نتایج جستجو برای: articular chondrocyte

تعداد نتایج: 32509  

2011
Sung Won Lee Yeon Suk Song Sang Yeob Lee Young Geol Yoon Sang Hwa Lee Bong Soo Park Il Yun Hyantae Choi Kunhong Kim Won Tae Chung Young Hyun Yoo

Despite the numerous studies of protein kinase CK2, little progress has been made in understanding its function in chondrocyte death. Our previous study first demonstrated that CK2 is involved in apoptosis of rat articular chondrocytes. Recent studies have suggested that CK2 downregulation is associated with aging. Thus examining the involvement of CK2 downregulation in chondrocyte death is an ...

2012
E. K. Moo Abu Osman

INTRODUCTION Mechanical impact loading is known to cause cell death and to lead to the onset and progression of osteoarthritis [1]. In order to understand why in-situ cells die readily following impact loading but remain unaffected when the same load is applied at a slow rate, we used a Finite Element model of articular cartilage and chondrocytes to study the in-situ cell mechanics, which canno...

Journal: :Erzincan University Journal of Science and Technology 2021

Articular cartilage is a low-friction white connective tissue. The only cell type in articular are chondrocytes. They permit smooth articulation cartilage. have insufficient regenerative capacity. Response surface methodology very useful tool for the modelling of any processes using polynomials. This study investigated depth-dependent chondrocyte area from bovine Confocal microscope was utilize...

Journal: :Genes & development 1999
B St-Jacques M Hammerschmidt A P McMahon

The mechanisms that control cell proliferation and cell differentiation during morphogenesis of the endochondral skeleton of vertebrates are poorly understood. Indian hedgehog (Ihh) signaling from prehypertrophic chondrocytes has been implicated in the control of chondrocyte maturation by way of feedback control of a second secreted factor parathyroid hormone-related peptide (PTHrP) at the arti...

2018
Kazunori Shimomura Wataru Ando Hiromichi Fujie David A. Hart Hideki Yoshikawa Norimasa Nakamura

Articular cartilage does not heal spontaneously due to its limited healing capacity, and thus effective treatments for cartilage injuries has remained challenging. Since the first report by Brittberg et al. in 1994, autologous chondrocyte implantation (ACI) has been introduced into the clinic. Recently, as an alternative for chondrocyte-based therapy, mesenchymal stem cell (MSC)-based therapy h...

2013
Eleonora Olivotto Miguel Otero Annalisa Astolfi Daniela Platano Annalisa Facchini Stefania Pagani Flavio Flamigni Andrea Facchini Mary B. Goldring Rosa Maria Borzì Kenneth B. Marcu

BACKGROUND The non-canonical NF-κB activating kinase IKKα, encoded by CHUK (conserved-helix-loop-helix-ubiquitous-kinase), has been reported to modulate pro- or anti- inflammatory responses, cellular survival and cellular differentiation. Here, we have investigated the mechanism of action of IKKα as a novel effector of human and murine chondrocyte extracellular matrix (ECM) homeostasis and diff...

2017
Zhen Cao Yun Bai Chuan Liu Ce Dou Jianmei Li Junyu Xiang Chunrong Zhao Zhao Xie Qiang Xiang Shiwu Dong

Chondrocyte hypertrophy is a physiological process in endochondral ossification. However, the hypertrophic‑like alterations of chondrocytes at the articular surface may result in osteoarthritis (OA). In addition, the generation of fibrocartilage with a decreased biological function in tissue engineered cartilage, has been attributed to chondrocyte hypertrophy. Therefore, suppressing chondrocyte...

Donald M. Salter, Mahmoud Orazizadeh,

Background: Integrins are a family of transmembrane proteins that allow communication between the extracellular matrix and the interior of cells. Chondrocytes, cells of articular cartilage, express integrins and these molecules appear to have a variety of roles including mechanotransduction. Integrins are known to associate with a number of accessory molecules such as CD147 that may act to regu...

Journal: :The Journal of bone and joint surgery. British volume 1973
A G Rothwell G Bentley

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