Estradiol-induced inhibition of endoplasmic reticulum stress normalizes splenic CD4 + T lymphocytes following hemorrhagic shock
Abstract The aim is to investigate that 17β-estradiol (E2)/estrogen receptors (ERs) activation normalizes splenic CD4 + T lymphocytes proliferation and cytokine production through inhibition of endoplasmic reticulum stress (ERS) following hemorrhage. The results showed that hemorrhagic shock (hemorr...
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2021
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oai:doaj.org-article:a7003911e25a4c46b264cfff998517cb2021-12-02T18:15:33ZEstradiol-induced inhibition of endoplasmic reticulum stress normalizes splenic CD4 + T lymphocytes following hemorrhagic shock10.1038/s41598-021-87159-12045-2322https://doaj.org/article/a7003911e25a4c46b264cfff998517cb2021-04-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-87159-1https://doaj.org/toc/2045-2322Abstract The aim is to investigate that 17β-estradiol (E2)/estrogen receptors (ERs) activation normalizes splenic CD4 + T lymphocytes proliferation and cytokine production through inhibition of endoplasmic reticulum stress (ERS) following hemorrhage. The results showed that hemorrhagic shock (hemorrhage through femoral artery, 38–42 mmHg for 90 min followed by resuscitation of 30 min and subsequent observation period of 180 min) decreased the CD4+ T lymphocytes proliferation and cytokine production after isolation and incubation with Concanavalin A (5 μg/mL) for 48 h, induced the splenic injury with evidences of missed contours of the white pulp, irregular cellular structure, and typical inflammatory cell infiltration, upregulated the expressions of ERS biomarkers 78 kDa glucose-regulated protein (GRP78) and activating transcription factor 6 (ATF6). Either E2, ER-α agonist propyl pyrazole triol (PPT) or ERS inhibitor 4-Phenylbutyric acid administration normalized these parameters, while ER-β agonist diarylpropionitrile administration had no effect. In contrast, administrations of either ERs antagonist ICI 182,780 or G15 abolished the salutary effects of E2. Likewise, ERS inducer tunicamycin induced an adverse effect similarly to that of hemorrhagic shock in sham rats, and aggravated shock-induced effects, also abolished the beneficial effects of E2 and PPT, respectively. Together, the data suggest that E2 produces salutary effects on CD4+ T lymphocytes function, and these effects are mediated by ER-α and GPR30, but not ER-β, and associated with the attenuation of hemorrhagic shock-induced ERS.Peng WangLi-Na JiangChen WangYing LiMeng YinHui-Bo DuHong ZhangZe-Hua FanYan-Xu LiuMeng ZhaoAn-Ling KangDing-Ya FengShu-Guang LiChun-Yu NiuZi-Gang ZhaoNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-11 (2021) |
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Medicine R Science Q |
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Medicine R Science Q Peng Wang Li-Na Jiang Chen Wang Ying Li Meng Yin Hui-Bo Du Hong Zhang Ze-Hua Fan Yan-Xu Liu Meng Zhao An-Ling Kang Ding-Ya Feng Shu-Guang Li Chun-Yu Niu Zi-Gang Zhao Estradiol-induced inhibition of endoplasmic reticulum stress normalizes splenic CD4 + T lymphocytes following hemorrhagic shock |
| description |
Abstract The aim is to investigate that 17β-estradiol (E2)/estrogen receptors (ERs) activation normalizes splenic CD4 + T lymphocytes proliferation and cytokine production through inhibition of endoplasmic reticulum stress (ERS) following hemorrhage. The results showed that hemorrhagic shock (hemorrhage through femoral artery, 38–42 mmHg for 90 min followed by resuscitation of 30 min and subsequent observation period of 180 min) decreased the CD4+ T lymphocytes proliferation and cytokine production after isolation and incubation with Concanavalin A (5 μg/mL) for 48 h, induced the splenic injury with evidences of missed contours of the white pulp, irregular cellular structure, and typical inflammatory cell infiltration, upregulated the expressions of ERS biomarkers 78 kDa glucose-regulated protein (GRP78) and activating transcription factor 6 (ATF6). Either E2, ER-α agonist propyl pyrazole triol (PPT) or ERS inhibitor 4-Phenylbutyric acid administration normalized these parameters, while ER-β agonist diarylpropionitrile administration had no effect. In contrast, administrations of either ERs antagonist ICI 182,780 or G15 abolished the salutary effects of E2. Likewise, ERS inducer tunicamycin induced an adverse effect similarly to that of hemorrhagic shock in sham rats, and aggravated shock-induced effects, also abolished the beneficial effects of E2 and PPT, respectively. Together, the data suggest that E2 produces salutary effects on CD4+ T lymphocytes function, and these effects are mediated by ER-α and GPR30, but not ER-β, and associated with the attenuation of hemorrhagic shock-induced ERS. |
| format |
article |
| author |
Peng Wang Li-Na Jiang Chen Wang Ying Li Meng Yin Hui-Bo Du Hong Zhang Ze-Hua Fan Yan-Xu Liu Meng Zhao An-Ling Kang Ding-Ya Feng Shu-Guang Li Chun-Yu Niu Zi-Gang Zhao |
| author_facet |
Peng Wang Li-Na Jiang Chen Wang Ying Li Meng Yin Hui-Bo Du Hong Zhang Ze-Hua Fan Yan-Xu Liu Meng Zhao An-Ling Kang Ding-Ya Feng Shu-Guang Li Chun-Yu Niu Zi-Gang Zhao |
| author_sort |
Peng Wang |
| title |
Estradiol-induced inhibition of endoplasmic reticulum stress normalizes splenic CD4 + T lymphocytes following hemorrhagic shock |
| title_short |
Estradiol-induced inhibition of endoplasmic reticulum stress normalizes splenic CD4 + T lymphocytes following hemorrhagic shock |
| title_full |
Estradiol-induced inhibition of endoplasmic reticulum stress normalizes splenic CD4 + T lymphocytes following hemorrhagic shock |
| title_fullStr |
Estradiol-induced inhibition of endoplasmic reticulum stress normalizes splenic CD4 + T lymphocytes following hemorrhagic shock |
| title_full_unstemmed |
Estradiol-induced inhibition of endoplasmic reticulum stress normalizes splenic CD4 + T lymphocytes following hemorrhagic shock |
| title_sort |
estradiol-induced inhibition of endoplasmic reticulum stress normalizes splenic cd4 + t lymphocytes following hemorrhagic shock |
| publisher |
Nature Portfolio |
| publishDate |
2021 |
| url |
https://doaj.org/article/a7003911e25a4c46b264cfff998517cb |
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| _version_ |
1718378350980890624 |