scholarly journals Protective Effects of 5-Aminolevulinic Acid on Heat Stress in Bovine Mammary Epithelial Cells

2020 ◽  
Author(s):  
Md Aminul Islam ◽  
Yoko Noguchi ◽  
Shin Taniguchi ◽  
Shinichi Yonekura
Keyword(s):  
Heat Stress ◽  
Epithelial Cells ◽  
Aminolevulinic Acid ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Protective Effects ◽  
Bovine Mammary Epithelial Cells

scholarly journals 5-ALA Attenuates the Palmitic Acid-Induced ER Stress and Apoptosis in Bovine Mammary Epithelial Cells

Molecules ◽  
2021 ◽  
Vol 26 (4) ◽  
pp. 1183
Author(s):  
Mst Mamuna Sharmin ◽  
Md Aminul Islam ◽  
Itsuki Yamamoto ◽  
Shin Taniguchi ◽  
Shinichi Yonekura
Keyword(s):  
T Cells ◽  
Epithelial Cells ◽  
Palmitic Acid ◽  
Er Stress ◽  
Aminolevulinic Acid ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Protective Effects ◽  
Bovine Mammary Epithelial Cells ◽  
Induced Apoptosis

The conservation of mammary gland physiology by maintaining the maximum number of mammary epithelial cells (MECs) is of the utmost importance for the optimum amount of milk production. In a state of negative energy balance, palmitic acid (PA) reduces the number of bovine MECs. However, there is no effective strategy against PA-induced apoptosis of MECs. In the present study, 5-aminolevulinic acid (5-ALA) was established as a remedial agent against PA-induced apoptosis of MAC-T cells (an established line of bovine MECs). In PA-treated cells, the apoptosis-related genes BCL2 and BAX were down- and upregulated, respectively. The elevated expression of major genes of the unfolded protein response (UPR), such as CHOP, a proapoptotic marker (C/EBP homologous protein), reduced the viability of PA-treated MAC-T cells. In contrast, 5-ALA pretreatment increased and decreased BCL2 and BAX expression, respectively. Moreover, cleaved caspase-3 protein expression was significantly reduced in the 5-ALA-pretreated group in comparison with the PA group. The downregulation of major UPR-related genes, including CHOP, extended the viability of MAC-T cells pretreated with 5-ALA and also reduced the enhanced intensity of the PA-induced expression of phospho-protein kinase R-like ER kinase. Moreover, the enhanced expression of HO-1 (antioxidant gene heme oxygenase) by 5-ALA reduced PA-induced oxidative stress (OxS). HO-1 is not only protective against OxS but also effective against ER stress. Collectively, these findings offer new insights into the protective effects of 5-ALA against PA-induced apoptosis of bovine MECs.

Effect of heat stress on the interaction of Streptococcus uberis with bovine mammary epithelial cells

2018 ◽  
Vol 85 (1) ◽  
pp. 53-56 ◽  
Author(s):  
Raúl A. Almeida ◽  
Oudessa Kerro-Dego ◽  
Agustín G. Rius
Keyword(s):  
Heat Stress ◽  
Epithelial Cells ◽  
Mammary Epithelial Cells ◽  
Cell Metabolism ◽  
Membrane Damage ◽  
Membrane Integrity ◽  
Mammary Epithelial ◽  
Host Cells ◽  
Bovine Mammary Epithelial Cells ◽  
Streptococcus Uberis

Heat stress (HS) negatively affects milk production and has been associated with decreased immune function, and increased rate of intramammary infections (IMI). Research has shown that HS affects gene expression, cell cycle, and cell metabolism in bovine mammary epithelial cells (BMEC). Since BMEC are an initial target of mastitis pathogens, we studied adherence to and internalisation of S. uberis into HS-BMEC, as well as the effect that this interaction has on host cells by measuring HS-BMEC viability and membrane integrity. Results reported in this Research Communication showed that HS reduced cell viability and induced membrane damage. However, these pathological changes, as well as the rate of adherence and internalisation of S. uberis into BMEC, were augmented when S. uberis was cocultured with HS-BMEC. These results may help to understand the pathogenesis of S. uberis IMI as well as the increased susceptibility of mammary glands to IMI in cows subjected to HS.

scholarly journals MicroRNA-216b inhibits heat stress-induced cell apoptosis by targeting Fas in bovine mammary epithelial cells

2018 ◽  
Vol 23 (5) ◽  
pp. 921-931 ◽  
Author(s):  
Mingcheng Cai ◽  
Yongsong Hu ◽  
Tianhao Zheng ◽  
Hongbing He ◽  
Wudian Xiao ◽  
...  
Keyword(s):  
Heat Stress ◽  
Epithelial Cells ◽  
Cell Apoptosis ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Bovine Mammary Epithelial Cells

scholarly journals SIRT3 protects bovine mammary epithelial cells from heat stress damage by activating the AMPK signaling pathway

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Xiao-Chun Sun ◽  
Yue Wang ◽  
Han-Fang Zeng ◽  
Yu-Meng Xi ◽  
Hong Lin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heat Stress ◽  
High Temperature ◽  
Epithelial Cells ◽  
Mammary Epithelial Cells ◽  
Mitochondrial Fission ◽  
Mammary Epithelial ◽  
Bovine Mammary Epithelial Cells ◽  
Ampk Signaling ◽  
Stress Damage

AbstractWith global warming, heat stress has become an important challenge for the global dairy industry. Sirtuin 3 (SIRT3), an important mitochondrial NAD+dependent decarboxylase and a major regulator of cellular energy metabolism and antioxidant defense, is integral to maintaining normal mitochondrial function. The aim of this study was to assess the protective effect of SIRT3 on damage to bovine mammary epithelial cells (BMECs) induced by heat stress and to explore its potential mechanism. Our results indicate that SIRT3 is significantly downregulated in heat-stressed mammary tissue and high-temperature-treated BMECs. SIRT3 knockdown significantly increased the expression of HSP70, Bax, and cleaved-caspase 3 and inhibited the production of antioxidases, thus promoting ROS production and cell apoptosis in BMECs. In addition, SIRT3 knockdown can aggravate mitochondrial damage by mediating the expression of genes related to mitochondrial fission and fusion, including dynamin-related protein 1, mitochondrial fission 1 protein, and mitochondrial fusion proteins 1and 2. In addition, SIRT3 knockdown substantially decreased AMPK phosphorylation in BMECs. In contrast, SIRT3 overexpression in high-temperature treatment had the opposite effect to SIRT3 knockdown in BMECs. SIRT3 overexpression reduced mitochondrial damage and weakened the oxidative stress response of BMECs induced by heat stress and promoted the phosphorylation of AMPK. Taken together, our results indicate that SIRT3 can protect BMECs from heat stress damage through the AMPK signaling pathway. Therefore, the reduction of oxidative stress by SIRT3 may be the primary molecular mechanism underlying resistance to heat stress in summer cows.

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