An article published in “Stem Cell Research” using our Polyclonal Antibody Development Service by our customers from the, University of Extremadura, Spain, in the analysis of how Lung regeneration after toxic injury is improved in absence of dioxin receptor. Congrats and thanks.
Summary:
Recent
experimental evidences from cellular systems and from mammalian and
non-mammalian animal models highlight novel functions for the aryl
hydrocarbon/dioxin receptor (AhR) in maintaining cell differentiation and
tissue homeostasis. Notably, AhR depletion stimulates an undifferentiated and
pluripotent phenotype likely associated to a mesenchymal transition in
epithelial cells and to increased primary tumorigenesis and metastasis in
melanoma. In this work, we have used a lung model of epithelial regeneration to
investigate whether AhR regulates proper tissue repair by adjusting the
expansion of undifferentiated stem-like cells. AhR-null mice developed a faster
and more efficient repair of the lung bronchiolar epithelium upon naphthalene
injury that required increased cell proliferation and the earlier activation of
stem-like Clara, Basal and neuroepithelial cells precursors. Increased basal
content in multipotent Sca1+/CD31−/CD4− cells and in cells expressing
pluripotency factors NANOG and OCT4 could also improve re-epithelialization in
AhR-null lungs. The reduced response of AhRdeficient lungs to Sonic Hedgehog
(Shh) repression shortly after injury may also help their improved bronchiolar
epithelium repair. These results support a role for AhR in the regenerative
response against toxins, and open the possibility of modulating its activation
level to favor recovery from lesions caused by environmental contaminants.
Reference:
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