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The role of Voclosporin administration and Inmt TG in renal proximal tubules.

ABSTRACT: Indolethylamine N-methyltransferase (Inmt), an enzyme responsible for detoxifying local uremic toxins, including indole. We next investigated a strategy for preventing the significant decrease in Inmt expression in proximal tubules induced by high‑dose Voc administration and I/R. Accordingly, we used transgenic (Tg) mice with proximal tubule-specific Inmt overexpression and comparatively analyzed the changes with WT mice. Both WT and Tg mice were treated with high‑dose Voc, followed by I/R or sham operation for controls. Two experimental groups were campared using RNA-seq as follows: 1. I/R+WT+Voc (WT mice subjected to I/R and treated with high‑dose Voc)=WT+AKI, 2. I/R+Tg+Voc (Tg mice subjected to I/R and treated with high‑dose voclosporin)=TG+AKI. Results: Inmt-overexpressing mice treated with high-dose voclosporin exhibited absence of peroxisomal abnormalities and resistance to I/R injury.

ORGANISM(S): Mus musculus

PROVIDER: GSE316216 | GEO | 2026/03/28

REPOSITORIES: GEO

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Project description:The hepatocyte growth factor (HGF)/c-Met signaling pathway is known to mediate vascularization. We have previously demonstrated that expression of a human HGF transgene in the small airways produced mice (HGF TG) that were more susceptible to the tobacco carcinogen, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). We also have observed that HGF TG mice display significantly enhanced vascularization in the lungs that increases over time compared to wild-type (WT) littermates. To analyze which genes might contribute to increased vascularization from HGF overexpression in the airways, RNA and protein were isolated from whole lungs of individual HGF TG and WT adult mice. We profiled the mRNA expression of several hundred genes representative of six biological pathways involved in transformation, angiogenesis, and tumorigenesis using two commercial microarrays. Significant changes in expression over a 1.5-fold boundary were also observed in lung tumors derived from NNK-treated HGF TG mice. Lung tumors were induced by exposing mice to four weekly i.p. injections of 3mg NNK (15μg/μl) over 2 weeks. Whole lungs from control untreated animals were dissected after sacrifice at 10, 20, or 40 wks of age, and NNK induced lung tumors were dissected from the animals at 20 or 40 weeks of age. Total RNA was extracted from whole lung or isolated tumors from HGF TG or WT mice using TRIzol reagent and the Array Grade Total RNA Isolation Kit. The cDNA was generated and labeled using the TrueLabeling-AMP Linear RNA Amplication Kit. RNA was analyzed from 28 mice in total. The angiogenesis array was used to analyze 10 samples taken from 40 week old mice (HGF TG untreated [n=4], WT untreated [n=4], HGF TG NNK treated [n=1], WT NNK treated [n=1]) and 6 samples from 20 week old mice (HGF TG untreated [n=2], WT untreated [n=2], HGF TG NNK treated [n=1], WT NNK treated [n=1]). The cancer gene array was used to analyze 8 samples taken from 40 week old mice (HGF TG untreated [n=2], WT untreated [n=2], HGF TG NNK treated [n=2], WT NNK treated [n=2]) and 4 samples from 20 week old mice (HGF TG untreated [n=2], WT untreated [n=2]).

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The role of Voclosporin administration and Inmt TG in renal proximal tubules.

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