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10.1038/labinvest.2014.85 http://scihub22266oqcxt.onion/10.1038/labinvest.2014.85 C5919187!5919187 !25068659     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25068659 &cmd=llinks): Failed to open stream: HTTP request failed! 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TRPA1 is required for TGF-? signaling and its loss blocks inflammatory fibrosis in mouse corneal stroma |pdf=|usr=}}{{25068659 }} gab.com Text TRPA1 is required for TGF- signaling and its loss blocks inflammatory fibrosis in mouse corneal stroma JO: Lab Invest http://www.kidney.de/pget.php?&tw=1&pmid=25068659 #FOAvip We examined whether the loss of transient receptor potential ankyrin 1 (TRPA1), an irritant-sensing ion channel, or TRPA1 antagonist treatment affects the severity inflammation and scarring during tissue wound healing in a mouse cornea injury model. In addition, the effects of the absence of TRPA1 on transforming growth factor ?1 (TGF-?1)-signaling activation were studied in cell culture. The lack of TRPA1 in cultured ocular fibroblasts attenuated expression of TGF-?1, interleukin-6, and ?-smooth muscle actin, a myofibroblast the marker, but suppressed the activation of Smad3, p38 MAPK, ERK, and JNK. Stroma of the healing corneas of TRPA1(-/-) knockout (KO) mice appeared more transparent compared with those of wild-type mice post-alkali burn. Eye globe diameters were measured from photographs. An examination of the corneal surface and eye globes suggested the loss of TRPA1 suppressed post-alkali burn inflammation and fibrosis/scarring, which was confirmed by histology, immunohistochemistry, and gene expression analysis. Reciprocal bone marrow transplantation between mice showed that KO corneal tissue resident cells, but not KO bone marrow-derived cells, are responsible for KO mouse wound healing with reduced inflammation and fibrosis. Systemic TRPA1 antagonists reproduced the KO phenotype of healing. In conclusion, a loss or blocking of TRPA1 in mice reduces inflammation and fibrosis/scarring in the corneal stroma during wound healing following an alkali burn. The responsible mechanism may include the inhibition of TGF-?1-signaling cascades in fibroblasts by attenuated TRPA1 signaling. Inflammatory cells are considered to have a minimum involvement in the exhibition of the KO phenotype after injury. Twit Text FOAVip TRPA1 is required for TGF- signaling and its loss blocks inflammatory fibrosis in mouse corneal stroma ????Lab Invest http://www.kidney.de/pget.php?&tw=1&pmid=25068659 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25068659 #FOAvip English Wikipedia <ref>{{Cite pmid|25068659 }}</ref> TRPA1 is required for TGF-? signaling and its loss blocks inflammatory fibrosis in mouse corneal stroma #MMPMID25068659 Okada Y ; Shirai K ; Reinach PS ; Kitano-Izutani A ; Miyajima M ; Flanders KC ; Jester JV ; Tominaga M ; Saika S Lab Invest 2014[Sep]; 94 (9 ): 1030-41 PMID25068659 show ga We examined whether the loss of transient receptor potential ankyrin 1 (TRPA1), an irritant-sensing ion channel, or TRPA1 antagonist treatment affects the severity inflammation and scarring during tissue wound healing in a mouse cornea injury model. In addition, the effects of the absence of TRPA1 on transforming growth factor ?1 (TGF-?1)-signaling activation were studied in cell culture. The lack of TRPA1 in cultured ocular fibroblasts attenuated expression of TGF-?1, interleukin-6, and ?-smooth muscle actin, a myofibroblast the marker, but suppressed the activation of Smad3, p38 MAPK, ERK, and JNK. Stroma of the healing corneas of TRPA1(-/-) knockout (KO) mice appeared more transparent compared with those of wild-type mice post-alkali burn. Eye globe diameters were measured from photographs. An examination of the corneal surface and eye globes suggested the loss of TRPA1 suppressed post-alkali burn inflammation and fibrosis/scarring, which was confirmed by histology, immunohistochemistry, and gene expression analysis. Reciprocal bone marrow transplantation between mice showed that KO corneal tissue resident cells, but not KO bone marrow-derived cells, are responsible for KO mouse wound healing with reduced inflammation and fibrosis. Systemic TRPA1 antagonists reproduced the KO phenotype of healing. In conclusion, a loss or blocking of TRPA1 in mice reduces inflammation and fibrosis/scarring in the corneal stroma during wound healing following an alkali burn. The responsible mechanism may include the inhibition of TGF-?1-signaling cascades in fibroblasts by attenuated TRPA1 signaling. Inflammatory cells are considered to have a minimum involvement in the exhibition of the KO phenotype after injury. |Animals [MESH] |Corneal Diseases/pathology/*prevention & control [MESH] |Eye Burns/physiopathology [MESH] |Fibrosis/*prevention & control [MESH] |Inflammation/*prevention & control [MESH] |Mice [MESH] |Mice, Knockout [MESH] |Real-Time Polymerase Chain Reaction [MESH] |Signal Transduction/*physiology [MESH] |TRPA1 Cation Channel [MESH] |Transforming Growth Factor beta/*metabolism [MESH] |Transient Receptor Potential Channels/antagonists & inhibitors/genetics/*physiology [MESH]TRPA1 is required for TGF-? signaling and its loss blocks inflammatory(epmc).pdf DeepDyve Pubget Overpricing