Knocking down TCF8 inhibits high glucose- and angiotensin II-induced epithelial to mesenchymal transition in podocytes

Bai, Changhuan; Liang, Shu‐Chuan; Wang, Yunshan; Jiang, Bo

doi:10.5582/bst.2016.01224

Cited by 2 publications

(2 citation statements)

References 21 publications

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“…Additionally, SLFN5 is an IRF1-controlled factor downregulated by the CSC treatment. It is involved in the inhibition of endothelial mesenchymal transition (EMT) and of E-cadherin-repression, by downregulating the zinc finger E-box-binding homeobox 1 [ 55 ] as well as in the suppression of MMP expression and of cellular proliferation, migration, and invasiveness in different types of cancer [ 56 , 57 , 58 , 59 , 60 ]. The downregulation of SRP40 induced by CSC treatment may concur with SLFN5 in facilitating HSMC transdifferentiation and migration.…”

Section: Resultsmentioning

confidence: 99%

Smooth Muscle Cell Phenotypic Switch Induced by Traditional Cigarette Smoke Condensate: A Holistic Overview

Bianchi

Damiani

Castiglioni

et al. 2023

IJMS

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Cigarette smoke (CS) is a risk factor for inflammatory diseases, such as atherosclerosis. CS condensate (CSC) contains lipophilic components that may represent a systemic cardiac risk factor. To better understand CSC effects, we incubated mouse and human aortic smooth muscle cells (SMCs) with CSC. We evaluated specific markers for contractile [i.e., actin, aortic smooth muscle (ACTA2), calponin-1 (CNN1), the Kruppel-like factor 4 (KLF4), and myocardin (MYOCD) genes] and inflammatory [i.e., IL-1β, and IL-6, IL-8, and galectin-3 (LGALS-3) genes] phenotypes. CSC increased the expression of inflammatory markers and reduced the contractile ones in both cell types, with KLF4 modulating the SMC phenotypic switch. Next, we performed a mass spectrometry-based differential proteomic approach on human SMCs and could show 11 proteins were significantly affected by exposition to CSC (FC ≥ 2.7, p ≤ 0.05). These proteins are active in signaling pathways related to expression of pro-inflammatory cytokines and IFN, inflammasome assembly and activation, cytoskeleton regulation and SMC contraction, mitochondrial integrity and cellular response to oxidative stress, proteostasis control via ubiquitination, and cell proliferation and epithelial-to-mesenchymal transition. Through specific bioinformatics resources, we showed their tight functional correlation in a close interaction niche mainly orchestrated by the interferon-induced double-stranded RNA-activated protein kinase (alternative name: protein kinase RNA-activated; PKR) (EIF2AK2/PKR). Finally, by combining gene expression and protein abundance data we obtained a hybrid network showing reciprocal integration of the CSC-deregulated factors and indicating KLF4 and PKR as the most relevant factors.

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Section: Resultsmentioning

confidence: 99%

Smooth Muscle Cell Phenotypic Switch Induced by Traditional Cigarette Smoke Condensate: A Holistic Overview

Bianchi

Damiani

Castiglioni

et al. 2023

IJMS

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“…As an essential factor promoting the progression to renal fibrosis, EMT in podocytes will result in loss of epithelial markers with de novo expression of EMT markers; in more severe cases, it may lead to podocyte detachment from the glomerular basement membrane, thereby aggravating proteinuria and glomerulosclerosis (Li et al 2015;Loeffler and Wolf 2015). A recent study reported that a high concentration of glucose and Ang II promoted EMT in podocytes, which could be reversed by silencing TCF8 (Bai et al 2017).…”

Section: Activation Of Ras In Podocyte Injurymentioning

confidence: 99%

Role of Podocyte Injury in Glomerulosclerosis

Lü

Wang

Lü

et al. 2019

Advances in Experimental Medicine and Biology

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Finding new therapeutic targets of glomerulosclerosis treatment is an ongoing quest. Due to a living environment of various stresses and pathological stimuli, podocytes are prone to injuries; moreover, as a cell without proliferative potential, loss of podocytes is vital in the pathogenesis of glomerulosclerosis. Thus, sufficient understanding of factors and underlying mechanisms of podocyte injury facilitates the advancement of treating and prevention of glomerulosclerosis. The clinical symptom of podocyte injury is proteinuria, sometimes with loss of kidney functions progressing to glomerulosclerosis. Injury-induced changes in podocyte physiology and function are actually not a simple passive process, but a complex interaction of proteins that comprise the anatomical structure of podocytes at molecular levels. This chapter lists several aspects of podocyte injuries along with potential mechanisms, including glucose and lipid metabolism disorder, hypertension, RAS activation, micro-inflammation, immune disorder, and other factors. These aspects are not technically separated items, but intertwined with each other in the pathogenesis of podocyte injuries.

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Knocking down TCF8 inhibits high glucose- and angiotensin II-induced epithelial to mesenchymal transition in podocytes

Cited by 2 publications

References 21 publications

Smooth Muscle Cell Phenotypic Switch Induced by Traditional Cigarette Smoke Condensate: A Holistic Overview

Smooth Muscle Cell Phenotypic Switch Induced by Traditional Cigarette Smoke Condensate: A Holistic Overview

Role of Podocyte Injury in Glomerulosclerosis

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