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      Protective Effect and Mechanism of Bone Morphogenetic Protein-4 on Apoptosis of Human Lens Epithelium Cells under Oxidative Stress

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          Abstract

          Bone morphogenetic proteins (BMPs), a member of the transforming growth factor β (TGF- β) superfamily, are abundant in human ocular tissues and play an important role in lens development. Targeted deletion of BMP-4 in mice results in failure of lens placode formation. Following lens maturation, the formation of senile cataracts is demonstrably associated with free radical-related oxidative stress. Previous studies reported that BMPs play an antiapoptotic role in cells under oxidative stress, and the BMP-4 signal is important in inflammation regulation and homeostasis. BMP-4 evidently suppressed the apoptosis of human lens epithelial cells (HLECS) under oxidative stress induced by H 2O 2. This protective antiapoptotic effect is partly due to a decrease in caspase-3 activity and reactive oxygen species (ROS) level. Furthermore, the expression of activating transcription factor- (ATF-) 6 and Krüppel-like factor- (KLF-) 6 increased under oxidative stress and decreased after BMP-4 treatment.

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          Isolation of mitochondria-associated membranes and mitochondria from animal tissues and cells.

          Mariusz R. Wieckowski, Carlotta Giorgi, Magdalena Lebiedzinska … (2009)
          Many cellular processes require the proper cooperation between mitochondria and the endoplasmic reticulum (ER). Several recent works show that their functional interactions rely on dynamic structural contacts between both organelles. Such contacts, called mitochondria-associated membranes (MAMs), are crucial for the synthesis and intracellular transport of phospholipids, as well as for intracellular Ca(2+) signaling and for the determination of mitochondrial structure. Although several techniques are available to isolate mitochondria, only few are specifically tuned to the isolation of MAM, containing unique regions of ER membranes attached to the outer mitochondrial membrane and mitochondria without contamination from other organelles (i.e., pure mitochondria). Here we provide optimized protocols to isolate these fractions from tissues and cells. These procedures require 4-5 h and can be easily modified and adapted to different tissues and cell types.
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            Mitochondrial Dysfunction and Myocardial Ischemia-Reperfusion: Implications for Novel Therapies.

            Charles Hoppel, Bernard Tandler, Qun Chen … (2017)
            Mitochondria have emerged as key participants in and regulators of myocardial injury during ischemia and reperfusion. This review examines the sites of damage to cardiac mitochondria during ischemia and focuses on the impact of these defects. The concept that mitochondrial damage during ischemia leads to cardiac injury during reperfusion is addressed. The mechanisms that translate ischemic mitochondrial injury into cellular damage, during both ischemia and early reperfusion, are examined. Next, we discuss strategies that modulate and counteract these mechanisms of mitochondrial-driven injury. The new concept that mitochondria are not merely stochastic sites of oxidative and calcium-mediated injury but that they activate cellular responses of mitochondrial remodeling and cellular reactions that modulate the balance between cell death and recovery is reviewed, and the therapeutic implications of this concept are discussed.
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              Biology of endoplasmic reticulum stress in the heart.

              Jody Groenendyk, Pradeep Kumar Sreenivasaiah, Do Han Kim … (2010)
              The endoplasmic reticulum (ER) is a multifunctional intracellular organelle supporting many processes required by virtually every mammalian cell, including cardiomyocytes. It performs diverse functions, including protein synthesis, translocation across the membrane, integration into the membrane, folding, posttranslational modification including N-linked glycosylation, and synthesis of phospholipids and steroids on the cytoplasmic side of the ER membrane, and regulation of Ca(2+) homeostasis. Perturbation of ER-associated functions results in ER stress via the activation of complex cytoplasmic and nuclear signaling pathways, collectively termed the unfolded protein response (UPR) (also known as misfolded protein response), leading to upregulation of expression of ER resident chaperones, inhibition of protein synthesis and activation of protein degradation. The UPR has been associated with numerous human pathologies, and it may play an important role in the pathophysiology of the heart. ER stress responses, ER Ca(2+) buffering, and protein and lipid turnover impact many cardiac functions, including energy metabolism, cardiogenesis, ischemic/reperfusion, cardiomyopathies, and heart failure. ER proteins and ER stress-associated pathways may play a role in the development of novel UPR-targeted therapies for cardiovascular diseases.
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                Author and article information

                Contributors
                Li-Jie Dong:
                ORCID: https://orcid.org/0000-0001-9720-8227
                Journal
                Journal ID (nlm-ta): Biomed Res Int
                Journal ID (iso-abbrev): Biomed Res Int
                Journal ID (publisher-id): BMRI
                Title: BioMed Research International
                Publisher: Hindawi
                ISSN (Print): 2314-6133
                ISSN (Electronic): 2314-6141
                Publication date Collection: 2021
                Publication date (Electronic): 29 January 2021
                Volume: 2021
                Electronic Location Identifier: 8109134
                Affiliations
                1Tianjin Key Laboratory of Retinal Functions and Diseases, Eye Institute and School of Optometry, Tianjin Medical University Eye Hospital, Tianjin 300384, China
                2Eye Hospital, Nanjing Medical University, Nanjing, China
                3First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, China
                Author notes

                Academic Editor: Claudio Acu a Castillo

                Author information
                https://orcid.org/0000-0002-0947-1541
                https://orcid.org/0000-0001-9720-8227
                Article
                DOI: 10.1155/2021/8109134
                PMC ID: 7864734
                PubMed ID: 33575344
                SO-VID: 38a7530b-a394-4a46-91c2-a60da131b918
                Copyright © Copyright © 2021 Bei Du et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 5 July 2020
                Date revision received : 15 January 2021
                Date accepted : 21 January 2021
                Funding
                Funded by: Tianjin Medical University
                Award ID: YDYYRCXM-C2018-02
                Funded by: Young Medical Talents Program of Tianjin Health and Family Planning Commission
                Funded by: Tianjin Science and Technology Committee
                Award ID: 15JCYBJC24900
                Funded by: Science and Technology Project of Health Commission of Tianjin Binhai New Area
                Award ID: 2019BWKY019
                Funded by: Tianjin Clinical Key Discipline Project
                Award ID: TJLCZDXKQ012
                Funded by: Clinical Research Fund of Tianjin Medical University Eye Institute
                Award ID: 16YKYJS003
                Funded by: National Natural Science Foundation of China
                Award ID: 81570872
                Categories
                Subject: Research Article

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