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診療報酬「本体」0.55%引き上げ 前回と同水準 政府方針 (毎日新聞)

麻生太郎副総理兼財務相=川田雅浩撮影 [PR] 政府は13日、2020年度の診療報酬の改定で、医師の技術料にあたる「本体部分」を0・55%引き上げる方針を固めた...

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Fibrotic scar after experimental autoimmune encephalomyelitis inhibits oligodendrocyte differentiation.

著者 Yahn SL , Li J , Goo I , Gao H , Brambilla R , Lee JK
Neurobiol Dis.2019 Nov 12 ; ():104674.
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Remyelination failure is a crucial component of disease progression in the autoimmune demyelinating disease Multiple Sclerosis (MS). The regenerative capacity of oligodendrocyte progenitor cells (OPCs) to replace myelinating oligodendrocytes is likely influenced by many aspects of the lesion environment including inflammatory signaling and extracellular matrix (ECM) deposition. These features of MS lesions are typically attributed to infiltrating leukocytes and reactive astrocytes. Here we demonstrate that fibroblasts also contribute to the inhibitory environment in the animal model of MS, experimental autoimmune encephalomyelitis (EAE). Using Col1α1 transgenic mice, we show that perivascular fibroblasts are activated in the spinal cord at EAE onset, and infiltrate the parenchyma by the peak of behavioral deficits where they are closely associated with areas of demyelination, myeloid cell accumulation, and ECM deposition. We further show that both fibroblast conditioned media and fibroblast ECM inhibit the differentiation of OPCs into mature oligodendrocytes. Taken together, our results indicate that the fibrotic scar is a major component of EAE pathology that leads to an inhibitory environment for remyelination, thus raising the possibility that anti-fibrotic mechanisms may serve as novel therapeutic targets for MS.
PMID: 31731043 [PubMed - as supplied by publisher]
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