Heme oxygenase-1(HO-1) regulates Golgi stress and attenuates endotoxin-induced acute lung injury through hypoxia inducible factor-1α (HIF-1α)/HO-1 signaling pathway

Li, Xiangyun; Yu, Jianbo; Gong, Lirong; Zhang, Yuan; Dong, Shuying; Shi, Jia; Li, Cui; Li, Yuting; Zhang, Yanfang; Li, Haibo

doi:10.1016/j.freeradbiomed.2021.01.028

Cited by 47 publications

(37 citation statements)

References 62 publications

(39 reference statements)

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“…Herein, H 2 O 2 was employed to induce oxidative stress an in vitro in A549 cells. Our data showed that H 2 O 2 treatment obviously induced oxidative stress and apoptosis in A549 cells, both of which were proved to play an important role in the pathogenesis of ALI [ 18–20 ].…”

Section: Discussionmentioning

confidence: 99%

24-Dehydrocholesterol Reductase alleviates oxidative damage-induced apoptosis in alveolar epithelial cells via regulating Phosphatidylinositol-3-Kinase/Protein Kinase B activation

Yao

et al. 2021

Bioengineered

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Apoptosis of alveolar epithelial cells during acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is a critical pathological event that seriously endangers the health of patients. Suppressing apoptosis of alveolar epithelial cells was shown to alleviate functional damage of lung, and modulator of the reactive oxygen species (ROS)-induced apoptosis becomes a promising approach to the ALI therapy. Previous little studies showed that DHCR24 possessed anti-oxidative and anti-apoptotic property in ALI. Thus, H 2 O 2 was utilized to mimic oxidative damage in vitro in alveolar epithelial cell line A549 in the present study. Our results exhibited that H 2 O 2 treatment of A549 cells reduced the level of SOD and increased the level of ROS. Moreover, H 2 O 2 inhibited Bcl-2 expression in A549 cells, but increased Bax and the activity of Caspase-3. In addition, the apoptosis rate in the H 2 O 2 treatment group also increased significantly. And the expression of 24-dehydrocholesterol reductase (DHCR24) was markedly reduced in the H 2 O 2 treatment group. Overexpression of DHCR24 can remarkably inhibit H 2 O 2 -induced oxidative stress and apoptosis. We found that overexpression of DHCR24 increased the phosphorylation level of PI3K and AKT, however, the PI3K inhibitor LY294002 (LY) eliminated the protective effect of DHCR24 in ALI. DHCR24 was down-regulated in H 2 O 2 -induced ALI, and overexpression of DHCR24 could inhibit H 2 O 2 -induced oxidative stress and apoptosis of A549 cells by activating the Phosphatidylinositol-3-Kinase/Protein Kinase B (PI3K/AKT) signaling pathway. The above exhibited a protective effect of DHCR24 on alveolar epithelial cells exposed to oxidative stress-mediated apoptosis and provided a novel therapeutic method for ALI.

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Section: Discussionmentioning

confidence: 99%

24-Dehydrocholesterol Reductase alleviates oxidative damage-induced apoptosis in alveolar epithelial cells via regulating Phosphatidylinositol-3-Kinase/Protein Kinase B activation

Yao

et al. 2021

Bioengineered

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“…Hypoxia has also been shown to down-or up-regulate enzymes that synthetize nucleotide sugars in the cytoplasm, Golgilocalized glycosyltransferases, fucosyltransferases, and sialyltransferases (Kellokumpu, 2019). Additionally, activation of the hypoxia inducible factor-1α (HIF-1α)/heme-oxygenase-1 (HO-1) pathway by oxidative stress upregulates the expression of Golgi proteins: GM130, Golgin-97 and mannosidase II (Li et al, 2021). It has been proposed that upregulation of Golgi associated genes during cellular stress serves to increase Golgi function as a compensatory mechanism.…”

Section: Golgi Response To Stressmentioning

confidence: 99%

Adaptation of the Golgi Apparatus in Cancer Cell Invasion and Metastasis

Bui

Mejia

Díaz

et al. 2021

Front. Cell Dev. Biol.

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The Golgi apparatus plays a central role in normal cell physiology by promoting cell survival, facilitating proliferation, and enabling cell-cell communication and migration. These roles are partially mediated by well-known Golgi functions, including post-translational modifications, lipid biosynthesis, intracellular trafficking, and protein secretion. In addition, accumulating evidence indicates that the Golgi plays a critical role in sensing and integrating external and internal cues to promote cellular homeostasis. Indeed, the unique structure of the mammalian Golgi can be fine-tuned to adapt different Golgi functions to specific cellular needs. This is particularly relevant in the context of cancer, where unrestrained proliferation and aberrant survival and migration increase the demands in Golgi functions, as well as the need for Golgi-dependent sensing and adaptation to intrinsic and extrinsic stressors. Here, we review and discuss current understanding of how the structure and function of the Golgi apparatus is influenced by oncogenic transformation, and how this adaptation may facilitate cancer cell invasion and metastasis.

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“…Similarly to nrf2, these factors can combine with the cis-regulatory element of the Ho-1 gene, resulting in an increase in Ho-1 expression (21). HiF-1, a redox-responsive transcription factor, induces Ho-1 expression in different cell types under hypoxic conditions (23)(24)(25)(26). However, a specific mutant of HiF-1 lost its dna-binding activity, which resulted in inhibition of HO-1 expression (27).…”

Section: Regulation Of Ho-1 Expressionmentioning

confidence: 99%

Association between HO‑1 gene promoter polymorphisms and diseases (Review)

Sun

Wang

et al. 2021

Mol Med Rep

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Heme oxygenase-1 (Ho-1) is an inducible cytoprotective enzyme that degrades heme into free iron, carbon monoxide and biliverdin, which is then rapidly converted into bilirubin. These degradation products serve an important role in the regulation of inflammation, oxidative stress and apoptosis. While the expression level of Ho-1 is typically low in most cells, it may be highly expressed when induced by a variety of stimulating factors, a process that contributes to the regulation of cell homeostasis. in the 5'-non-coding region of the Ho-1 gene, there are two polymorphic sites, namely the (GT)n dinucleotide and T(-413)a single nucleotide polymorphism sites, which regulate the transcriptional activity of Ho-1. These polymorphisms have been shown to be closely associated with the occurrence and progression of numerous diseases, including cardiovascular, pulmonary, liver and kidney, various types of cancer and viral diseases. The present article reviews the progress that has been made in research on the association between the two types of polymorphisms and these diseases, which is expected to provide novel strategies for the diagnosis, treatment and prognosis of various diseases. Contents1. introduction 2. regulation of Ho-1 expression 3. Ho-1 promoter polymorphism 4. association between Ho-1 gene polymorphism and clinical diseases 5. conclusions and prospects

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Heme oxygenase-1(HO-1) regulates Golgi stress and attenuates endotoxin-induced acute lung injury through hypoxia inducible factor-1α (HIF-1α)/HO-1 signaling pathway

Cited by 47 publications

References 62 publications

24-Dehydrocholesterol Reductase alleviates oxidative damage-induced apoptosis in alveolar epithelial cells via regulating Phosphatidylinositol-3-Kinase/Protein Kinase B activation

24-Dehydrocholesterol Reductase alleviates oxidative damage-induced apoptosis in alveolar epithelial cells via regulating Phosphatidylinositol-3-Kinase/Protein Kinase B activation

Adaptation of the Golgi Apparatus in Cancer Cell Invasion and Metastasis

Association between HO‑1 gene promoter polymorphisms and diseases (Review)

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