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Delayed Cutaneous Wound Healing and Aberrant Expression of Hair Follicle Stem Cell Markers in Mice Selectively Lacking Ctip2 in Epidermis

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dc.creator Liang, Xiaobo
dc.creator Bhattacharya, Shreya
dc.creator Bajaj, Gaurav
dc.creator Guha, Gunjan
dc.creator Wang, Zhixing
dc.creator Jang, Hyo-Sang
dc.creator Leid, Mark
dc.creator Indra, Arup Kumar
dc.creator Ganguli-Indra, Gitali
dc.date.accessioned 2012-07-30T22:22:16Z
dc.date.available 2012-07-30T22:22:16Z
dc.date.issued 2012-02-21
dc.identifier.citation Liang X, Bhattacharya S, Bajaj G, Guha G, Wang Z, Jang H... (2012) Delayed Cutaneous Wound Healing and Aberrant Expression of Hair Follicle Stem Cell Markers in Mice Selectively Lacking Ctip2 in Epidermis. PLoS ONE 7(2): e29999. doi:10.1371/journal.pone.0029999 en_US
dc.identifier.uri http://hdl.handle.net/1957/31679
dc.description This is the publisher’s final pdf. The published article is copyrighted by PLoS and can be found at: http://www.plosone.org/home.action. en_US
dc.description.abstract Background: COUP-TF interacting protein 2 [(Ctip2), also known as Bcl11b] is an important regulator of skin homeostasis, and is overexpressed in head and neck cancer. Ctip2(ep-/-) mice, selectively ablated for Ctip2 in epidermal keratinocytes, exhibited impaired terminal differentiation and delayed epidermal permeability barrier (EPB) establishment during development, similar to what was observed in Ctip2 null (Ctip2(-/-)) mice. Considering that as an important role of Ctip2, and the fact that molecular networks which underlie cancer progression partially overlap with those responsible for tissue remodeling, we sought to determine the role of Ctip2 during cutaneous wound healing. Methodology/Principal Findings: Full thickness excisional wound healing experiments were performed on Ctip2(L2/L2) and Ctip2(ep-/-) animals per time point and used for harvesting samples for histology, immunohistochemistry (IHC) and immunoblotting. Results demonstrated inherent defects in proliferation and migration of Ctip2 lacking keratinocytes during re-epithelialization. Mutant mice exhibited reduced epidermal proliferation, delayed keratinocyte activation, altered cell-cell adhesion and impaired ECM development. Post wounding, Ctip2(ep-/-) mice wounds displayed lack of E-Cadherin suppression in the migratory tongue, insufficient expression of alpha smooth muscle actin (alpha SMA) in the dermis, and robust induction of K8. Importantly, dysregulated expression of several hair follicle (HF) stem cell markers such as K15, NFATc1, CD133, CD34 and Lrig1 was observed in mutant skin during wound repair. Conclusions/Significance: Results confirm a cell autonomous role of keratinocytic Ctip2 to modulate cell migration, proliferation and/or differentiation, and to maintain HF stem cells during cutaneous wounding. Furthermore, Ctip2 in a non-cell autonomous manner regulated granulation tissue formation and tissue contraction during wound closure. en_US
dc.language.iso en_US en_US
dc.publisher PLoS en_US
dc.relation.ispartofseries PLoS ONE en_US
dc.relation.ispartofseries Vol. 7 no. 2 en_US
dc.subject Growth factor receptor en_US
dc.subject Keratin 15 expression en_US
dc.subject dermal papilla cells en_US
dc.subject Migration in-vitro en_US
dc.subject Mouse skin en_US
dc.subject Mammalian epidermis en_US
dc.subject Newborn mice en_US
dc.subject Basal layer en_US
dc.subject E-cadherin en_US
dc.subject Repair en_US
dc.title Delayed Cutaneous Wound Healing and Aberrant Expression of Hair Follicle Stem Cell Markers in Mice Selectively Lacking Ctip2 in Epidermis en_US
dc.type Article en_US
dc.identifier.doi 10.1371/journal.pone.0029999


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