Ctip2 is a dynamic regulator of epidermal proliferation and differentiation by integrating EGFR and Notch signaling

Zhang, Ling-juan; Bhattacharya, Shreya; Leid, Mark; Ganguli‐Indra, Gitali; Indra, Arup K.

doi:10.1242/jcs.108969

Cited by 35 publications

(41 citation statements)

References 56 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Cells at 60~80% confluence were starved overnight without EDGS prior to treatment. Primary neonatal mouse epidermal keratinocytes (mKCs) were isolated from newborn Mavs +/+ , Mavs −/+ or Mavs −/− littermate pups as described previously (Zhang et al, 2012) and mKCs were cultured in EpiLife supplemented with 0.04mM CaCl 2 and EDGS until cells reached 80% confluency before starvation overnight followed by indicated treatments. Control siRNA, TLR3 siRNA and MAVS siRNA were purchased from Dharmacon (Chicago, IL).…”

Section: Methodsmentioning

confidence: 99%

Antimicrobial Peptide LL37 and MAVS Signaling Drive Interferon-β Production by Epidermal Keratinocytes during Skin Injury

et al. 2016

Self Cite

View full text Add to dashboard Cite

SUMMARY Type 1 interferons (IFN) promote inflammation in the skin but the mechanisms responsible for inducing these cytokines are not well understood. We found that IFNβ was abundantly produced by epidermal keratinocytes (KCs) in psoriasis and during wound repair. KC IFNβ production depended on stimulation of mitochondrial antiviral-signaling protein (MAVS) by the antimicrobial peptide LL37 and double stranded-RNA released from necrotic cells. MAVS activated downstream TBK1 (TANK-Binding Kinase 1)-AKT (AKT serine/threonine kinase 1)-IRF3 (interferon regulatory factor 3) signaling cascade leading to IFNβ production, and then promoted maturation of dendritic cells. In mice, the production of epidermal IFNβ by LL37 required MAVS, and human wounded and/or psoriatic skin showed activation of MAVS-associated IRF3 and induction of MAVS and IFNβ gene signatures. These findings show that KCs are an important source of IFNβ and MAVS is critical to this function, and demonstrates how the epidermis triggers unwanted skin inflammation under disease conditions.

show abstract

Section: Methodsmentioning

confidence: 99%

Antimicrobial Peptide LL37 and MAVS Signaling Drive Interferon-β Production by Epidermal Keratinocytes during Skin Injury

et al. 2016

Self Cite

View full text Add to dashboard Cite

show abstract

“…The calcium gradient also develops coincidently with the emergence of a component permeability barrier, which supports that calcium signaling plays a critical role of KC differentiation. In vitro , low calcium (0.02-0.1 mM) maintains the proliferation of basal KCs as a monolayer, whereas high calcium (>0.1 mM) induces a rapid and irreversible commitment of the cells to terminal differentiation as demonstrated by tight-junction formation and induction of LOR and INV upon high calcium treatment to the basal KCs 4,5 .…”

Section: Introductionmentioning

confidence: 99%

Isolation and Culture of Primary Mouse Keratinocytes from Neonatal and Adult Mouse Skin

Adase

Zhang

2017

JoVE

Self Cite

View full text Add to dashboard Cite

The keratinocyte (KC) is the predominant cell type in the epidermis, the outermost layer of the skin. Epidermal KCs play a critical role in providing skin defense by forming an intact skin barrier against environmental insults, such as UVB irradiation or pathogens, and also by initiating an inflammatory response upon those insults. Here we describe methods to isolate KCs from neonatal mouse skin and from adult mouse tail skin. We also describe culturing conditions using defined growth supplements (dGS) in comparison to chelexed fetal bovine serum (cFBS). Functionally, we show that both neonatal and adult KCs are highly responsive to high calcium-induced terminal differentiation, tight junction formation and stratification. Additionally, cultured adult KCs are susceptible to UVB-triggered cell death and can release large amounts of TNF upon UVB irradiation. Together, the methods described here will be useful to researchers for the setup of in vitro models to study epidermal biology in the neonatal mouse and/or the adult mouse.

show abstract

“…BCL11B can interact with COUP-TF or HDACs and other chromatin-associated proteins to repress transcription (Avram et al, 2000; Marban et al, 2007). Transcriptional targets of BCL11B include cell cycle regulators (Cherrier et al, 2009; Topark-Ngarm et al, 2006) and signaling pathways affected include those of FGF, SHH, EGF, and NOTCH (Kyrylkova et al, 2012; Zhang et al, 2012). During embryonic development, BCL11B is expressed in the brain, thymus, skin epidermis, dermis, and hair follicles, oral and gut epithelia, and teeth (Arlotta et al, 2005; Golonzhka et al, 2007, 2009b; Leid et al, 2004).…”

mentioning

confidence: 99%

BCL11B expression in intramembranous osteogenesis during murine craniofacial suture development

Holmes

Bakel

Zhou

et al. 2015

Gene Expression Patterns

View full text Add to dashboard Cite

Sutures, where neighboring craniofacial bones are separated by undifferentiated mesenchyme, are major growth sites during craniofacial development. Pathologic fusion of bones within sutures occurs in a wide variety of craniosynostosis conditions and can result in dysmorphic craniofacial growth and secondary neurologic deficits. Our knowledge of the genes involved in suture formation is poor. Here we describe the novel expression pattern of the BCL11B transcription factor protein during murine embryonic craniofacial bone formation. We examined BCL11B protein expression at E14.5, E16.5, and E18.5 in 14 major craniofacial sutures of C57BL/6J mice. We found BCL11B expression to be associated with all intramembranous craniofacial bones examined. The most striking aspects of BCL11B expression were its high levels in suture mesenchyme and increasingly complementary expression with RUNX2 in differentiating osteoblasts during development. BCL11B was also expressed in mesenchyme at the non-sutural edges of intramembranous bones. No expression was seen in osteoblasts involved in endochondral ossification of the cartilaginous cranial base. BCL11B is expressed to potentially regulate the transition of mesenchymal differentiation and suture formation within craniofacial intramembranous bone.

show abstract

Ctip2 is a dynamic regulator of epidermal proliferation and differentiation by integrating EGFR and Notch signaling

Cited by 35 publications

References 56 publications

Antimicrobial Peptide LL37 and MAVS Signaling Drive Interferon-β Production by Epidermal Keratinocytes during Skin Injury

Antimicrobial Peptide LL37 and MAVS Signaling Drive Interferon-β Production by Epidermal Keratinocytes during Skin Injury

Isolation and Culture of Primary Mouse Keratinocytes from Neonatal and Adult Mouse Skin

BCL11B expression in intramembranous osteogenesis during murine craniofacial suture development

Contact Info

Product

Resources

About