocytes leads to white matter dysfunction through the loss of myelin. On the contrary, during the chronic phase, white matter components promote an environment, which is favorable for neural repair, vascular remodeling, and remyelination. For effective remyelination to take place, oligodendrocyte precursor cells (OPCs) play critical roles by proliferating and differentiating into mature oligodendrocytes, which help to decrease the burden of axonal injury. Notably, other types of cells contribute to these OPC responses under the ischemic conditions. This mini-review summarizes the non-cell autonomous mechanisms in oligodendrogenesis and remyelination after white matter damage, focusing on how OPCs receive support from their neighboring cells.

Source: CLICK HERE

Keywords:

White matter, Stroke, Oligodendrocyte precursor cell, Cell–cell interaction

The axon–glia unit in white matter stroke: Mechanisms of damage and recovery

Shira Rosenzweig, S. Thomas Carmichael

Abstract

Approximately one quarter of all strokes in humans occur in white matter, and the progressive nature of white matter lesions often results in severe physical and mental disability. Unlike cortical grey matter stroke, the pathology of white matter stroke revolves around disrupted connectivity and injured axons and glial cells, rather than neuronal cell bodies. Consequently, the mechanisms behind ischemic damage to white matter elements, the regenerative responses of glial cells and their signaling pathways, all differ significantly from those in grey matter. Development of effective therapies for white matter stroke would require an enhanced understanding of the complex cellular and molecular interactions within the white matter, leading to the identification of new therapeutic targets. This review will address the unique properties of the axon–glia unit during white matter stroke, describe the challenging process of promoting effective white matter repair, and discuss recently-identified signaling pathways which may hold potential targets for repair in this disease.

Source: CLICK HERE

Keywords:

White matter, Stroke, Ischemia, Repair, Oligodendrocytes, Myelin

The evolving roles of pericyte in early brain injury after subarachnoid hemorrhage

Yujie Chen, Qiang Li, Jiping Tang, Hua Feng, John H Zhang

Abstract

Despite accumulated understanding on the mechanisms of early brain injury and improved management of subarachnoid hemorrhage (SAH), it is still one of the serious and refractory health problems around the world. Traditionally, pericyte, served as capillary contraction handler, is recently considered as the main participant of microcirculation regulation in SAH pathophysiology. However, accumulate evidences indicate that pericyte is much more than we already know. Therefore, we briefly review the characteristics, regulation pathways and functions of pericyte, aim to summarize the evolving new pathophysiological roles of pericyte that are implicated in early brain injury after SAH and to improve our understanding in order to explore potential novel therapeutic options for patients with SAH.

Source: CLICK HERE

Keywords:

Pericyte, Subarachnoid hemorrhage, Early brain injury, Vascular neural network

Intercellular cross-talk in intracerebral hemorrhage

Yusuke Egashira, Ya Hua, Richard F. Keep, Guohua Xi

Abstract

Intracerebral hemorrhage (ICH) is a devastating cerebrovascular disorder with high mortality and morbidity. Currently, there are few treatment strategies for ICH-induced brain injury. A recent increase in interest in the pathophysiology of ICH has led to elucidation of the pathways underlying ICH-induced brain injury, pathways where intercellular and hematoma to cell signaling play important roles. In this review, we summarize recent advances in ICH research focusing on intercellular and hematoma:cell cross-talk related to brain injury and recovery after ICH.

Source: CLICK HERE

Keywords:

Brain injury, Experimental model, Intracerebral hemorrhage, Injury mechanism, Intercellular signaling

Cellular connections, microenvironment and brain angiogenesis in diabetes: Lost communication signals in the post-stroke period

Adviye Ergul, John Paul Valenzuela, Abdelrahman Y. Fouda, Susan C. Fagan

Abstract

Diabetes not only increases the risk but also worsens the motor and cognitive recovery after stroke, which is the leading cause of disability worldwide. Repair after stroke requires coordinated communication among various cell types in the central nervous system as well as circulating cells. Vascular restoration is critical for the enhancement of neurogenesis and neuroplasticity. Given that vascular disease is a major component of all complications associated with diabetes including stroke, this review will focus on cellular communications that are important for vascular restoration in the context of diabetes.

