Pericytes are specialized mural cells located at the abluminal surface of capillary blood vessels, embedded within the basement membrane. In the vascular network these multifunctional cells fulfil diverse functions, which are indispensable for proper homoeostasis. They serve as microvascular stabilizers, are potential regulators of microvascular blood flow and have a central role in angiogenesis, as they for example regulate endothelial cell proliferation. Furthermore, pericytes, as part of the neurovascular unit, are a major component of the blood-retina/brain barrier. CNS pericytes are a heterogenic cell population derived from mesodermal and neuro-ectodermal germ layers acting as modulators of stromal and niche environmental properties. In addition, they display multipotent differentiation potential making them an intriguing target for regenerative therapies. Pericyte-deficiencies can be cause or consequence of many kinds of diseases. In diabetes, for instance, pericyte-loss is a severe pathological process in diabetic retinopathy (DR) with detrimental consequences for eye sight in millions of patients. In this review, we provide an overview of our current understanding of CNS pericyte origin and function, with a special focus on the retina in the healthy and diseased. Finally, we highlight the role of pericytes in de- and regenerative processes.
Since YFP-positive PCs and vSMCs are colocalized with NG2 and PDGFRβ, we propose that capillary PCs and vSMCs in the retina and the optic nerve, both parts of the central nervous system, as well as in the choroid, a tissue of mesodermal origin, derive from the neural crest.
Summary1. Plant-soil feedback (PSF) may affect above-ground higher trophic levels in glasshouse experiments, but evidence from field studies on the relevance of these multitrophic interactions for plant performance is lacking. Therefore, we examined whether PSF effects of several native and invasive plant species occur also in the field and influence plant damage by above-ground herbivores. 2. Root zone soil from an abandoned urban field was used as inocula for the PSF experiment. First, we grew eight urban grassland plant species (five natives and three invasive species) separately in a glasshouse, with soil biota communities conditioned by the respective species itself ('home soil') or by a mixture of all other species ('foreign soil'). After 13 weeks, one cohort of the plants was placed on an urban field in Berlin to assess damage by naturally colonizing herbivores, while another cohort of the plants stayed in the glasshouse. 3. We observed that the extent of the PSF effects differed between the field and glasshouse cohorts of plants. While we found positive PSF responses for five of the eight plant species in the glasshouse, we found no PSF effects in the field. Further, there was no trend that invasive or native species differed in the direction or extent of PSF responses. Concerning the leaf damage by herbivores of the field plants, we found no evidence that the soil history (home vs. foreign soil) affected the effects of above-ground herbivores on the plants. 4. Synthesis. We conclude that PSF effects are more likely to be found under glasshouse conditions. In the field, PSFs seem to play a minor role for the selected urban grassland species. More generally, our study highlights the need to focus on PSFs under natural conditions and in natural communities (including higher trophic levels), which is often overlooked in PSF research.
Based on previous findings of visual field defects after LASIK, and as a consequence of the present study, it seems feasible to design patient interfaces in a more physiologic manner to prevent high IOPs during refractive procedures.
Autophagy is an important cellular mechanism for maintaining cellular homeostasis, and its impairment correlates highly with age and age-related diseases. Retinal pigment epithelial (RPE) cells of the eye represent a crucial model for studying autophagy, as RPE functions and integrity are highly dependent on an efficient autophagic process. Cysteinyl leukotriene receptor 1 (CysLTR1) acts in immunoregulation and cellular stress responses and is a potential regulator of basal and adaptive autophagy. As basal autophagy is a dynamic process, the aim of this study was to define the role of CysLTR1 in autophagy regulation in a chronobiologic context using the ARPE-19 human RPE cell line. Effects of CysLTR1 inhibition on basal autophagic activity were analyzed at inactive/low and high lysosomal degradation activity with the antagonists zafirlukast (ZTK) and montelukast (MTK) at a dosage of 100 nM for 3 hours. Abundances of the autophagy markers LC3-II and SQSTM1 and LC3B particles were analyzed in the absence and presence of lysosomal inhibitors using western blot analysis and immunofluorescence microscopy. CysLTR1 antagonization revealed a biphasic effect of CysLTR1 on autophagosome formation and lysosomal degradation that depended on the autophagic activity of cells at treatment initiation. ZTK and MTK affected lysosomal degradation, but only ZTK regulated autophagosome formation. In addition, dexamethasone treatment and serum shock induced autophagy, which was repressed by CysLTR1 antagonization. As a newly identified autophagy modulator, CysLTR1 appears to be a key player in the chronobiological regulation of basal autophagy and adaptive autophagy in RPE cells.
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