[Platelet-derived growth factor].

Over a century ago, hypertrophy of astrocytes was noted as a pathology of multiple sclerosis (MS) and was hypothesized to play an important role in this disease, yet the contribution of astrocytes has been largely underemphasized in the pathophysiology of CNS demyelination. Astrocytes perform many homeostatic functions within the developing and adult CNS, including enhancing formation and maintenance of the blood–brain barrier, moderating neuronal connections through the tripartite synapse, and perhaps evenoffering intercellular communication independently of neurons. Although there is a significant body of literature characterizing different types of MS lesions, the inflammatory demyelination in an active MS lesion is accompanied by the presence of macrophages, lymphocytes, and large reactive astrocytes. The astrocyte has long been viewed as a cell that promotes inflammation and demyelination, while also forming the glial scar, thus hindering remyelination and axon growth. Renewed interest in the astrocyte has been brought about by recent studies demonstrating that astrocytes can also function as cellular mediators of CNS myelination by promoting oligodendrocyte progenitor migration, proliferation, and differentiation. Thus, refining our knowledge of astrocytic functions in the regulation of CNS myelination may help us to better understand why remyelination fails in MS. © 2010 Wiley-Liss, Inc.

How factors secreted from astrocytes impact myelin repair.

Platelet-derived growth factors (PDGFs) and their receptors (PDGFRs) represent one of the most intensively studied families of growth factors in the last four decades. PDGF signaling plays an essential role in cell proliferation, differentiation, migration, and survival. In vivo studies have documented an important role of PDGF signaling in the normal development of several organs, such as the kidney, eye, or lung. PDGF signaling is essential for the formation of intact mesenchymal cells during embryogenesis. Recently, this knowledge has been extended to a role of PDGF signaling in diseases in general, such as cancer and atherosclerosis, and more importantly in lung diseases, including pulmonary arterial hypertension, lung cancer, and lung fibrosis. In this review, we provide an up-to-date overview of PDGF signaling, including tissue- and cell-type-specific expression patterns and effects. We highlight current therapeutic approaches modifying PDGF signaling in lung diseases and summarize clinical trials in which PDGF signaling has been inhibited. In conclusion, although PDGF inhibition has been used in multiple clinical trials, we suggest that more elaborate and specific approaches for spatio-temporal control of PDGF signaling are required for developing personalized approaches involving PDGF signaling in lung disease.

Platelet-derived growth factor signaling in the lung. From lung development and disease to clinical studies.

Platelet-derived growth factor mediates survival of leukemic large granular lymphocytes via an autocrine regulatory pathway

Considerable attention has focused on the study of neural stem cells (NSCs) as therapy for neurodegenerative diseases. The mammalian brain harbors NSCs throughout life mainly in the subventricular zone (SVZ) as well as the subgranular zone. NSCs in the SVZ are a specialized subpopulation of astrocytes that maintain contact with the ventricle and vascular structures. Components of the SVZ microenvironment, or niche, include intercellular interactions, extracellular matrix proteins, and soluble factors, all of which aid in NSC proliferation, self-renewal, and multipotentiality. Multiple studies demonstrate that endogenous neurogenesis responds to insults such as ischemic stroke, multiple sclerosis and other neurodegenerative diseases, and even brain tumors, supporting the existence of remarkable plasticity and significant regenerative potential in the mammalian brain. Further, in response to recruitment cues from damaged brain tissue NSCs not only "home" to sites of disease but also integrate into functional tissues and appear to acquire the morphological and physiological properties of neurons, astrocytes, and oligodendrocytes. In this review we focus on neurogenesis in the SVZ and on recruitment cues that promote homing and integration of NSCs to sites of disease in the brain. We also discuss animal models of important human neurodegenerative diseases in which transplantation of neural stem cells has been tested.

/pdf/neural-stem-cell-niches-and-homing-recruitment-and-4xp5xhop88.pdf

Neural stem cell niches and homing: recruitment and integration into functional tissues

In multiple sclerosis (MS) and its animal model, experimental allergic encephalomyelitis (EAE), clinical disease is associated with infiltration of the central nervous system (CNS) by immune cells. Subsequent remission with remyelination has been linked to an increased occurrence of oligodendrocyte progenitor (O2A) cells. Platelet-derived growth factor (PDGF) and fibroblast growth factor–2 (FGF-2) are key growth factors for O2A cells, yet little is known about their relevance in EAE and MS. We analyzed the expression of PDGF, FGF-2, and their receptors by peripheral-blood leukocytes (PBLs) and lymphocyte subsets during MBP-induced EAE. Strong up-regulation of PDGF, but not FGF-2, was observed in PBLs, with the highest expression after the disease maximum. T, NK, and NKT cells expressed PDGF, which is a novel observation because thus far only monocytes/macrophages have been reported to express PDGF. These results extend the idea that growth factors may contribute to improved CNS tissue repair, including PDGF, which is secreted by lesion-homing immune cells. The production of PDGF by lymphocytes may have potential therapeutic value when activating or modulating T-cell responses in demyelinating diseases. © 2007 Wiley-Liss, Inc.

Up‐regulation of platelet‐derived growth factor by peripheral‐blood leukocytes during experimental allergic encephalomyelitis

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Up‐regulation of platelet‐derived growth factor by peripheral‐blood leukocytes during experimental allergic encephalomyelitis