Source: CLICK HERE

Keywords:

Diabetes, Angiogenesis, Vascular restoration, Stroke

SIRP/CD47 signaling in neurological disorders

Haiyue Zhanga, Fengwu Li, Yuanyuan Yang, Jun Chena, Xiaoming Hu

Abstract

Microglia play important roles in the process of neuronal injury and recovery. Numeous surface receptors have been described to regulate microglial activation. These receptors tightly mediate normal microglial functions including cell mobility, phagocytosis, and production of inflammatory mediators or trophic factors. In recent years, significant progresses have been achieved for understanding the signaling mechanisms underlying these receptors. Their specific roles in neurological diseases have been documented. This review will focus on the signal regulatory protein (SIRP) and its ligand CD47, two surface receptors expressed on microglia and other cells in the central nervous system (CNS) such as neurons. We will discuss the involvement of SIRP/CD47 signaling in microglial activation and in the interplay between microglia and other CNS cells. Current studies reveal the importance of CD47 and SIRPα in the process of neuroinflammation in the CNS disorders. The dual and contradictory role of CD47 suggests that targeting the SIRPα/CD47 signaling may achieve different effects depending on disease stage.

Source: CLICK HERE

Keywords:

Signal regulatory protein (SIRP), CD47, Microglia, Neuroinflammation

Interaction of astrocytes and T cells in physiological and pathological conditions

Luokun Xie, Shao-Hua Yang

Abstract

The central nervous system (CNS) has long been recognized as a site of ‘immune privilege’ because of the existence of the blood brain barrier (BBB) which presumably isolates CNS from the peripheral immunosurveillance. Different from the peripheral organs, CNS is unique in response to all forms of CNS injury and disease which is mainly mediated by resident microglia and astrocyte. There is increasing evidence that immune cells are not only involved in neuroinflammation process but also the maintenance of CNS homeostasis. T cells, an important immune cell population, are involved in the pathogenesis of some neurological diseases by inducing either innate or adaptive immune responses. Astrocytes, which are the most abundant cell type in the CNS, maintain the integrity of BBB and actively participate in the initiation and progression of neurological diseases. Surprisingly, how astrocytes and T cells interact and the consequences of their interaction are not clear. In this review we briefly summarized T cells diversity and astrocyte function. Then, we examined the evidence for the astrocytes and T cells interaction under physiological and pathological conditions including ischemic stroke, multiple sclerosis, viral infection, and Alzheimer’s disease.

Source: CLICK HERE

Keywords:

T cells, Astrocyte, Central nervous system, Stroke, Alzheimer’s disease, Multiple sclerosis

Complexity of the cell–cell interactions in the innate immune response after cerebral ischemia

Maria I. Cuartero, Ivan Ballesteros, Ignacio Lizasoain, Maria A. Moro

Abstract

In response to brain ischemia a cascade of signals leads to the activation of the brain innate immune system and to the recruitment of blood borne derived cells to the ischemic tissue. These processes have been increasingly shown to play a role on stroke pathogenesis. Here, we discuss the key features of resident microglia and different leukocyte subsets implicated in cerebral ischemia with special emphasis of neutrophils, monocytes and microglia. We focus on how leukocytes are recruited to injured brain through a complex interplay between endothelial cells, platelets and leukocytes and describe different strategies used to inhibit their recruitment. Finally, we discuss the possible existence of different leukocyte subsets in the ischemic tissue and the repercussion of different myeloid phenotypes on stroke outcome. The knowledge of the nature of these heterogeneous cell–cell interactions may open new lines of investigation on new therapies to promote protective immune responses and tissue repair after cerebral ischemia or to block harmful responses.

Source: CLICK HERE

Keywords:

Neuroinflammation, Stroke, Cerebral ischemia, Leukocyte, Microglia, Neuroimmune, Interactions