北海道大学 · 医学
Takako Chikenji教授の研究室は、線維化疾患、特にカルポスチルン症候群(CTS)や自己免疫疾患における細胞外マトリックスの制御機構に注目し、TGF-βやCTGFをはじめとする成長因子の役割を解明しています。特に、慢性炎症環境における間質幹細幹細胞(MSCs)の若年化的修復作用や、サルコイドーシスやSLEにおける神経障害と骨髄機能障害の関連性についても探求しています。その基盤として、細胞老化と免疫応答の交差メカニズムを解明し、新たな治療戦略の開発を目指しています。
Figures are computed from collected data and may differ slightly.
Non-inflammatory fibrosis of the subsynovial connective tissue (SSCT) is a hallmark of carpal tunnel syndrome (CTS). The etiology of this finding and its relationship to the development of CTS remain poorly understood. Recent studies have found that transforming growth factor-β (TGF-β) plays a central role in fibrosis. The purpose of this study was to investigate the expression of TGF-β and connective tissue growth factor (CTGF), a downstream mediator of TGF-β, in the pathogenesis of CTS. We com
MSCs may exert their effect by remodelling the chronic inflammatory environment via senescence-related regenerative processes.
Rheumatoid arthritis (RA) is an autoimmune disease caused by inflammation of the synovium and characterized by chronic polyarthritis that destroys bone and cartilage. Fibroblast-like synoviocytes (FLSs) in the synovium of patients with RA can promote cartilage and bone destruction by producing proteins such as matrix metalloproteinases and receptor activator of NF-κB ligand, thereby representing an important therapeutic target for RA. FLSs have several phenotypes depending on which cell surface
Carpal tunnel syndrome (CTS) is an idiopathic disease that results from increased fibrosis of the subsynovial connective tissue (SSCT). A recent study found overexpression of both transforming growth factor-β (TGF-β) and connective tissue growth factor (CTGF) in the SSCT of CTS patients. This study investigated TGF-β and CTGF expression in a rabbit model of CTS, in which SSCT fibrosis is induced by a surgical injury. Levels of TGF-β1 and CTGF at 6, 12, 24 weeks after injury were determined by im
Up to 60% of patients with systemic lupus erythematosus (SLE) experience autonomic symptom. Sympathetic nervous system damage can cause dysfunction of the bone marrow that activates inflammatory cells, potentially causing multiple organ damage. We hypothesized that sympathetic nervous system damage would induce bone marrow dysfunction with multiple organ damage in SLE, and that multiple organ damage could be improved by therapy targeting the nervous system. Here, we showed that damage to autonom
Senescent cells create a microenvironment that directs cytotoxic T cell-mediated responses against normal epidermis in patients with CLE, contributing to disease pathology. Targeting senescent cells and their signaling pathways may offer novel therapeutic strategies for patients with skin lesions from CLE and SLE.
The purpose of this study was to investigate the strengths of four intrinsic muscles of the hand of college baseball players. The strengths of four intrinsic muscle groups were measured by the Rotterdam Intrinsic Hand Myometer (RIHM) which has been developed to assess the abduction of the little finger and index finger, and palmar abduction and opposition of the thumb. The strengths of these four intrinsic muscle groups were compared between baseball players and inexperienced sports players. The
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