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10.1111/jcmm.12661 http://scihub22266oqcxt.onion/10.1111/jcmm.12661 C4687706!4687706 !26337045     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26337045 &cmd=llinks): Failed to open stream: HTTP request failed! 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The I?B kinase inhibitor ACHP strongly attenuates TGF?1-induced myofibroblast formation and collagen synthesis |pdf=|usr=}}{{26337045 }} gab.com Text The I B kinase inhibitor ACHP strongly attenuates TGF 1-induced myofibroblast formation and collagen synthesis JO: J Cell Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=26337045 #FOAvip Excessive accumulation of a collagen-rich extracellular matrix (ECM) by myofibroblasts is a characteristic feature of fibrosis, a pathological state leading to serious organ dysfunction. Transforming growth factor beta1 (TGF?1) is a strong inducer of myofibroblast formation and subsequent collagen production. Currently, there are no remedies for the treatment of fibrosis. Activation of the nuclear factor kappa B (NF-?B) pathway by phosphorylating I?B with the enzyme I?B kinase (IKK) plays a major role in the induction of fibrosis. ACHP {2-Amino-6-[2-(cyclopropylmethoxy)-6-hydroxyphenyl]-4-(4-piperidinyl)-3 pyridinecarbonitrile}, a selective inhibitor of IKK, prohibits the activation of the NF-?B pathway. It is not known whether ACHP has potential anti-fibrotic properties. Using adult human dermal and lung fibroblasts we have investigated whether ACHP has the ability to inhibit the TGF?1-induced transition of fibroblasts into myofibroblasts and its excessive synthesis of ECM. The presence of ACHP strongly suppressed the induction of the myofibroblast markers alpha-smooth muscle actin (?SMA) and SM22?, as well as the deposition of the ECM components collagen type I and fibronectin. Furthermore, post-treatment with ACHP partly reversed the expression of ?SMA and collagen type I production. Finally, ACHP suppressed the expression of the three collagen-modifying enzymes lysyl hydroxylase (PLOD1, PLOD2 and PLOD3) in dermal fibroblasts, but did not do so in lung fibroblasts. We conclude that the IKK inhibitor ACHP has potent antifibrotic properties, and that the NF-?B pathway plays an important role in myofibroblast biology. Twit Text FOAVip The I B kinase inhibitor ACHP strongly attenuates TGF 1-induced myofibroblast formation and collagen synthesis ????J Cell Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=26337045 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26337045 #FOAvip English Wikipedia <ref>{{Cite pmid|26337045 }}</ref> The I?B kinase inhibitor ACHP strongly attenuates TGF?1-induced myofibroblast formation and collagen synthesis #MMPMID26337045 Mia MM ; Bank RA J Cell Mol Med 2015[Dec]; 19 (12 ): 2780-92 PMID26337045 show ga Excessive accumulation of a collagen-rich extracellular matrix (ECM) by myofibroblasts is a characteristic feature of fibrosis, a pathological state leading to serious organ dysfunction. Transforming growth factor beta1 (TGF?1) is a strong inducer of myofibroblast formation and subsequent collagen production. Currently, there are no remedies for the treatment of fibrosis. Activation of the nuclear factor kappa B (NF-?B) pathway by phosphorylating I?B with the enzyme I?B kinase (IKK) plays a major role in the induction of fibrosis. ACHP {2-Amino-6-[2-(cyclopropylmethoxy)-6-hydroxyphenyl]-4-(4-piperidinyl)-3 pyridinecarbonitrile}, a selective inhibitor of IKK, prohibits the activation of the NF-?B pathway. It is not known whether ACHP has potential anti-fibrotic properties. Using adult human dermal and lung fibroblasts we have investigated whether ACHP has the ability to inhibit the TGF?1-induced transition of fibroblasts into myofibroblasts and its excessive synthesis of ECM. The presence of ACHP strongly suppressed the induction of the myofibroblast markers alpha-smooth muscle actin (?SMA) and SM22?, as well as the deposition of the ECM components collagen type I and fibronectin. Furthermore, post-treatment with ACHP partly reversed the expression of ?SMA and collagen type I production. Finally, ACHP suppressed the expression of the three collagen-modifying enzymes lysyl hydroxylase (PLOD1, PLOD2 and PLOD3) in dermal fibroblasts, but did not do so in lung fibroblasts. We conclude that the IKK inhibitor ACHP has potent antifibrotic properties, and that the NF-?B pathway plays an important role in myofibroblast biology. |Actins/genetics/metabolism [MESH] |Adult [MESH] |Cell Differentiation/drug effects [MESH] |Cells, Cultured [MESH] |Collagen Type I/*biosynthesis/genetics [MESH] |Fibroblasts/cytology/drug effects/metabolism [MESH] |Fibronectins/genetics/metabolism [MESH] |Gene Expression/drug effects [MESH] |Humans [MESH] |I-kappa B Kinase/*antagonists & inhibitors/metabolism [MESH] |Lung/cytology [MESH] |Microfilament Proteins/genetics/metabolism [MESH] |Microscopy, Confocal [MESH] |Muscle Proteins/genetics/metabolism [MESH] |Myofibroblasts/cytology/*drug effects/metabolism [MESH] |Nicotinic Acids/*pharmacology [MESH] |Nitriles/*pharmacology [MESH] |Procollagen-Lysine, 2-Oxoglutarate 5-Dioxygenase/genetics/metabolism [MESH] |Reverse Transcriptase Polymerase Chain Reaction [MESH] |Skin/cytology [MESH] |Smad Proteins/metabolism [MESH] |Transcription Factor RelA/metabolism [MESH]The I?B kinase inhibitor ACHP strongly attenuates TGF?1-induced myofib(epmc).pdf DeepDyve Pubget Overpricing