Редактирование: PDGFB

Platelet-derived growth factor subunit B precursor (PDGF subunit B) (PDGF-2) (Platelet-derived growth factor B chain) (Platelet-derived growth factor beta polypeptide) (Proto-oncogene c-Sis) (Becaplermin) [PDGF2] [SIS]

==Publications==

{{medline-entry
|title=Skin-resident stem cells and wound healing.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/28539548
|abstract=CD271 is common stem cell marker for the epidermis and dermis. We assessed a kinetic movement of epidermal and dermal CD271  cells in the wound healing process to elucidate the possible involvement with chronic skin ulcers. Epidermal CD271  cells were proliferated and migrated from 3 days after wounding. Purified epidermal CD271  cells expressed higher TGFβ2 and V[[EGF]]α transcripts than CD271  cells. Delayed wound healing was observed in the aged mice compared with young mice. During the wound healing process, the peak of dermal CD271  cell accumulation was delayed in aged mice compared with young mice. The expression levels of collagen-1, -3, -5, F4-80, [[EGF]], [[FGF2]], TGFβ1, and IL-1α were significantly increased in young mice compared with aged mice. Furthermore, purified dermal CD271  cells expressed higher [[FGF2]], [[EGF]], [[PDGFB]], and TGFβ1 gene transcripts than CD271  cells. These results suggested that epidermal and dermal CD271  cells were closely associated with wound healing process by producing various growth factors. Epidermal and dermal CD271  cells in chronic skin ulcer patients were significantly reduced compared with healthy controls. Thus, both epidermal and dermal stem cells can play an important role in wound healing process.
|mesh-terms=* Aging
* Animals
* Cell Movement
* Cell Proliferation
* Chronic Disease
* Disease Models, Animal
* Humans
* Mice
* Receptors, Nerve Growth Factor
* Skin
* Skin Physiological Phenomena
* Skin Ulcer
* Stem Cells
* Transforming Growth Factor beta
* Vascular Endothelial Growth Factor A
* Wound Healing
|keywords=* CD271
* stem cell
* wound healing
|full-text-url=https://sci-hub.do/10.2177/jsci.40.1
}}
{{medline-entry
|title=The choroid plexus transcriptome reveals changes in type I and II interferon responses in a mouse model of Alzheimer's disease.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/26092102
|abstract=Alzheimer's disease (AD) is a neurodegenerative disorder characterized by a marked decline in cognition and memory function. Increasing evidence highlights the essential role of neuroinflammatory and immune-related molecules, including those produced at the brain barriers, on brain immune surveillance, cellular dysfunction and amyloid beta (Aβ) pathology in AD. Therefore, understanding the response at the brain barriers may unravel novel pathways of relevance for the pathophysiology of AD. Herein, we focused on the study of the choroid plexus ([[CP]]), which constitutes the blood-cerebrospinal fluid barrier, in aging and in AD. Specifically, we used the [[PDGFB]]-APPSwInd (J20) transgenic mouse model of AD, which presents early memory decline and progressive Aβ accumulation, and littermate age-matched wild-type (WT) mice, to characterize the [[CP]] transcriptome at 3, 5-6 and 11-12months of age. The most striking observation was that the [[CP]] of J20 mice displayed an overall overexpression of type I interferon (IFN) response genes at all ages. Moreover, J20 mice presented a high expression of type II IFN genes in the [[CP]] at 3months, which became lower than WT at 5-6 and 11-12months. Importantly, along with a marked memory impairment and increased glial activation, J20 mice also presented a similar overexpression of type I IFN genes in the dorsal hippocampus at 3months. Altogether, these findings provide new insights on a possible interplay between type I and II IFN responses in AD and point to IFNs as targets for modulation in cognitive decline. 
|mesh-terms=* Aging
* Alzheimer Disease
* Amyloid beta-Peptides
* Animals
* Astrocytes
* Choroid Plexus
* Disease Models, Animal
* Interferon Type I
* Interferon-gamma
* Male
* Maze Learning
* Mice
* Mice, Inbred C57BL
* Neurons
* Transcriptome
|keywords=* Aging
* Alzheimer’s disease
* Cerebrospinal fluid
* Choroid plexus
* Glial cells
* Hippocampus
* Interferons
* Memory
* Neuroinflammation
* Transcriptome
|full-text-url=https://sci-hub.do/10.1016/j.bbi.2015.06.008
}}