2019
DOI: 10.1002/jcp.29356
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MKL1 mediates TGF‐β‐induced CTGF transcription to promote renal fibrosis

Abstract: Aberrant fibrogenesis impairs the architectural and functional homeostasis of the kidneys. It also predicts poor diagnosis in patients with end-stage renal disease (ESRD). Renal tubular epithelial cells (RTEC) can trans-differentiate into myofibro-

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Cited by 36 publications
(29 citation statements)
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“…Here we provide examples of “famous” target genes that were shown to be (a) MRTF-dependent in kidney cells and/or (b) directly related to renal pathologies. These include the contractility protein myosin [ 16 , 141 ], the myofibroblast hallmark α-SMA [ 16 , 20 , 104 , 142 , 143 ], actin-severing (cofilin), capping (CapZ) [ 20 ]) and bundling (filamin) [ 144 ]) proteins; focal adhesion and cell-matrix components (α and β integrins [ 145 ]), tenascin [ 144 , 146 ]); extracellular matrix proteins (collagen [ 62 , 147 ], CTGF [ 124 , 148 , 149 , 150 ]); caveolar proteins (caveolin 1 [ 144 , 151 ]), fibrogenic cytokines (TGFβ [ 124 ]), cell cycle regulators (p21 [ 152 ]), NADPH oxidases [ 153 , 154 ]; and transcription factors, encompassing SRF itself [ 20 ], the EMT drivers Snai1/2 and ZEB2 [ 155 , 156 , 157 ] and the Hippo effector TAZ [ 22 , 95 ]. Moreover, SRF/MRTF-targeted CArG motifs are frequently located in the vicinity of AP1 and TEAD sites (that are activated by YAP/TAZ), showing that these TFs often regulate the same genes, and may act synergistically with MRTF [ 23 ].…”
Section: Targets Functions Actionsmentioning
confidence: 99%
“…Here we provide examples of “famous” target genes that were shown to be (a) MRTF-dependent in kidney cells and/or (b) directly related to renal pathologies. These include the contractility protein myosin [ 16 , 141 ], the myofibroblast hallmark α-SMA [ 16 , 20 , 104 , 142 , 143 ], actin-severing (cofilin), capping (CapZ) [ 20 ]) and bundling (filamin) [ 144 ]) proteins; focal adhesion and cell-matrix components (α and β integrins [ 145 ]), tenascin [ 144 , 146 ]); extracellular matrix proteins (collagen [ 62 , 147 ], CTGF [ 124 , 148 , 149 , 150 ]); caveolar proteins (caveolin 1 [ 144 , 151 ]), fibrogenic cytokines (TGFβ [ 124 ]), cell cycle regulators (p21 [ 152 ]), NADPH oxidases [ 153 , 154 ]; and transcription factors, encompassing SRF itself [ 20 ], the EMT drivers Snai1/2 and ZEB2 [ 155 , 156 , 157 ] and the Hippo effector TAZ [ 22 , 95 ]. Moreover, SRF/MRTF-targeted CArG motifs are frequently located in the vicinity of AP1 and TEAD sites (that are activated by YAP/TAZ), showing that these TFs often regulate the same genes, and may act synergistically with MRTF [ 23 ].…”
Section: Targets Functions Actionsmentioning
confidence: 99%
“…Whole-cell lysates were obtained by re-suspending cell pellets in RIPA buffer (50 mM Tris pH7.4, 150 mM NaCl, 1% Triton X-100) with freshly added protease inhibitor (Roche) as previously described [55][56][57][58][59] . Specific antibodies or pre-immune IgGs (P.I.I.)…”
Section: Protein Extraction Immunoprecipitation and Western Blotmentioning
confidence: 99%
“…Histological analyses were performed essentially as previously described ( Zhao et al, 2019 ; Dong et al, 2020 ; Mao et al, 2020 ). Paraffin sections of heart tissue from the mice receiving different treatments were incubated with anti-MRTF-A primary antibody (1:100 dilution, Proteintech, China) and anti-actinin primary antibody (1:100 dilution, Abcam, United Kingdom) overnight at 4°C, then incubated with af594-labeled secondary antibody (1:100 dilution, Life Technologies, United States) for actinin and AF488-labeled secondary antibody (1:100 dilution, Life Technologies, United States) for MRTF-A at room temperature for 1 h. After stained with 4′,6-diamidino-2-phenylindole (DAPI) to label nuclei, the samples were observed under a confocal microscope (LSM 710, Zeiss, Germany).…”
Section: Methodsmentioning
confidence: 99%