RE: Onuma H, Tsuji K, Hoshino T, Inomata K, Udo M, Nakagawa Y, Katagiri H, Miyatake K, Watanabe T, Sekiya I, Muneta T, Koga H. Fibrotic changes in the infrapatellar fat pad induce new vessel formation and sensory nerve fiber endings that associate prolong
RE: Onuma H, Tsuji K, Hoshino T, Inomata K, Udo M, Nakagawa Y, Katagiri H, Miyatake K, Watanabe T, Sekiya I, Muneta T, Koga H. Fibrotic changes in the infrapatellar fat pad induce new vessel formation and sensory nerve fiber endings that associate prolong
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RE: Onuma H、Tsuji K、Hoshino T、Inomata K、Udo M、Nakakawa Y、Katagiri H、Miyatake K、Watanabe T、Sekiya I、Muneta T、Koga H。髌下脂肪垫的纤维化变化诱导新血管形成和
DOI：
10.1002/jor.24966
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发表时间：
2021
影响因子：
2.8
通讯作者：
Macchi Veronica
中科院分区：
文献类型：
--
作者：
Stocco Elena;Porzionato Andrea;De Caro Raffaele;Macchi Veronica
根据OA-IFPs中神经纤维末梢的增加，我们评估了终末期OA-IFPs和健康IFPs中神经元蛋白S-100的表达。在OA-IFP组织形态描述之后，我们专注于可能负责这种组织修饰的关键元素的分离/表征：OA-IFP干细胞。相反，在OA中通常上调的I CD38/NADase I的零表达意味着OA- ifp干细胞无法抵抗NAD SP+ SP介导的OA炎症，从而导致细胞应激（I钙网蛋白I基因的显著表达）。[文章节选]
Referring to the increase in nerve-fiber endings in OA-IFPs, we evaluated the neuronal protein S-100 expression, in both end-stage-OA IFPs and healthy-IFPs. After OA-IFP tissue morphological description, we focused on the isolation/characterization of the key elements likely responsible of such tissue modification: the OA-IFP stem cells. In contrast, the null-expression of I CD38/NADase i, commonly upregulated in OA, implied OA-IFP stem cells inability to counteract NAD SP+ sp-mediated OA inflammation thus causing cellular stress (significant expression of I calreticulin i gene).[Extracted from the article]