@article {1160,
	title = {Cytoplasmic poly (A)-binding protein critically regulates epidermal maintenance and turnover in the planarian .},
	journal = {Development},
	volume = {144},
	year = {2017},
	month = {2017 09 01},
	pages = {3066-3079},
	abstract = {<p>Identifying key cellular events that facilitate stem cell function and tissue organization is crucial for understanding the process of regeneration. Planarians are powerful model system to study regeneration and stem cell (neoblast) function. Here, using planaria, we show that the initial events of regeneration, such as epithelialization and epidermal organization are critically regulated by a novel cytoplasmic poly A-binding protein, SMED-PABPC2. Knockdown leads to defects in epidermal lineage specification, disorganization of epidermis and ECM, and deregulated wound healing, resulting in the selective failure of neoblast proliferation near the wound region. Polysome profiling suggests that epidermal lineage transcripts, including , are translationally regulated by SMED-PABPC2 Together, our results uncover a novel role for SMED-PABPC2 in the maintenance of epidermal and ECM integrity, critical for wound healing and subsequent processes for regeneration.</p>
},
	keywords = {Animals, Cell Lineage, Cell Proliferation, Cytoplasm, Epidermis, Epithelium, Extracellular Matrix, Gene Knockdown Techniques, Homeostasis, Models, Biological, Planarians, Poly(A)-Binding Protein I, Regeneration, RNA, Messenger, Wound Healing},
	issn = {1477-9129},
	doi = {10.1242/dev.152942},
	author = {Bansal, Dhiru and Kulkarni, Jahnavi and Nadahalli, Kavana and Lakshmanan, Vairavan and Krishna, Srikar and Sasidharan, Vidyanand and Geo, Jini and Dilipkumar, Shilpa and Pasricha, Renu and Gulyani, Akash and Raghavan, Srikala and Palakodeti, Dasaradhi}
}
@article {1168,
	title = {Sterile Inflammation Enhances ECM Degradation in Integrin β1 KO Embryonic Skin.},
	journal = {Cell Rep},
	volume = {16},
	year = {2016},
	month = {2016 09 20},
	pages = {3334-3347},
	abstract = {<p>Epidermal knockout of integrin β1 results in complete disorganization of the basement membrane (BM), resulting in neonatal lethality. Here, we report that this disorganization is exacerbated by an early\&nbsp;embryonic inflammatory response involving the recruitment of tissue-resident and monocyte-derived macrophages to the dermal-epidermal junction, associated with increased matrix metalloproteinase activity. Remarkably, the skin barrier in the integrin β1 knockout animals is intact, suggesting that this inflammatory response is initiated in a sterile environment. We demonstrate that the molecular mechanism involves de novo expression of integrin αvβ6 in the basal epidermal cells, which activates a TGF-β1 driven inflammatory cascade resulting in upregulation of dermal NF-κB in a Tenascin C-dependent manner. Importantly, treatment of β1 KO embryos in utero with small molecule inhibitors of TGF-βR1 and NF-κB results in marked rescue of the BM defects and amelioration of immune response, revealing an unconventional immuno-protective role for integrin β1 during BM remodeling.</p>
},
	keywords = {Animals, Extracellular Matrix, Inflammation, Integrin beta1, Macrophages, Mice, Mice, Knockout, Signal Transduction, Skin},
	issn = {2211-1247},
	doi = {10.1016/j.celrep.2016.08.062},
	author = {Kurbet, Ambika S and Hegde, Samarth and Bhattacharjee, Oindrila and Marepally, Srujan and Vemula, Praveen K and Raghavan, Srikala}
}
