Alternative Negative Feedback Control in the Aryl Hydrocarbon Receptor Signaling Pathway

Matthews, Jason

doi:10.4172/2157-7609.1000e116

Cited by 3 publications

(1 citation statement)

References 21 publications

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“…PARP7 is a CCCH-zinc finger domain containing PARP with high evolutionary conservation with PARP12 and PARP13, the latter of which is also mono-ADP-ribosylated by PARP7 [1,4,10]. PARP7 expression is induced by platelet-derived growth factors [11], viral infection [12,13], nuclear hormone receptors [14,15], hypoxia [16], and aryl hydrocarbon receptor (AHR) [17]. In the latter case, PARP7 in turn represses AHR signaling through a negative feedback loop that is dependent on its catalytic activity [9,18].…”

Section: Introductionmentioning

confidence: 99%

Reduced Colonic Mucosal Injury in 2,3,7,8-Tetrachlorodibenzo-p-Dioxin Poly ADP-Ribose Polymerase (TIPARP/PARP7)-Deficient Mice

Hutin

Hagen

Shao

et al. 2022

IJMS

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Poly-ADP-ribose polymerases (PARPs) are important regulators of the immune system, including TCDD-inducible poly-ADP-ribose polymerase (TIPARP), also known as poly-ADP-ribose polymerase 7 (PARP7). PARP7 negatively regulates aryl hydrocarbon receptor (AHR) and type I interferon (IFN-I) signaling, both of which have been implicated in intestinal homeostasis and immunity. Since the loss of PARP7 expression increases AHR and IFN-I signaling, we used a murine dextran sulfate sodium (DSS)-induced colitis model to investigate the effect of PARP7 loss on DSS-induced intestinal inflammation. DSS-exposed Parp7−/− mice had less body weight loss, lower disease index scores, and reduced expression of several inflammation genes, including interleukin IL-6, C-x-c motif chemokine ligand 1 (Cxcl1), and lipocalin-2, when compared with wild-type mice. However, no significant difference was observed between genotypes in the colonic expression of the AHR target gene cytochrome P450 1A1 (Cyp1a1). Moreover, no significant differences in microbial composition were observed between the genotypes. Our findings demonstrate that the absence of PARP7 protein results in an impaired immune response to colonic inflammation and suggests that PARP7 may participate in the recruitment of immune cells to the inflammation site, which may be due to its role in IFN-I signaling rather than AHR signaling.

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