Deletion of Negative Elongation Factor B in epithelial stem cells accelerates mouse skin wound healing
Open AccessFollowing injury, keratinocytes rapidly coordinate changes in gene expression to contribute to stages of inflammation and proliferation that are required for healing. One mechanism that cells utilize to regulate gene expression is through promotor proximal pausing of RNA Pol II through the Negative Elongation Factor (NELF) complex. To date, little is known about how the NELF complex and RNA Pol II pausing contribute to changes in gene expression that occur during wound healing. To investigate this, we used a conditional knockout mouse model of the Nelfb gene in keratinocytes (KC-KO) to disrupt the NELF complex. Using immunofluorescence tissue analysis, we observed greater re-epithelialization and angiogenesis during the proliferation phase of repair in KC-KO mice compared to controls . Subsequent flow cytometry analysis of the myeloid leukocytes revealed that populations of macrophages were significantly increased at very early time points post-wounding, suggesting that an altered immune cell response promotes accelerated tissue repair when Nelfb is knocked out of keratinocytes. These data indicate that the NELF complex has a pivotal role in regulating injury-induced responses of keratinocytes during wound healing and may be a suitable target in treating patients that suffer from delayed wound healing
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