ArticleVeterinary world2022
Effect of leptin on the growth and expression of STAT3 in yak mammary epithelial cells.
Article in Veterinary world, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed, 0 citations in OpenAlex.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background and Aim: Leptin (LEP) is an autocrine and paracrine factor produced by the fat pad and acinar epithelial cells of the breast. This study aimed to investigate the effects of LEP on yak mammary epithelial cells (YMECs) and the expression of STAT3. In addition, we evaluated the possible effects of prolactin (PRL) on the function of LEP. Materials and Methods: The YMECs were treated with 0, 50, 100, 200, 400, and 800 ng/mL LEP for 48 h in the absence of PRL and the presence of 500 ng/mL PRL. The growth activity of YMECs was measured using the cell counting kit-8 assay. The changes in the lactation signaling pathway-related factor STAT3 were detected at the mRNA, protein, and protein phosphorylation levels using the reverse transcriptase-quantitative polymerase chain reaction and Western blotting. To explore whether LEP affects the activation of STAT3 through JAK2/JAK3 in YMECs, the JAK2/3 signaling pathway inhibitor AG490 was used at a fixed concentration of LEP. Results: Each concentration of LEP significantly promoted the expression of STAT3 mRNA (p < 0.05) in YMECs in the presence of PRL. In the absence of PRL, all concentrations of LEP were found to inhibit the expression of the STAT3 protein (p < 0.05). The expression of the STAT3 protein in YMECs was found to first increase followed by a decrease with an increase in the concentration of LEP. In addition, the phosphorylation level of STAT3 increased in all groups, except the 100 ng/mL concentration group. The STAT3 phosphorylation trend and protein expression were different, such that the level of protein phosphorylation was higher than that of the STAT3 protein (p < 0.05). The addition of AG490 reduced the expression of the STAT3 mRNA, STAT3 protein, and STAT3 phosphorylation in the LEP and LEP + PRL groups. Conclusion: Altogether, the results indicated that different concentrations of LEP exerted varying effects on the growth of YMECs and the expression of STAT3, and the activity of STAT3 was primarily activated by JAK2. The addition of LEP can effectively inhibit the downregulation of the JAK2/STAT3 signal pathway by AG490, mitigate its inhibitory effect on the proliferation of YMECs, and reduce apoptosis. We believe that these findings will provide a theoretical and experimental basis for future research in this field.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.