MiR- 223 alleviates the heat-stress-induced inhibition of cell proliferation by targeting PRDM1
Abstract Background Heat stress, exacerbated by global warming, has emerged as a significant concern for both the health of dairy cattle and the quality of milk production. In vitro investigations suggest that primary bovine mammary epithelial cells exhibit enhanced levels of programmed cell death w...
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BMC
2025-05-01
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| Series: | BMC Genomics |
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| Online Access: | https://doi.org/10.1186/s12864-025-11567-0 |
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| author | Siqi Xia Huimei Fan Jianghai Xiao Ci Shen Yongping Yan Meigui Wang Tao Tang Wenqiang Sun Jie Wang Xianbo Jia Songjia Lai |
| author_facet | Siqi Xia Huimei Fan Jianghai Xiao Ci Shen Yongping Yan Meigui Wang Tao Tang Wenqiang Sun Jie Wang Xianbo Jia Songjia Lai |
| author_sort | Siqi Xia |
| collection | DOAJ |
| description | Abstract Background Heat stress, exacerbated by global warming, has emerged as a significant concern for both the health of dairy cattle and the quality of milk production. In vitro investigations suggest that primary bovine mammary epithelial cells exhibit enhanced levels of programmed cell death when subjected to elevated ambient temperatures, potentially resulting in a reduction in the total number of mammary epithelial cells within the mammary gland, thereby partially elucidating the diminished milk yield in lactating cows under heat stress. In vivo, heat stress affects both milk synthesis and secretion by directly acting on mammary epithelial cells and by altering hormonal levels and metabolic pathways, which can lead to long-term effects on mammary growth. Future research should focus on elucidating the molecular mechanisms by which heat stress regulates mammary development. Previous studies have demonstrated that heat stress induction results in a significant downregulation of miR- 223 in MAC-T cells; therefore, miR- 223 may play a crucial role in the response to heat stress. Nevertheless, the mechanism by which miR- 223 confers resistance to heat stress in MAC-T remains unclear. Methods Here, to investigate how miR- 223 regulates the proliferation of MAC-T cells, we performed a combination of miRNA- 223 overexpression and inhibition strategies. We transfected MAC-T cells with miR- 223 mimics or inhibitors and evaluated the impact on cell proliferation using CCK- 8 assay, EdU assay, and RT-qPCR. Additionally, MAC-T cells subjected to heat stress were used to investigate how miR- 223 and its target gene regulate cell proliferation under heat stress, either by promoting or alleviating the inhibition of cell proliferation, as assessed by EdU assay, CCK- 8 assay, and RT-qPCR. Results In this study, we investigated the effects of heat stress on MAC-T cell proliferation and gene expression. Bioinformatics analysis identified PRDM1 as a key regulator of proliferation, and it was selected for further investigation. RT-qPCR validated the upregulation of PRDM1 under heat stress, confirming its role in regulating cell proliferation. The results revealed that miR- 223 mimic promoted cell proliferation, with PRDM1 identified as its target gene. Importantly, after heat stress, the miR- 223 mimic or the knockdown of PRDM1 in MAC-T was proven to partially reverse the inhibition of proliferation. Conclusion Consequently, the miR- 223 targeting PRDM1 might be important in alleviating heat-stress-induced inhibition of cell proliferation. This would potentially alleviate heat stress-induced damage to the mammary gland, thereby improving milk production in dairy cows. |
| format | Article |
| id | doaj-art-86eae10067034c74af47c0073b6003cd |
| institution | OA Journals |
| issn | 1471-2164 |
| language | English |
| publishDate | 2025-05-01 |
| publisher | BMC |
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| series | BMC Genomics |
| spelling | doaj-art-86eae10067034c74af47c0073b6003cd2025-08-20T01:51:59ZengBMCBMC Genomics1471-21642025-05-0126111310.1186/s12864-025-11567-0MiR- 223 alleviates the heat-stress-induced inhibition of cell proliferation by targeting PRDM1Siqi Xia0Huimei Fan1Jianghai Xiao2Ci Shen3Yongping Yan4Meigui Wang5Tao Tang6Wenqiang Sun7Jie Wang8Xianbo Jia9Songjia Lai10State Key Laboratory of Swine and Poultry Breeding Industrycollege of Animal Science and Technology, Sichuan Agricultural UniversityState Key Laboratory of Swine and Poultry Breeding Industrycollege of Animal Science and Technology, Sichuan Agricultural UniversityState Key Laboratory of Swine and Poultry Breeding Industrycollege of Animal Science and Technology, Sichuan Agricultural UniversityState Key Laboratory of Swine and Poultry Breeding Industrycollege of Animal Science and Technology, Sichuan