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Estradiol-induced inhibition of endoplasmic reticulum stress normalizes splenic CD4 + T lymphocytes following hemorrhagic shock. | LitMetric

AI Article Synopsis

  • The study investigates how 17β-estradiol (E2) and estrogen receptors (ERs) influence the function of CD4+ T lymphocytes after a hemorrhagic shock event, focusing on the reduction of endoplasmic reticulum stress (ERS).
  • Results show that hemorrhagic shock decreases CD4+ T lymphocyte activity and disrupts splenic structure, correlating with increased ERS biomarkers, but E2 can restore these functions when administered.
  • E2's beneficial effects are linked to ER-α and GPR30 activation, while ER-β appears ineffective; ER antagonists and ERS inducers negate these positive outcomes.

Article 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.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8021564PMC
http://dx.doi.org/10.1038/s41598-021-87159-1DOI Listing

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