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Administration of retinoic acid to pregnant mice increases the number of fetal mouse glomeruli.

ABSTRACT: The prevalence of chronic kidney disease (CKD) is increasing worldwide, and CKD is a serious global health problem. Low glomerular number is one of the risk factors for CKD; therefore, the glomerular number is associated with the risk of CKD. Increasing the glomerular number above normal levels may reduce the risk of CKD. It has been reported that, in vitro, the addition of retinoic acid (RA) to the culture medium increases the glomerular number. However, there is no report of an increase in glomerular number above normal levels with the addition of RA in vivo. In this study, RA (20 mg/kg) was administered intraperitoneally to pregnant mice once at embryonic day (E) 10.5, E12.5, E14.5, or E16.5. The fetuses were harvested at E18.5 and fetal mouse kidneys were evaluated. Fetal kidney volume and weight were significantly increased in the E16.5 group compared to the control group. The total glomerular number in the E16.5 group was also approximately 1.46 times higher than that in the control group. In summary, we established a method to increase the glomerular number in the fetal kidney by administration of RA to pregnant mice at E16.5. These results will facilitate the investigation of whether CKD risk is reduced when the glomerular number increases above normal.

SUBMITTER: Fukunaga S

PROVIDER: S-EPMC8907684 | biostudies-literature | 2022 Jul

REPOSITORIES: biostudies-literature

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Administration of retinoic acid to pregnant mice increases the number of fetal mouse glomeruli.

Fukunaga Shohei S Ogawa Noriko N Matsumoto Akihiro A Ito Takafumi T Tanabe Kazuaki K Otani Hiroki H

Biochemistry and biophysics reports 20220308

The prevalence of chronic kidney disease (CKD) is increasing worldwide, and CKD is a serious global health problem. Low glomerular number is one of the risk factors for CKD; therefore, the glomerular number is associated with the risk of CKD. Increasing the glomerular number above normal levels may reduce the risk of CKD. It has been reported that, in vitro, the addition of retinoic acid (RA) to the culture medium increases the glomerular number. However, there is no report of an increase in glo ...[more]

PMID: 35280524

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Project description:This study investigated whether vitamin A (VA) administration during the neonatal stage could increase the number of intramuscular adipocytes in Hu sheep by promoting vascularity. A total of 56 newborn male Hu sheep were divided into four groups and received intramuscular injections of either 0, 7500 IU retinoic acid (RA), 7500 IU VA, or a combination of 7500 IU VA and 5 mg SU5416 (an angiogenic inhibitor), at 1, 7, 14, and 21 days of age. At 15 days of age, 6 sheep from each group were randomly selected and sacrificed for intramuscular adipogenic capacity analysis. The remaining 8 sheep in each group were raised until they were 8 months old. VA-treated sheep exhibited an increase in preadipocytes, elevated expression of adipogenic genes (CCAAT enhancer binding protein alpha [CEBPA] and CCAAT enhancer binding protein beta [CEBPB]) and angiogenic genes (vascular endothelial growth factor A [VEGFA]), and stromal vascular fraction cells in the longissimus dorsi (LD) muscle with enhanced adipogenic capacity (P ＜ 0.05). These effects were entirely negated by SU5416. Upon slaughter, VA increased final weight, carcass weight, and average daily gain (P ＜ 0.05) but did not affect feed intake at 21 to 32 weeks (P = 0.824). VA increased the number of intramuscular adipocytes in the LD and semitendinosus (ST) muscle (P ＜ 0.05) without changing the adipocyte number of the omentum, perirenal and subcutaneous fats (P ＞ 0.05). VA injections also increased intramuscular triglyceride (TG) content (P = 0.016) without changing the omentum fat weight or subcutaneous fat thickness (P ＞ 0.05), but it did increase the perirenal fat weight (P = 0.011). Consistently, SU5416 mitigated the effects of VA on intramuscular TG content and adipocyte count, correlating with a decrease in vascularity. In contrast, RA injections didn't affect the intramuscular fat (P = 0.744) but reduced the TG content of the omentum and perirenal fat (P ＜ 0.05). In conclusion, intramuscular injections of VA but not RA at the neonatal stage improved the growth performance of Hu sheep, increasing the number of intramuscular adipocytes and marbling by promoting angiogenesis.

Project description:BackgroundThe H9N2 virus can infect not only birds but also humans. The pathogenicity of H9N2 virus infection is determined by an excessive immune response in the lung. All-trans retinoic acid (ATRA), the active metabolite of vitamin A, plays an important regulatory role and has been widely used in the clinical practice. This study was aimed to investigate whether ATRA could regulate the immune response to H9N2 virus infection in the lungs of mice, thereby reducing the pathogenicity of the H9N2 virus in mice.MethodsMice were infected intranasally with H9N2 virus, and injected intraperitoneally with 0.2 mL of ATRA at low (1 mg/kg), medium (5 or 10 mg/kg), or high therapeutic dose (20 mg/kg), and toxic dose (40, 60, or 80 mg/kg), once per day for 10 days. Clinical signs, survival rates, and lung gross pathology were compared between the ATRA-treated H9N2-infected group, the ATRA group, and the H9N2-infected group, to investigate the effect of different doses of ATRA on the pathogenicity of H9N2 virus. Additionally, the viral load and cytokine concentration of lungs were measured at 3, 5, 7, and 9 days after infection, to investigate the potential mechanism of ATRA in affecting the pathogenicity of the H9N2 virus. Expression levels of cellular retinoic acid-binding protein 1 (CRABP1), cellular retinoic acid-binding protein 2 (CRABP2), and Retinoic acid-inducible gene-I (RIG-I) were detected using Western blotting.ResultsThe ATRA-treated H9N2-infected mice showed more severe clinical signs compared with the H9N2-infected group. The medium and high therapeutic doses of ATRA reduced the survival rates, aggravated lung tissue damage, decreased the expression of interferon beta (IFN-β), and increased the concentrations of interleukin-1 beta (IL-1β), tumor necrosis factor alpha (TNF-α), and C-C motif chemokine ligand 2 (CCL2) in the lungs of the H9N2-infected mice. At the same time, the expression patterns of CRABP1, CRABP2, and RIG-I were changed in mice infected by H9N2 and treated with different concentrations of ATRA.ConclusionsOur findings suggest that the therapeutic dose of ATRA can increase the pathogenicity of the H9N2 virus. Therefore, the consequences of those infected by influenza virus would be more severe after ATRA treatment.

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Administration of retinoic acid to pregnant mice increases the number of fetal mouse glomeruli.

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Administration of retinoic acid to pregnant mice increases the number of fetal mouse glomeruli.

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