Krüppel-like factor 4 interacts with p300 to activate mitofusin 2 gene expression induced by all-trans retinoic acid in VSMCs

Zhang, Rui; Han, Mei; Zheng, Bin; Li, Yingjie; Shu, Ya-Nan; Wen, Jin‐Kun

doi:10.1038/aps.2010.96

Cited by 27 publications

(17 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Recently, we published that KLF15 is a critical transcriptional regulator of podocyte differentiation (21). Furthermore, KLF4 was found to play a critical role in regulating mitochondrial fusion proteins in vascular smooth muscle differentiation (22). In addition, paralogs of KLF1 (specificity proteins) have been shown to transcriptionally regulate cytochrome c subunit genes in primary neurons (23).…”

Section: Discussionmentioning

confidence: 99%

Krüppel-like factor 6 regulates mitochondrial function in the kidney

Mallipattu¹,

Horne²,

D’Agati³

et al. 2015

J. Clin. Invest.

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

Krüppel-like factor 6 regulates mitochondrial function in the kidney

Mallipattu¹,

Horne²,

D’Agati³

et al. 2015

J. Clin. Invest.

View full text Add to dashboard Cite

“…These data support a cell-type specific regulation of KLF4 expression, and potentially function. Although MAPK, Pi3K and NF-κB have been mentioned to be important in KLF4 expression or function in different cell types (42)(43)(44)(45), the pneumococci-related KLF4 expression was strictly independent of the Pi3K and MAPK signaling pathways or NF-κB activation. The non-receptor protein tyrosine kinase family src includes nine members: src, yes, fyn, lck, hck, blk, lyn, fgr.and frk (46).…”

Section: Discussionmentioning

confidence: 99%

Role of Pneumococcal Autolysin for KLF4 Expression and Chemokine Secretion in Lung Epithelium

Zahlten

Herta

Kabus

et al. 2015

Am J Respir Cell Mol Biol

View full text Add to dashboard Cite

In severe pneumococcal pneumonia, the delicate balance between a robust inflammatory response necessary to kill bacteria and the loss of organ function determines the outcome of disease. In this study, we tested the hypothesis that Krueppel-like factor (KLF) 4 may counter-regulate Streptococcus pneumoniae-related human lung epithelial cell activation using the potent proinflammatory chemokine IL-8 as a model molecule. Pneumococci induced KLF4 expression in human lung, in primary human bronchial epithelial cells, and in the lung epithelial cell line BEAS-2B. Whereas proinflammatory cell activation depends mainly on the classical Toll-like receptor 2-mitogen-activated protein kinase or phosphatidylinositide 3-kinase and NF-κB pathways, the induction of KLF4 occurred independently of these molecules but relied, in general, on tyrosine kinase activation and, in part, on the src kinase family member yamaguchi sarcoma viral oncogene homolog (yes) 1. The up-regulation of KLF4 depended on the activity of the main pneumococcal autolysin LytA. KLF4 overexpression suppressed S. pneumoniae-induced NF-κB and IL-8 reporter gene activation and release, whereas small interfering RNA-mediated silencing of KLF4 or yes1 kinase led to an increase in IL-8 release. The KLF4-dependent down-regulation of NF-κB luciferase activity could be rescued by the overexpression of the histone acetylase p300/cAMP response element-binding protein-associated factor. In conclusion, KLF4 acts as a counter-regulatory transcription factor in pneumococci-related proinflammatory activation of lung epithelial cells, thereby potentially preventing lung hyperinflammation and subsequent organ failure.

show abstract

“…Expression-Previous studies showed that in VSMCs ATRA induces KLF4 expression and its post-translational modifications, including phosphorylation and acetylation (15,16,35). However, the underlying mechanism by which ATRA regulates Klf4 transcription in VSMCs remains largely unknown.…”

Section: Rar␣-mediated Atra-induced Klf4mentioning

confidence: 99%