Agricultural UniversityState Key Laboratory of Swine and Poultry Breeding Industrycollege of Animal Science and Technology, Sichuan Agricultural UniversityState Key Laboratory of Swine and Poultry Breeding Industrycollege of Animal Science and Technology, Sichuan Agricultural UniversityState Key Laboratory of Swine and Poultry Breeding Industrycollege of Animal Science and Technology, Sichuan Agricultural UniversityState Key Laboratory of Swine and Poultry Breeding Industrycollege of Animal Science and Technology, Sichuan Agricultural UniversityState Key Laboratory of Swine and Poultry Breeding Industrycollege of Animal Science and Technology, Sichuan Agricultural UniversityState Key Laboratory of Swine and Poultry Breeding Industrycollege of Animal Science and Technology, Sichuan Agricultural UniversityState Key Laboratory of Swine and Poultry Breeding Industrycollege of Animal Science and Technology, Sichuan Agricultural UniversityAbstract Background Heat stress, exacerbated by global warming, has emerged as a significant concern for both the health of dairy cattle and the quality of milk production. In vitro investigations suggest that primary bovine mammary epithelial cells exhibit enhanced levels of programmed cell death when subjected to elevated ambient temperatures, potentially resulting in a reduction in the total number of mammary epithelial cells within the mammary gland, thereby partially elucidating the diminished milk yield in lactating cows under heat stress. In vivo, heat stress affects both milk synthesis and secretion by directly acting on mammary epithelial cells and by altering hormonal levels and metabolic pathways, which can lead to long-term effects on mammary growth. Future research should focus on elucidating the molecular mechanisms by which heat stress regulates mammary development. Previous studies have demonstrated that heat stress induction results in a significant downregulation of miR- 223 in MAC-T cells; therefore, miR- 223 may play a crucial role in the response to heat stress. Nevertheless, the mechanism by which miR- 223 confers resistance to heat stress in MAC-T remains unclear. Methods Here, to investigate how miR- 223 regulates the proliferation of MAC-T cells, we performed a combination of miRNA- 223 overexpression and inhibition strategies. We transfected MAC-T cells with miR- 223 mimics or inhibitors and evaluated the impact on cell proliferation using CCK- 8 assay, EdU assay, and RT-qPCR. Additionally, MAC-T cells subjected to heat stress were used to investigate how miR- 223 and its target gene regulate cell proliferation under heat stress, either by promoting or alleviating the inhibition of cell proliferation, as assessed by EdU assay, CCK- 8 assay, and RT-qPCR. Results In this study, we investigated the effects of heat stress on MAC-T cell proliferation and gene expression. Bioinformatics analysis identified PRDM1 as a key regulator of proliferation, and it was selected for further investigation. RT-qPCR validated the upregulation of PRDM1 under heat stress, confirming its role in regulating cell proliferation. The results revealed that miR- 223 mimic promoted cell proliferation, with PRDM1 identified as its target gene. Importantly, after heat stress, the miR- 223 mimic or the knockdown of PRDM1 in MAC-T was proven to partially reverse the inhibition of proliferation. Conclusion Consequently, the miR- 223 targeting PRDM1 might be important in alleviating heat-stress-induced inhibition of cell proliferation. This would potentially alleviate heat stress-induced damage to the mammary gland, thereby improving milk production in dairy cows.https://doi.org/10.1186/s12864-025-11567-0MiR- 223Cell proliferationHeat stressPRDM1 |
| spellingShingle | Siqi Xia Huimei Fan Jianghai Xiao Ci Shen Yongping Yan Meigui Wang Tao Tang Wenqiang Sun Jie Wang Xianbo Jia Songjia Lai MiR- 223 alleviates the heat-stress-induced inhibition of cell proliferation by targeting PRDM1 BMC Genomics MiR- 223 Cell proliferation Heat stress PRDM1 |
| title | MiR- 223 alleviates the heat-stress-induced inhibition of cell proliferation by targeting PRDM1 |
| title_full | MiR- 223 alleviates the heat-stress-induced inhibition of cell proliferation by targeting PRDM1 |
| title_fullStr | MiR- 223 alleviates the heat-stress-induced inhibition of cell proliferation by targeting PRDM1 |
| title_full_unstemmed | MiR- 223 alleviates the heat-stress-induced inhibition of cell proliferation by targeting PRDM1 |
| title_short | MiR- 223 alleviates the heat-stress-induced inhibition of cell proliferation by targeting PRDM1 |
| title_sort | mir 223 alleviates the heat stress induced inhibition of cell proliferation by targeting prdm1 |
| topic | MiR- 223 Cell proliferation Heat stress PRDM1 |
| url | https://doi.org/10.1186/s12864-025-11567-0 |
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