دورية أكاديمية
Sestrin2 Protects Human Lens Epithelial Cells (HLECs) Against Apoptosis in Cataracts Formation: Interaction Between Endoplasmic Reticulum (ER) Stress and Oxidative Stress (OS) is Involved.
| العنوان: | Sestrin2 Protects Human Lens Epithelial Cells (HLECs) Against Apoptosis in Cataracts Formation: Interaction Between Endoplasmic Reticulum (ER) Stress and Oxidative Stress (OS) is Involved. |
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| المؤلفون: | Sun D; Chinese PLA Medical School, Beijing, China.; Senior Department of Ophthalmology, 3rd Medical Center of Chinese, PLA General Hospital, Beijing, China., Cui H; Chinese PLA Medical School, Beijing, China.; Senior Department of Ophthalmology, 3rd Medical Center of Chinese, PLA General Hospital, Beijing, China., Rong L; Senior Department of Ophthalmology, 3rd Medical Center of Chinese, PLA General Hospital, Beijing, China., Ma T; Senior Department of Ophthalmology, 3rd Medical Center of Chinese, PLA General Hospital, Beijing, China., Li X; Chinese PLA Medical School, Beijing, China.; Senior Department of Ophthalmology, 3rd Medical Center of Chinese, PLA General Hospital, Beijing, China., Ye Z; Senior Department of Ophthalmology, 3rd Medical Center of Chinese, PLA General Hospital, Beijing, China., Li Z; Senior Department of Ophthalmology, 3rd Medical Center of Chinese, PLA General Hospital, Beijing, China. |
| المصدر: | Current eye research [Curr Eye Res] 2024 Sep; Vol. 49 (9), pp. 949-960. Date of Electronic Publication: 2024 May 23. |
| نوع المنشور: | Journal Article |
| اللغة: | English |
| بيانات الدورية: | Publisher: Informa Healthcare Country of Publication: England NLM ID: 8104312 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1460-2202 (Electronic) Linking ISSN: 02713683 NLM ISO Abbreviation: Curr Eye Res Subsets: MEDLINE |
| أسماء مطبوعة: | Publication: London : Informa Healthcare Original Publication: London : IRL Press, [c1981- |
| مواضيع طبية MeSH: | Endoplasmic Reticulum Stress*/physiology , Apoptosis* , Oxidative Stress* , Lens, Crystalline*/metabolism , Lens, Crystalline*/pathology , Endoplasmic Reticulum Chaperone BiP* , Epithelial Cells*/metabolism , Cataract*/metabolism , Cataract*/pathology , Cataract*/genetics , Blotting, Western* , Nuclear Proteins*/metabolism , Nuclear Proteins*/genetics, Humans ; Cells, Cultured ; Reactive Oxygen Species/metabolism ; Real-Time Polymerase Chain Reaction ; Flow Cytometry ; NF-E2-Related Factor 2/metabolism ; NF-E2-Related Factor 2/genetics ; Gene Expression Regulation ; Sestrins |
| مستخلص: | Purpose: To explore the correlation of endoplasmic reticulum stress (ERS) and oxidative stress (OS), and the protective effect of Sestrin2 (SESN2) on human lens epithelial cells (HLECs). Methods: Tunicamycin (TM) was used to induce ERS in HLECs. 4-Phenylbutyric acid (4-PBA) was used to inhibit ERS. Eupatilin applied to HLECs as SESN2 agonist. SESN2 expression was knocked down via si-RNA in HLECs. The morphological changes of HLECs were observed by microscope. ER-tracker to evaluate ERS, ROS production assay to measure ROS, flow cytometry to calculate cell apoptosis rate. Immunofluorescence to observe Nrf2 translocation, and effects of TM or EUP on SESN2. Western blot and qPCR were used to evaluate the expression of GRP78, PERK, ATF4, CHOP, Nrf2, and SESN2 expression in HLECs with different treatment groups. Results: ERS can elevate the expression of ROS and Nrf2 to induce OS. Upregulation of SESN2 was observed in ERS-mediate OS. Overexpression of SESN2 can reduce the overexpression of ERS-related protein GRP78, PERK, ATF4, proapoptotic protein CHOP, OS-related protein Nrf2, as well as ROS, and alleviate ERS injury at the same time. Whereas knockdown of SESN2 can upregulate the expression of GRP78, PERK, ATF4, CHOP, Nrf2, ROS, and deteriorate ERS damage. Conclusions: ERS can induce OS, they form a vicious cycle to induce apoptosis in HLECs, which may contribute to cataract formation. SESN2 could protect HLECs against the apoptosis by regulating the vicious cycle between ERS and OS. |
| فهرسة مساهمة: | Keywords: Endoplasmic reticulum stress; Sestrin2; apoptosis; human lens epithelial cells; oxidative stress |
| المشرفين على المادة: | 0 (SESN2 protein, human) 0 (HSPA5 protein, human) 0 (Endoplasmic Reticulum Chaperone BiP) 0 (Nuclear Proteins) 0 (Reactive Oxygen Species) 0 (NF-E2-Related Factor 2) 0 (NFE2L2 protein, human) 0 (Sestrins) |
| تواريخ الأحداث: | Date Created: 20240523 Date Completed: 20240809 Latest Revision: 20240826 |
| رمز التحديث: | 20240826 |
| DOI: | 10.1080/02713683.2024.2352058 |
| PMID: | 38780907 |
| قاعدة البيانات: | MEDLINE |
PDF full text from Publisher | تدمد: | 1460-2202 |
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| DOI: | 10.1080/02713683.2024.2352058 |