Sam68 Promotes NF-κB Activation and Apoptosis Signaling in Articular Chondrocytes during Osteoarthritis

Inflammation Research : Official Journal of the European Histamine Research Society ... [et Al.]
Libin XuDongmei Zhang

Abstract

To investigate the expression of Sam68 in articular cartilage of knee osteoarthritis (OA) and the relationship between Sam68 and NF-κB activation and apoptosis signaling in OA articular chondrocytes. Sam68 expression in normal and osteoarthritic cartilage was assessed by immunohistochemistry and RT-PCR on both meniscal/ligamentous injury (MLI)-induced OA rat model and the clinical human OA cartilage tissues. Sam68 expression in chondrocytes under tumor necrosis factor-alpha (TNF-α) stimuli was also assessed by immunoblot. Inhibiting Sam68 in chondrocytes under TNF-α stimuli was conducted using small interfering RNA (siRNA) and its influence on the expression of apoptotic marker and catabolic genes was examined by immunoblot. The mechanism of how Sam68 stimulates NF-κB activity was determined by co-immunoprecipitation and immunoblot analysis of nuclear and cytoplasmic fractions of TNF-α-treated chondrocytes for p65 and Sam68. Sam68 expression was increased in OA cartilage tissues and chondrocytes under TNF-α stimuli. Inhibition of Sam68 by siRNA significantly decreased the expression of apoptotic markers (cleaved caspase-3 and cleaved PARP) in chondrocytes following TNF-α-stimulation. Sam68 knockdown suppressed Iκ-B degradation ...Continue Reading

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Citations

Apr 26, 2016·Evidence-based Complementary and Alternative Medicine : ECAM·Huaqi TangYikun Sun
Jul 20, 2019·Cells·Moon-Chang ChoiYoonkyung Park
Dec 31, 2019·Experimental and Therapeutic Medicine·Feida WangYinpeng Yuan
Sep 21, 2018·Experimental and Therapeutic Medicine·Zhaozong FuShanshan Xiang
Mar 20, 2020·Mediators of Inflammation·Yoke Yue Chow, Kok-Yong Chin
Jan 7, 2018·Biomedicine & Pharmacotherapy = Biomédecine & Pharmacothérapie·Chuandong Yu, Yongkun Wang

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Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis

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