Autophagic degradation of SQSTM1 enables fibroblast activation to accelerate wound healing
Yujiao Xu, Xin Gu, Wenshu Li, Boyang Lin, Yiting Xu, Qingcheng Wei, Qingyuan Liu, Yamin Zhao, Rongzhuo Long, Hu‐Lin Jiang, Zhao‐Qiu Wu, Yunyao Liu, Lei Qiang
Abstract
: 3-MA: 3-methyladenine; ACTA2/α-SMA: actin alpha 2, smooth muscle; ACTB: actin beta; AMPK: AMP-activated protein kinase; ATG: autophagy related; BiFC: bimolecular fluorescence complementation; COL1A2: collagen type I alpha 2 chain; ECM: extracellular matrix; FGF: fibroblast growth factor; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; HDF: human dermal fibroblast; HVGs: highly variable genes; KO: knockout; LMNB1: lamin B1; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MKI67/Ki-67: marker of proliferation Ki-67; MTOR/mTOR: mechanistic target of rapamycin kinase; NFE2L2/NRF2: NFE2 like bZIP transcription factor 2; NFKB: nuclear factor kappa B; NLRP3: NLR family pyrin domain containing 3; PCA: principal component analysis; PI3K: phosphoinositide 3-kinase; R-SMAD: receptor-regulated SMAD; SBE: SMAD binding element; shCON: small hairpin negative control; siNC: negative control; siRNA: small interfering RNA; SMAD: SMAD family member; SQSTM1/p62: sequestosome 1; ssGSEA: single-sample gene set enrichment analysis; TGFB/TGF-β: transforming growth factor beta; TGFBR1: transforming growth factor beta receptor 1; TGFBR2: transforming growth factor beta receptor 2; VIM: vimentin; WT: wild-type; ZFYVE9/SARA: zinc finger FYVE-type containing 9.